PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 19002263-7 2008 Utilizing the validated CIMP marker panel (including the 5 markers), multivariate logistic regression demonstrated that CIMP-high was independently associated with older age, proximal location, poor differentiation, MSI-high, BRAF mutation, and inversely with LINE-1 hypomethylation and beta-catenin (CTNNB1) activation. Cyclic IMP 120-124 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 226-230 19002263-7 2008 Utilizing the validated CIMP marker panel (including the 5 markers), multivariate logistic regression demonstrated that CIMP-high was independently associated with older age, proximal location, poor differentiation, MSI-high, BRAF mutation, and inversely with LINE-1 hypomethylation and beta-catenin (CTNNB1) activation. Cyclic IMP 120-124 catenin beta 1 Homo sapiens 287-299 19002263-7 2008 Utilizing the validated CIMP marker panel (including the 5 markers), multivariate logistic regression demonstrated that CIMP-high was independently associated with older age, proximal location, poor differentiation, MSI-high, BRAF mutation, and inversely with LINE-1 hypomethylation and beta-catenin (CTNNB1) activation. Cyclic IMP 120-124 catenin beta 1 Homo sapiens 301-307 19002263-12 2008 Our data also suggest that KRAS mutation is related with a random CpG island methylation pattern which may lead to CIMP-low tumors. Cyclic IMP 115-119 KRAS proto-oncogene, GTPase Homo sapiens 27-31 18084616-5 2007 IGFBP3 methylation was far more frequent in non-MSI-high CIMP-high tumors (85% = 35/41) than in MSI-high CIMP-high (49% = 44/90, P < .0001), MSI-high non-CIMP-high (17% = 6/36, P < .0001), and non-MSI-high non-CIMP-high tumors (22% = 152/680, P < .0001). Cyclic IMP 57-61 insulin like growth factor binding protein 3 Homo sapiens 0-6 18084616-7 2007 IGFBP3 methylation was associated inversely with TGFBR2 mutation in MSI-high non-CIMP-high tumors (P = .02). Cyclic IMP 81-85 insulin like growth factor binding protein 3 Homo sapiens 0-6 18084616-7 2007 IGFBP3 methylation was associated inversely with TGFBR2 mutation in MSI-high non-CIMP-high tumors (P = .02). Cyclic IMP 81-85 transforming growth factor beta receptor 2 Homo sapiens 49-55 18084616-8 2007 In conclusion, IGFBP3 methylation is inversely associated with MSI in CIMP-high colorectal cancers, and this relationship is limited to p53-negative tumors. Cyclic IMP 70-74 insulin like growth factor binding protein 3 Homo sapiens 15-21 18003927-9 2007 CIMP-negative cases have a high rate of p53 mutations (71%) and lower rates of MSI (12%) or mutations of BRAF (2%) or KRAS (33%). Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 105-109 18003927-9 2007 CIMP-negative cases have a high rate of p53 mutations (71%) and lower rates of MSI (12%) or mutations of BRAF (2%) or KRAS (33%). Cyclic IMP 0-4 tumor protein p53 Homo sapiens 40-43 18003927-9 2007 CIMP-negative cases have a high rate of p53 mutations (71%) and lower rates of MSI (12%) or mutations of BRAF (2%) or KRAS (33%). Cyclic IMP 0-4 KRAS proto-oncogene, GTPase Homo sapiens 118-122 18000779-12 2007 Simultaneous multiple genes hypermethylation represented by CIMP may be an epigenetic mechanism competing with the genetic mechanism of CIN. Cyclic IMP 60-64 pyridoxal phosphatase Homo sapiens 136-139 17339237-8 2007 Among the CIMP-low group, tumours with both MGMT methylation and loss were far more frequent in MSI-low tumours (67%, 12/18) than MSI-high tumours (5.6%, 1/18; p = 0.0003) and microsatellite stable (MSS) tumours (33%, 52/160; p = 0.008). Cyclic IMP 10-14 O-6-methylguanine-DNA methyltransferase Homo sapiens 44-48 17339237-10 2007 CONCLUSION: The relationship between MGMT methylation/silencing and MSI-low is limited to only CIMP-low tumours, supporting the suggestion that CIMP-low in colorectal cancer may be a different molecular phenotype from CIMP-high and CIMP-0. Cyclic IMP 95-99 O-6-methylguanine-DNA methyltransferase Homo sapiens 37-41 17339237-10 2007 CONCLUSION: The relationship between MGMT methylation/silencing and MSI-low is limited to only CIMP-low tumours, supporting the suggestion that CIMP-low in colorectal cancer may be a different molecular phenotype from CIMP-high and CIMP-0. Cyclic IMP 144-148 O-6-methylguanine-DNA methyltransferase Homo sapiens 37-41 17339237-10 2007 CONCLUSION: The relationship between MGMT methylation/silencing and MSI-low is limited to only CIMP-low tumours, supporting the suggestion that CIMP-low in colorectal cancer may be a different molecular phenotype from CIMP-high and CIMP-0. Cyclic IMP 144-148 RB binding protein 4, chromatin remodeling factor Homo sapiens 68-71 17339237-11 2007 Our data support a molecular difference between MSI-low and MSS in colorectal cancer, and a possible link between CIMP-low, MSI-low, MGMT methylation/loss and KRAS mutation. Cyclic IMP 114-118 KRAS proto-oncogene, GTPase Homo sapiens 159-163 17710160-8 2007 MSI-high, CIMP-high, and BRAF mutation were associated inversely with cytoplasmic and nuclear beta-catenin expressions (i.e., beta-catenin activation) and associated positively with membrane expression. Cyclic IMP 10-14 catenin beta 1 Homo sapiens 94-106 17947473-12 2007 Concurrent methylation of two or more genes of the CIMP-associated subset (MINT1, MINT31, p14ARF and p16INK4a) defined a group of cases with markedly reduced overall survival and hazard ratio was 3.22 (P < 0.0001 in multivariate analyses). Cyclic IMP 51-55 amyloid beta precursor protein binding family A member 1 Homo sapiens 75-80 17947473-12 2007 Concurrent methylation of two or more genes of the CIMP-associated subset (MINT1, MINT31, p14ARF and p16INK4a) defined a group of cases with markedly reduced overall survival and hazard ratio was 3.22 (P < 0.0001 in multivariate analyses). Cyclic IMP 51-55 cyclin dependent kinase inhibitor 2A Homo sapiens 90-96 17947473-12 2007 Concurrent methylation of two or more genes of the CIMP-associated subset (MINT1, MINT31, p14ARF and p16INK4a) defined a group of cases with markedly reduced overall survival and hazard ratio was 3.22 (P < 0.0001 in multivariate analyses). Cyclic IMP 51-55 cyclin dependent kinase inhibitor 2A Homo sapiens 101-109 17898258-8 2007 The rates for the CIMP-related genes were 25% for RUNX3, 5% for NEUROG1 and CACNA1G, and 0 for SOCS-1 and IGF-2. Cyclic IMP 18-22 RUNX family transcription factor 3 Homo sapiens 50-55 17898258-8 2007 The rates for the CIMP-related genes were 25% for RUNX3, 5% for NEUROG1 and CACNA1G, and 0 for SOCS-1 and IGF-2. Cyclic IMP 18-22 neurogenin 1 Homo sapiens 64-71 17898258-8 2007 The rates for the CIMP-related genes were 25% for RUNX3, 5% for NEUROG1 and CACNA1G, and 0 for SOCS-1 and IGF-2. Cyclic IMP 18-22 calcium voltage-gated channel subunit alpha1 G Homo sapiens 76-83 17898258-8 2007 The rates for the CIMP-related genes were 25% for RUNX3, 5% for NEUROG1 and CACNA1G, and 0 for SOCS-1 and IGF-2. Cyclic IMP 18-22 suppressor of cytokine signaling 1 Homo sapiens 95-101 17898258-8 2007 The rates for the CIMP-related genes were 25% for RUNX3, 5% for NEUROG1 and CACNA1G, and 0 for SOCS-1 and IGF-2. Cyclic IMP 18-22 insulin like growth factor 2 Homo sapiens 106-111 17449906-4 2007 CIMP- or CIMP+ phenotype was based on five CpG island markers: MINT1, MINT2, MINT31, p16 and MLH1. Cyclic IMP 0-4 amyloid beta precursor protein binding family A member 1 Homo sapiens 63-68 17591929-6 2007 A CIMP-high cutoff was set at > or = 6/8 or > or = 5/8 methylated promoters, based on tumor distribution and BRAF/KRAS mutation frequencies. Cyclic IMP 2-6 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 115-119 17591929-6 2007 A CIMP-high cutoff was set at > or = 6/8 or > or = 5/8 methylated promoters, based on tumor distribution and BRAF/KRAS mutation frequencies. Cyclic IMP 2-6 KRAS proto-oncogene, GTPase Homo sapiens 120-124 17710160-5 2007 However, no study has examined the relationship between beta-catenin activation and CIMP status. Cyclic IMP 84-88 catenin beta 1 Homo sapiens 56-68 17710160-8 2007 MSI-high, CIMP-high, and BRAF mutation were associated inversely with cytoplasmic and nuclear beta-catenin expressions (i.e., beta-catenin activation) and associated positively with membrane expression. Cyclic IMP 10-14 catenin beta 1 Homo sapiens 126-138 17710160-9 2007 The inverse relation between beta-catenin activation and CIMP was independent of MSI. Cyclic IMP 57-61 catenin beta 1 Homo sapiens 29-41 17710160-10 2007 COX-2 overexpression correlated with cytoplasmic beta-catenin expression (even after tumors were stratified by CIMP status), but did not correlate significantly with nuclear or membrane expression. Cyclic IMP 111-115 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 17710160-11 2007 In conclusion, beta-catenin activation is inversely associated with CIMP-high independent of MSI status. Cyclic IMP 68-72 catenin beta 1 Homo sapiens 15-27 16699497-10 2006 BRAF mutations were present in only CIMP-positive tumors. Cyclic IMP 36-40 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 0-4 17474983-3 2007 A recent study has shown an inverse correlation between CIN and CIMP (determined by MINTs, p16, p14 and MLH1 methylation) in colorectal cancer. Cyclic IMP 64-68 cyclin dependent kinase inhibitor 2A Homo sapiens 91-94 17474983-3 2007 A recent study has shown an inverse correlation between CIN and CIMP (determined by MINTs, p16, p14 and MLH1 methylation) in colorectal cancer. Cyclic IMP 64-68 cyclin dependent kinase inhibitor 2A Homo sapiens 96-99 17474983-3 2007 A recent study has shown an inverse correlation between CIN and CIMP (determined by MINTs, p16, p14 and MLH1 methylation) in colorectal cancer. Cyclic IMP 64-68 mutL homolog 1 Homo sapiens 104-108 17474983-5 2007 METHODS: Utilizing MethyLight technology (real-time PCR), we quantified DNA methylation in 8 CIMP-specific promoters {CACNA1G, CDKN2A (p16), CRABP1, IGF2, MLH1, NEUROG1, RUNX3 and SOCS1} in 758 non-MSI-high colorectal cancers obtained from two large prospective cohorts. Cyclic IMP 93-97 cyclin dependent kinase inhibitor 2A Homo sapiens 135-138 17270239-6 2007 After stratification by sex, location, tumor differentiation, RUNX3 status, KRAS/BRAF status, or p53 status, CIMP-high was persistently correlated with TGFBR2 mutation. Cyclic IMP 109-113 RUNX family transcription factor 3 Homo sapiens 62-67 17270239-6 2007 After stratification by sex, location, tumor differentiation, RUNX3 status, KRAS/BRAF status, or p53 status, CIMP-high was persistently correlated with TGFBR2 mutation. Cyclic IMP 109-113 KRAS proto-oncogene, GTPase Homo sapiens 76-80 17270239-6 2007 After stratification by sex, location, tumor differentiation, RUNX3 status, KRAS/BRAF status, or p53 status, CIMP-high was persistently correlated with TGFBR2 mutation. Cyclic IMP 109-113 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 81-85 17270239-6 2007 After stratification by sex, location, tumor differentiation, RUNX3 status, KRAS/BRAF status, or p53 status, CIMP-high was persistently correlated with TGFBR2 mutation. Cyclic IMP 109-113 tumor protein p53 Homo sapiens 97-100 17270239-6 2007 After stratification by sex, location, tumor differentiation, RUNX3 status, KRAS/BRAF status, or p53 status, CIMP-high was persistently correlated with TGFBR2 mutation. Cyclic IMP 109-113 transforming growth factor beta receptor 2 Homo sapiens 152-158 16759796-4 2007 Among the remaining cases without N-myc amplification, CIMP(+) cases (n=27) had a poorer OS (HR=4.5; P=0.02) and DFS (HR=5.2; P<0.0001) than CIMP(-) cases (n=95). Cyclic IMP 55-59 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 34-39 17289889-9 2007 There is a significant association between CIMP and methylation of P14, P15, P16, ER, RSAAF1A, and WT1 (P<0.05) and serum alpha-fetoprotein (AFP) level (P=0.017). Cyclic IMP 43-47 cyclin dependent kinase inhibitor 2A Homo sapiens 67-70 17289889-9 2007 There is a significant association between CIMP and methylation of P14, P15, P16, ER, RSAAF1A, and WT1 (P<0.05) and serum alpha-fetoprotein (AFP) level (P=0.017). Cyclic IMP 43-47 cyclin dependent kinase inhibitor 2B Homo sapiens 72-75 17289889-9 2007 There is a significant association between CIMP and methylation of P14, P15, P16, ER, RSAAF1A, and WT1 (P<0.05) and serum alpha-fetoprotein (AFP) level (P=0.017). Cyclic IMP 43-47 cyclin dependent kinase inhibitor 2A Homo sapiens 77-80 17289889-9 2007 There is a significant association between CIMP and methylation of P14, P15, P16, ER, RSAAF1A, and WT1 (P<0.05) and serum alpha-fetoprotein (AFP) level (P=0.017). Cyclic IMP 43-47 WT1 transcription factor Homo sapiens 99-102 17289889-9 2007 There is a significant association between CIMP and methylation of P14, P15, P16, ER, RSAAF1A, and WT1 (P<0.05) and serum alpha-fetoprotein (AFP) level (P=0.017). Cyclic IMP 43-47 alpha fetoprotein Homo sapiens 125-142 17289889-9 2007 There is a significant association between CIMP and methylation of P14, P15, P16, ER, RSAAF1A, and WT1 (P<0.05) and serum alpha-fetoprotein (AFP) level (P=0.017). Cyclic IMP 43-47 alpha fetoprotein Homo sapiens 144-147 17289889-12 2007 CONCLUSIONS: Positive correlation of CIMP and AFP levels in HCC suggests that CIMP can serve as a molecular marker of late-stage HCC development. Cyclic IMP 78-82 alpha fetoprotein Homo sapiens 46-49 17087942-12 2007 CONCLUSIONS: The associations between methylation frequencies at CIMP-related markers and MSI or MSI-/LOH- sporadic CRCs suggest that the majority of these tumors evolve through CIMP. Cyclic IMP 65-69 RB binding protein 4, chromatin remodeling factor Homo sapiens 90-93 17087942-12 2007 CONCLUSIONS: The associations between methylation frequencies at CIMP-related markers and MSI or MSI-/LOH- sporadic CRCs suggest that the majority of these tumors evolve through CIMP. Cyclic IMP 65-69 RB binding protein 4, chromatin remodeling factor Homo sapiens 97-100 17087942-12 2007 CONCLUSIONS: The associations between methylation frequencies at CIMP-related markers and MSI or MSI-/LOH- sporadic CRCs suggest that the majority of these tumors evolve through CIMP. Cyclic IMP 178-182 RB binding protein 4, chromatin remodeling factor Homo sapiens 90-93 17087942-12 2007 CONCLUSIONS: The associations between methylation frequencies at CIMP-related markers and MSI or MSI-/LOH- sporadic CRCs suggest that the majority of these tumors evolve through CIMP. Cyclic IMP 178-182 RB binding protein 4, chromatin remodeling factor Homo sapiens 97-100 17086168-0 2007 Loss of nuclear p27 (CDKN1B/KIP1) in colorectal cancer is correlated with microsatellite instability and CIMP. Cyclic IMP 105-109 interferon alpha inducible protein 27 Homo sapiens 16-19 17086168-0 2007 Loss of nuclear p27 (CDKN1B/KIP1) in colorectal cancer is correlated with microsatellite instability and CIMP. Cyclic IMP 105-109 cyclin dependent kinase inhibitor 1B Homo sapiens 21-27 17086168-0 2007 Loss of nuclear p27 (CDKN1B/KIP1) in colorectal cancer is correlated with microsatellite instability and CIMP. Cyclic IMP 105-109 cyclin dependent kinase inhibitor 1B Homo sapiens 28-32 17086168-4 2007 However, no study to date has examined relationship between p27 and CIMP status in colorectal cancer. Cyclic IMP 68-72 interferon alpha inducible protein 27 Homo sapiens 60-63 17086168-8 2007 Loss of nuclear p27 expression {observed in 231 tumors (33%)} was significantly associated with CIMP-high, MSI-H and BRAF mutations, and these associations were much more pronounced among p53-negative tumors than p53-positive tumors. Cyclic IMP 96-100 interferon alpha inducible protein 27 Homo sapiens 16-19 17086168-9 2007 When CIMP-high and non-CIMP-high tumors were stratified by MSI status (or KRAS and BRAF status), CIMP-high and MSI-H (but not BRAF mutations) were still significantly associated with nuclear p27 loss. Cyclic IMP 5-9 RB binding protein 4, chromatin remodeling factor Homo sapiens 59-62 17086168-9 2007 When CIMP-high and non-CIMP-high tumors were stratified by MSI status (or KRAS and BRAF status), CIMP-high and MSI-H (but not BRAF mutations) were still significantly associated with nuclear p27 loss. Cyclic IMP 5-9 KRAS proto-oncogene, GTPase Homo sapiens 74-78 17086168-9 2007 When CIMP-high and non-CIMP-high tumors were stratified by MSI status (or KRAS and BRAF status), CIMP-high and MSI-H (but not BRAF mutations) were still significantly associated with nuclear p27 loss. Cyclic IMP 5-9 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 83-87 17086168-9 2007 When CIMP-high and non-CIMP-high tumors were stratified by MSI status (or KRAS and BRAF status), CIMP-high and MSI-H (but not BRAF mutations) were still significantly associated with nuclear p27 loss. Cyclic IMP 5-9 interferon alpha inducible protein 27 Homo sapiens 191-194 17086168-9 2007 When CIMP-high and non-CIMP-high tumors were stratified by MSI status (or KRAS and BRAF status), CIMP-high and MSI-H (but not BRAF mutations) were still significantly associated with nuclear p27 loss. Cyclic IMP 23-27 KRAS proto-oncogene, GTPase Homo sapiens 74-78 17086168-11 2007 We conclude that downregulation of nuclear p27 is associated with CIMP-high and MSI-H in colorectal cancer. Cyclic IMP 66-70 interferon alpha inducible protein 27 Homo sapiens 43-46 16850502-14 2006 When CIMP-high and non-CIMP-high tumours were stratified by MSI or KRAS/BRAF status, CIMP-high and MSI-H (but not BRAF mutations) were still inversely associated with p21 loss. Cyclic IMP 5-9 cyclin dependent kinase inhibitor 1A Homo sapiens 167-170 16850502-14 2006 When CIMP-high and non-CIMP-high tumours were stratified by MSI or KRAS/BRAF status, CIMP-high and MSI-H (but not BRAF mutations) were still inversely associated with p21 loss. Cyclic IMP 23-27 cyclin dependent kinase inhibitor 1A Homo sapiens 167-170 17350669-9 2007 The association between FASN overexpression and MSI-H persisted even after stratification by CIMP status. Cyclic IMP 93-97 fatty acid synthase Homo sapiens 24-28 17350669-12 2007 In conclusion, FASN overexpression in colorectal cancer is associated with MSI-H, independent of CIMP status. Cyclic IMP 97-101 fatty acid synthase Homo sapiens 15-19 17239930-2 2007 CIMP in colorectal cancer is characterized by extensive promoter methylation and is associated with MSI-MSI-H and BRAF mutations. Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 114-118 17239930-3 2007 We have recently shown a positive correlation between MSI/CIMP and loss of nuclear p27. Cyclic IMP 58-62 interferon alpha inducible protein 27 Homo sapiens 83-86 17239930-4 2007 However, no study has examined cytoplasmic p27 mislocalization in relation to CIMP and MSI in colorectal cancer. Cyclic IMP 78-82 interferon alpha inducible protein 27 Homo sapiens 43-46 17239930-8 2007 The inverse association of cytoplasmic p27 with CIMP-high (or MSI-H) was independent of MSI (or CIMP) status. Cyclic IMP 48-52 interferon alpha inducible protein 27 Homo sapiens 39-42 17239930-12 2007 In conclusion, cytoplasmic p27 expression is inversely associated with MSI-H and CIMP-high, particularly in p53-negative tumors, suggesting interplay of functional losses of p27 and p53 in the development of various molecular subtypes of colorectal cancer. Cyclic IMP 81-85 interferon alpha inducible protein 27 Homo sapiens 27-30 17239930-12 2007 In conclusion, cytoplasmic p27 expression is inversely associated with MSI-H and CIMP-high, particularly in p53-negative tumors, suggesting interplay of functional losses of p27 and p53 in the development of various molecular subtypes of colorectal cancer. Cyclic IMP 81-85 tumor protein p53 Homo sapiens 182-185 17148775-7 2006 CIMP was determined by sodium bisulfite modification of DNA followed by methylation-specific polymerase chain reaction amplification of CpG islands in hMLH1, p16, and MINTS1, -2, and -31. Cyclic IMP 0-4 mutL homolog 1 Homo sapiens 151-156 17148775-7 2006 CIMP was determined by sodium bisulfite modification of DNA followed by methylation-specific polymerase chain reaction amplification of CpG islands in hMLH1, p16, and MINTS1, -2, and -31. Cyclic IMP 0-4 cyclin dependent kinase inhibitor 2A Homo sapiens 158-161 17065427-4 2006 CIMP-low (defined as 1/5 to 3/5 methylated promoters) colorectal cancers were significantly more common among men (38 versus 30% in women, P = 0.01) and among KRAS-mutated tumors (44 versus 30% in KRAS/BRAF wild-type tumors, P = 0.0003; 19% in BRAF-mutated tumors, P < 0.0001). Cyclic IMP 0-4 KRAS proto-oncogene, GTPase Homo sapiens 159-163 17065427-4 2006 CIMP-low (defined as 1/5 to 3/5 methylated promoters) colorectal cancers were significantly more common among men (38 versus 30% in women, P = 0.01) and among KRAS-mutated tumors (44 versus 30% in KRAS/BRAF wild-type tumors, P = 0.0003; 19% in BRAF-mutated tumors, P < 0.0001). Cyclic IMP 0-4 KRAS proto-oncogene, GTPase Homo sapiens 197-201 17065427-4 2006 CIMP-low (defined as 1/5 to 3/5 methylated promoters) colorectal cancers were significantly more common among men (38 versus 30% in women, P = 0.01) and among KRAS-mutated tumors (44 versus 30% in KRAS/BRAF wild-type tumors, P = 0.0003; 19% in BRAF-mutated tumors, P < 0.0001). Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 202-206 17065427-4 2006 CIMP-low (defined as 1/5 to 3/5 methylated promoters) colorectal cancers were significantly more common among men (38 versus 30% in women, P = 0.01) and among KRAS-mutated tumors (44 versus 30% in KRAS/BRAF wild-type tumors, P = 0.0003; 19% in BRAF-mutated tumors, P < 0.0001). Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 244-248 16143123-8 2005 CIMP-high unstable tumors also were more likely to have the V600E BRAF mutation, be located proximally, and occur in older individuals (in univariate analyses). Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 66-70 16407376-8 2006 CIMP was significantly associated with female sex, MSI, BRAF mutations, and wild-type KRAS. Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 56-60 16407376-8 2006 CIMP was significantly associated with female sex, MSI, BRAF mutations, and wild-type KRAS. Cyclic IMP 0-4 KRAS proto-oncogene, GTPase Homo sapiens 86-90 16804544-5 2006 We found that CIMP-positive (CIMP+) tumors convincingly represent a distinct subset, encompassing almost all cases of tumors with BRAF mutation (odds ratio = 203). Cyclic IMP 14-18 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 130-134 16804544-6 2006 Sporadic cases of mismatch repair deficiency occur almost exclusively as a consequence of CIMP-associated methylation of MLH1 . Cyclic IMP 90-94 mutL homolog 1 Homo sapiens 121-125 16598760-6 2006 On the basis of the methylation profile, CRBP1 and CDH13 methylation were good indicators of CIMP in NSCLC, and were correlated with a poorer prognosis in adenocarcinomas. Cyclic IMP 93-97 retinol binding protein 1 Homo sapiens 41-46 16598760-6 2006 On the basis of the methylation profile, CRBP1 and CDH13 methylation were good indicators of CIMP in NSCLC, and were correlated with a poorer prognosis in adenocarcinomas. Cyclic IMP 93-97 cadherin 13 Homo sapiens 51-56 16598760-9 2006 CONCLUSIONS: The findings of the current study suggest that adenocarcinoma cases with CIMP have a poorer prognosis than adenocarcinoma cases without CIMP, and the EGFR mutation was shown to have an inverse correlation with methylation of SPARC and the p16INK4A gene in NSCLC. Cyclic IMP 86-90 epidermal growth factor receptor Homo sapiens 163-167 16598760-9 2006 CONCLUSIONS: The findings of the current study suggest that adenocarcinoma cases with CIMP have a poorer prognosis than adenocarcinoma cases without CIMP, and the EGFR mutation was shown to have an inverse correlation with methylation of SPARC and the p16INK4A gene in NSCLC. Cyclic IMP 86-90 secreted protein acidic and cysteine rich Homo sapiens 238-243 16598760-9 2006 CONCLUSIONS: The findings of the current study suggest that adenocarcinoma cases with CIMP have a poorer prognosis than adenocarcinoma cases without CIMP, and the EGFR mutation was shown to have an inverse correlation with methylation of SPARC and the p16INK4A gene in NSCLC. Cyclic IMP 86-90 cyclin dependent kinase inhibitor 2A Homo sapiens 252-260 16598760-9 2006 CONCLUSIONS: The findings of the current study suggest that adenocarcinoma cases with CIMP have a poorer prognosis than adenocarcinoma cases without CIMP, and the EGFR mutation was shown to have an inverse correlation with methylation of SPARC and the p16INK4A gene in NSCLC. Cyclic IMP 149-153 epidermal growth factor receptor Homo sapiens 163-167 16820091-4 2006 CIMP-high tumors were much less frequent in COX-2+/p53+ tumors (4.6%) than in COX-2+/p53- tumors (19%; P < .0001), COX-2-/p53+ tumors (17%; P = .04), and COX-2-/p53- tumors (28%; P < .0001). Cyclic IMP 0-4 prostaglandin-endoperoxide synthase 2 Homo sapiens 44-49 16820091-4 2006 CIMP-high tumors were much less frequent in COX-2+/p53+ tumors (4.6%) than in COX-2+/p53- tumors (19%; P < .0001), COX-2-/p53+ tumors (17%; P = .04), and COX-2-/p53- tumors (28%; P < .0001). Cyclic IMP 0-4 tumor protein p53 Homo sapiens 51-54 16820091-4 2006 CIMP-high tumors were much less frequent in COX-2+/p53+ tumors (4.6%) than in COX-2+/p53- tumors (19%; P < .0001), COX-2-/p53+ tumors (17%; P = .04), and COX-2-/p53- tumors (28%; P < .0001). Cyclic IMP 0-4 tumor protein p53 Homo sapiens 85-88 16820091-4 2006 CIMP-high tumors were much less frequent in COX-2+/p53+ tumors (4.6%) than in COX-2+/p53- tumors (19%; P < .0001), COX-2-/p53+ tumors (17%; P = .04), and COX-2-/p53- tumors (28%; P < .0001). Cyclic IMP 0-4 tumor protein p53 Homo sapiens 85-88 16820091-4 2006 CIMP-high tumors were much less frequent in COX-2+/p53+ tumors (4.6%) than in COX-2+/p53- tumors (19%; P < .0001), COX-2-/p53+ tumors (17%; P = .04), and COX-2-/p53- tumors (28%; P < .0001). Cyclic IMP 0-4 tumor protein p53 Homo sapiens 85-88 16820091-6 2006 In conclusion, COX-2 and p53 alterations were synergistically inversely correlated with both MSI-H and CIMP-high. Cyclic IMP 103-107 prostaglandin-endoperoxide synthase 2 Homo sapiens 15-20 16820091-6 2006 In conclusion, COX-2 and p53 alterations were synergistically inversely correlated with both MSI-H and CIMP-high. Cyclic IMP 103-107 tumor protein p53 Homo sapiens 25-28 16143123-9 2005 However, CIMP-high unstable tumors were significantly more likely than their stable counterparts to be KRAS2 wild type, TP53 wild type, poorly differentiated, proximally located, occur at lower stages, and have the BRAF V600E mutation (64.1% vs 17.6%). Cyclic IMP 9-13 KRAS proto-oncogene, GTPase Homo sapiens 103-108 16143123-9 2005 However, CIMP-high unstable tumors were significantly more likely than their stable counterparts to be KRAS2 wild type, TP53 wild type, poorly differentiated, proximally located, occur at lower stages, and have the BRAF V600E mutation (64.1% vs 17.6%). Cyclic IMP 9-13 tumor protein p53 Homo sapiens 120-124 16143123-9 2005 However, CIMP-high unstable tumors were significantly more likely than their stable counterparts to be KRAS2 wild type, TP53 wild type, poorly differentiated, proximally located, occur at lower stages, and have the BRAF V600E mutation (64.1% vs 17.6%). Cyclic IMP 9-13 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 215-219 15705880-5 2005 The presence of CIMP was sensitively detected by methylation of the PCDHB CGIs and associated with significantly poor survival (hazard ratio, 22.1; 95% confidence interval, 5.3-93.4; P < 0.0001). Cyclic IMP 16-20 protocadherin beta cluster Homo sapiens 68-73 16024606-1 2005 The BRAF V600E mutation has been associated with microsatellite instability and the CpG island methylator phenotype (CIMP) in colon cancer. Cyclic IMP 117-121 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 4-8 15681708-5 2005 Levels of PAR-1 in the left ventricle (LV) were increased at 2 and 8 wk (compared with 0 wk of no CIMP treatment) but were normal at 12 and 16 wk after CIMP treatment, as measured by Western blot analysis. Cyclic IMP 98-102 coagulation factor II (thrombin) receptor Mus musculus 10-15 15681708-7 2005 However, the levels of TIMP-4, endothelial cell density, and responses of cardiac rings to acetylcholine and bradykinin were attenuated at 2 and 8 wk and normalized after CIMP administration in AVF mice. Cyclic IMP 171-175 tissue inhibitor of metalloproteinase 4 Mus musculus 23-29 15681708-10 2005 CIMP treatment normalized PAR-1 expression and ameliorated endothelial-myocyte uncoupling by decreasing oxidant-mediated proteolytic stress in CHF. Cyclic IMP 0-4 coagulation factor II (thrombin) receptor Mus musculus 26-31 15705880-9 2005 However, CIMP was significantly associated with methylation of promoter CGIs of the RASSF1A and BLU tumor suppressor genes. Cyclic IMP 9-13 Ras association domain family member 1 Homo sapiens 84-91 15705880-9 2005 However, CIMP was significantly associated with methylation of promoter CGIs of the RASSF1A and BLU tumor suppressor genes. Cyclic IMP 9-13 zinc finger MYND-type containing 10 Homo sapiens 96-99 15069684-5 2004 CIMP status was investigated by examining the methylation status of MINT1, MINT2, MINT12, MINT25 and MINT31. Cyclic IMP 0-4 amyloid beta precursor protein binding family A member 1 Homo sapiens 68-73 15247181-8 2004 The BRAF mutation was identified more often in CIMP-high serrated polyps (72%) and CIMP-high CRC (77%) than in CIMP-low (30%) and CIMP-negative (13%) polyps (p = 0.002) as well as CIMP-low (18%) and CIMP-negative (0%) CRC (p<0.0001). Cyclic IMP 47-51 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 4-8 15247181-8 2004 The BRAF mutation was identified more often in CIMP-high serrated polyps (72%) and CIMP-high CRC (77%) than in CIMP-low (30%) and CIMP-negative (13%) polyps (p = 0.002) as well as CIMP-low (18%) and CIMP-negative (0%) CRC (p<0.0001). Cyclic IMP 83-87 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 4-8 15247181-8 2004 The BRAF mutation was identified more often in CIMP-high serrated polyps (72%) and CIMP-high CRC (77%) than in CIMP-low (30%) and CIMP-negative (13%) polyps (p = 0.002) as well as CIMP-low (18%) and CIMP-negative (0%) CRC (p<0.0001). Cyclic IMP 83-87 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 4-8 15247181-8 2004 The BRAF mutation was identified more often in CIMP-high serrated polyps (72%) and CIMP-high CRC (77%) than in CIMP-low (30%) and CIMP-negative (13%) polyps (p = 0.002) as well as CIMP-low (18%) and CIMP-negative (0%) CRC (p<0.0001). Cyclic IMP 83-87 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 4-8 15247181-8 2004 The BRAF mutation was identified more often in CIMP-high serrated polyps (72%) and CIMP-high CRC (77%) than in CIMP-low (30%) and CIMP-negative (13%) polyps (p = 0.002) as well as CIMP-low (18%) and CIMP-negative (0%) CRC (p<0.0001). Cyclic IMP 83-87 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 4-8 15247181-8 2004 The BRAF mutation was identified more often in CIMP-high serrated polyps (72%) and CIMP-high CRC (77%) than in CIMP-low (30%) and CIMP-negative (13%) polyps (p = 0.002) as well as CIMP-low (18%) and CIMP-negative (0%) CRC (p<0.0001). Cyclic IMP 83-87 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 4-8 15069684-5 2004 CIMP status was investigated by examining the methylation status of MINT1, MINT2, MINT12, MINT25 and MINT31. Cyclic IMP 0-4 amyloid beta precursor protein binding family A member 2 Homo sapiens 75-80 15069684-10 2004 Promoter hypermethylation of the RIZ1 gene was significantly associated with CIMP (p = 0.002). Cyclic IMP 77-81 PR/SET domain 2 Homo sapiens 33-37 15161007-12 2004 CONCLUSION: These results suggest that the haplotype with low enzymatic activity of MTHFR is linked with promoter hypermethylation and consequently modifies the risk of CIMP(+) proximal colon cancer development in the Japanese people. Cyclic IMP 169-173 methylenetetrahydrofolate reductase Homo sapiens 84-89 15087661-13 2004 Frequent K-ras mutations and infrequent CIMP distinguish the distal GCSP variant. Cyclic IMP 40-44 glycine decarboxylase Homo sapiens 68-72 17031233-7 2002 In sporadic colon cancer, CIMP has distinct epidemiologic and clinical features and is responsible for most cases of microsatellite instability related to hMLH1 inactivation. Cyclic IMP 26-30 mutL homolog 1 Homo sapiens 155-160 12210063-3 2002 In this study, methylation-specific polymerase chain reaction (PCR) was performed to study methylation of CpG islands in the promoters of the p16(INK4a), cadherin 1 (CDH1), and retinoic acid receptor-beta (RAR-beta) genes in 45 gastric carcinomas and to investigate whether CDH1 and RAR-beta promoter hypermethylation is associated with CIMP-positive gastric carcinoma. Cyclic IMP 337-341 cyclin dependent kinase inhibitor 2A Homo sapiens 142-145 12210063-3 2002 In this study, methylation-specific polymerase chain reaction (PCR) was performed to study methylation of CpG islands in the promoters of the p16(INK4a), cadherin 1 (CDH1), and retinoic acid receptor-beta (RAR-beta) genes in 45 gastric carcinomas and to investigate whether CDH1 and RAR-beta promoter hypermethylation is associated with CIMP-positive gastric carcinoma. Cyclic IMP 337-341 cyclin dependent kinase inhibitor 2A Homo sapiens 146-151 14556664-6 2003 Forty-two (41%) of 103 gastric carcinomas were positive for the CIMP. CIMP and hypermethylation of p16(INK4a) gene were found more frequently in intestinal and diffuse-adherent types than in diffuse-scattered type (P = 0.013 and 0.017, respectively). Cyclic IMP 64-68 cyclin dependent kinase inhibitor 2A Homo sapiens 99-102 14556664-6 2003 Forty-two (41%) of 103 gastric carcinomas were positive for the CIMP. CIMP and hypermethylation of p16(INK4a) gene were found more frequently in intestinal and diffuse-adherent types than in diffuse-scattered type (P = 0.013 and 0.017, respectively). Cyclic IMP 64-68 cyclin dependent kinase inhibitor 2A Homo sapiens 103-108 14556664-8 2003 In intestinal- and diffuse-adherent-type gastric carcinomas, we found significant associations between the presence of the CIMP and hypermethylation of several genes: hMLH1 (P = 0.006), p16(INK4a) (P = 0.018), CDH1 (P = 0.024), and RAR-beta (P = 0.044). Cyclic IMP 123-127 mutL homolog 1 Homo sapiens 167-172 14556664-8 2003 In intestinal- and diffuse-adherent-type gastric carcinomas, we found significant associations between the presence of the CIMP and hypermethylation of several genes: hMLH1 (P = 0.006), p16(INK4a) (P = 0.018), CDH1 (P = 0.024), and RAR-beta (P = 0.044). Cyclic IMP 123-127 cyclin dependent kinase inhibitor 2A Homo sapiens 186-189 14556664-8 2003 In intestinal- and diffuse-adherent-type gastric carcinomas, we found significant associations between the presence of the CIMP and hypermethylation of several genes: hMLH1 (P = 0.006), p16(INK4a) (P = 0.018), CDH1 (P = 0.024), and RAR-beta (P = 0.044). Cyclic IMP 123-127 cyclin dependent kinase inhibitor 2A Homo sapiens 190-195 14556664-8 2003 In intestinal- and diffuse-adherent-type gastric carcinomas, we found significant associations between the presence of the CIMP and hypermethylation of several genes: hMLH1 (P = 0.006), p16(INK4a) (P = 0.018), CDH1 (P = 0.024), and RAR-beta (P = 0.044). Cyclic IMP 123-127 cadherin 1 Homo sapiens 210-214 14556664-8 2003 In intestinal- and diffuse-adherent-type gastric carcinomas, we found significant associations between the presence of the CIMP and hypermethylation of several genes: hMLH1 (P = 0.006), p16(INK4a) (P = 0.018), CDH1 (P = 0.024), and RAR-beta (P = 0.044). Cyclic IMP 123-127 retinoic acid receptor beta Homo sapiens 232-240 12427779-8 2002 Females who were heterozygous or homozygous for the C677T MTHFR polymorphism were at increased risk of developing CIMP+ CRC (odds ratio 2.17, 95% confidence interval 1.03-4.57; p=0.037). Cyclic IMP 114-118 methylenetetrahydrofolate reductase Homo sapiens 58-63 12210063-3 2002 In this study, methylation-specific polymerase chain reaction (PCR) was performed to study methylation of CpG islands in the promoters of the p16(INK4a), cadherin 1 (CDH1), and retinoic acid receptor-beta (RAR-beta) genes in 45 gastric carcinomas and to investigate whether CDH1 and RAR-beta promoter hypermethylation is associated with CIMP-positive gastric carcinoma. Cyclic IMP 337-341 retinoic acid receptor beta Homo sapiens 177-204 10911911-11 2000 By contrast, CIMP- cases evolve along a more classic genetic instability pathway, with a high rate of p53 mutations and chromosomal changes. Cyclic IMP 13-17 tumor protein p53 Homo sapiens 102-105 10934201-2 2000 The cNMP-ligated CRP and mutants were cAMP, cGMP, and cIMP ligated with CRP, T127L CRP, S128A CRP, and T127L/S128A CRP. Cyclic IMP 54-58 C-reactive protein Homo sapiens 17-20 10934201-2 2000 The cNMP-ligated CRP and mutants were cAMP, cGMP, and cIMP ligated with CRP, T127L CRP, S128A CRP, and T127L/S128A CRP. Cyclic IMP 54-58 C-reactive protein Homo sapiens 72-75 10934201-2 2000 The cNMP-ligated CRP and mutants were cAMP, cGMP, and cIMP ligated with CRP, T127L CRP, S128A CRP, and T127L/S128A CRP. Cyclic IMP 54-58 C-reactive protein Homo sapiens 72-75 10934201-2 2000 The cNMP-ligated CRP and mutants were cAMP, cGMP, and cIMP ligated with CRP, T127L CRP, S128A CRP, and T127L/S128A CRP. Cyclic IMP 54-58 C-reactive protein Homo sapiens 72-75 10934201-2 2000 The cNMP-ligated CRP and mutants were cAMP, cGMP, and cIMP ligated with CRP, T127L CRP, S128A CRP, and T127L/S128A CRP. Cyclic IMP 54-58 C-reactive protein Homo sapiens 72-75 11531283-12 2001 CONCLUSIONS: We observed differential expression of the DNMT genes in some ovarian cancer cell lines and conclude that alterations in DNMT expression might contribute to the CIMP phenotype in ovarian cancer. Cyclic IMP 174-178 DNA methyltransferase 1 Homo sapiens 56-60 11531283-12 2001 CONCLUSIONS: We observed differential expression of the DNMT genes in some ovarian cancer cell lines and conclude that alterations in DNMT expression might contribute to the CIMP phenotype in ovarian cancer. Cyclic IMP 174-178 DNA methyltransferase 1 Homo sapiens 134-138 11146446-9 2001 Over-expression of DNMT1 mRNA was significantly associated with CIMP, whereas the level of DNMT3b mRNA was not associated with CIMP or DNA hypomethylation of peri-centromeric satellite regions. Cyclic IMP 64-68 DNA methyltransferase 1 Homo sapiens 19-24 25008768-6 2014 CIMP(pos) (IDH mutant) tumors showed a further separation based on copy-number status of chromosome arms 1p and 19q. Cyclic IMP 0-4 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 11-14 10639144-4 2000 We find that CIMP defines two groups of tumors with significantly different genetic lesions: frequent K-RAS mutations were found in CIMP(+) CRCs (28/41, 68%) compared with CIMP(-) cases (14/47, 30%, P = 0.0005). Cyclic IMP 13-17 KRAS proto-oncogene, GTPase Homo sapiens 102-107 10639144-4 2000 We find that CIMP defines two groups of tumors with significantly different genetic lesions: frequent K-RAS mutations were found in CIMP(+) CRCs (28/41, 68%) compared with CIMP(-) cases (14/47, 30%, P = 0.0005). Cyclic IMP 132-136 KRAS proto-oncogene, GTPase Homo sapiens 102-107 10639144-4 2000 We find that CIMP defines two groups of tumors with significantly different genetic lesions: frequent K-RAS mutations were found in CIMP(+) CRCs (28/41, 68%) compared with CIMP(-) cases (14/47, 30%, P = 0.0005). Cyclic IMP 132-136 KRAS proto-oncogene, GTPase Homo sapiens 102-107 10639144-5 2000 By contrast, p53 mutations were found in 24% (10/41) of CIMP(+) CRCs vs. 60% (30/46) of CIMP(-) cases (P = 0.002). Cyclic IMP 56-60 tumor protein p53 Homo sapiens 13-16 10639144-5 2000 By contrast, p53 mutations were found in 24% (10/41) of CIMP(+) CRCs vs. 60% (30/46) of CIMP(-) cases (P = 0.002). Cyclic IMP 88-92 tumor protein p53 Homo sapiens 13-16 11063215-7 2000 In this regard, the majority of sporadic colorectal cancers, exhibiting microsatellite instability (MSI) appear to be associated with CIMP, which leads to aberrant methylation of human MutL homologue (hMLH1) and the loss of its expression. Cyclic IMP 134-138 mutL homolog 1 Homo sapiens 201-206 10554013-5 1999 There was a significant concordance between CIMP and the methylation of known genes including p16, and hMLH1; methylation of p16 was detected in 16 (70%) of 23 CIMP+ tumors, 1 (8%) of 12 CIMP intermediate tumors, and 1 (5%) of 21 CIMP- tumors (P<0.0001). Cyclic IMP 160-164 cyclin dependent kinase inhibitor 2A Homo sapiens 125-128 10554013-5 1999 There was a significant concordance between CIMP and the methylation of known genes including p16, and hMLH1; methylation of p16 was detected in 16 (70%) of 23 CIMP+ tumors, 1 (8%) of 12 CIMP intermediate tumors, and 1 (5%) of 21 CIMP- tumors (P<0.0001). Cyclic IMP 160-164 cyclin dependent kinase inhibitor 2A Homo sapiens 125-128 10554013-5 1999 There was a significant concordance between CIMP and the methylation of known genes including p16, and hMLH1; methylation of p16 was detected in 16 (70%) of 23 CIMP+ tumors, 1 (8%) of 12 CIMP intermediate tumors, and 1 (5%) of 21 CIMP- tumors (P<0.0001). Cyclic IMP 160-164 cyclin dependent kinase inhibitor 2A Homo sapiens 125-128 10547343-9 1999 CIMP is a novel molecular instability pathway that appears to be responsible for most cases of aberrant TSG methylation in colorectal cancer, and which has important interactions with genetic pathways as well. Cyclic IMP 0-4 twisted gastrulation BMP signaling modulator 1 Homo sapiens 104-107 8948594-2 1996 The postulated pathway of cGMP-dependent protein kinase (PKG) activation of ADP-ribosyl cyclase for production of cADPR to activate the ryanodine receptor Ca2+ channel was tested with a variety of activators (cGMP analogs and cIMP) and inhibitors (Rp-8-pCPT-cGMPS, 3-aminopyridine NAD, nicotinamide, and spermine). Cyclic IMP 226-230 protein kinase cGMP-dependent 1 Homo sapiens 57-60 8948594-4 1996 PKG activity in the sea urchin egg was activated by cIMP, but was insensitive to cGMP analogs, which are potent activators of mammalian isoenzymes. Cyclic IMP 52-56 protein kinase cGMP-dependent 1 Homo sapiens 0-3 25008768-7 2014 CIMP(neg) (IDH wild type) tumors showed hallmark copy-number alterations of glioblastomas, and clustered together with CIMP(neg) glioblastomas without forming separate groups based on WHO grade. Cyclic IMP 0-4 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 11-14 34843679-7 2021 Genes hypermethylated in CIMP compared with LM melanomas included PTEN, VDR, PD-L1, TET2 and gene sets related to development/differentiation, the extracellular matrix and immunity. Cyclic IMP 25-29 phosphatase and tensin homolog Homo sapiens 66-70 34591983-6 2022 The CIMP group defined in our study revealed significant association with colon localization, either KRAS or BRAF mutation, and mostly minor chromosomal losses but no association with known histopathological features. Cyclic IMP 4-8 KRAS proto-oncogene, GTPase Homo sapiens 101-105 34591983-6 2022 The CIMP group defined in our study revealed significant association with colon localization, either KRAS or BRAF mutation, and mostly minor chromosomal losses but no association with known histopathological features. Cyclic IMP 4-8 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 109-113 34843679-7 2021 Genes hypermethylated in CIMP compared with LM melanomas included PTEN, VDR, PD-L1, TET2 and gene sets related to development/differentiation, the extracellular matrix and immunity. Cyclic IMP 25-29 vitamin D receptor Homo sapiens 72-75 34843679-7 2021 Genes hypermethylated in CIMP compared with LM melanomas included PTEN, VDR, PD-L1, TET2 and gene sets related to development/differentiation, the extracellular matrix and immunity. Cyclic IMP 25-29 CD274 molecule Homo sapiens 77-82 34843679-7 2021 Genes hypermethylated in CIMP compared with LM melanomas included PTEN, VDR, PD-L1, TET2 and gene sets related to development/differentiation, the extracellular matrix and immunity. Cyclic IMP 25-29 tet methylcytosine dioxygenase 2 Homo sapiens 84-88 34253388-12 2021 In addition, CIMP may reveal ECs benefitting from immune checkpoint inhibition and allows upfront identification of targetable alterations, such as HER2 amplification in p53 abn ECs. Cyclic IMP 13-17 erb-b2 receptor tyrosine kinase 2 Homo sapiens 148-152 35131383-4 2022 In this study, we demonstrate a causal role of ARID1A loss-of-function in CIMP induction. Cyclic IMP 74-78 AT-rich interaction domain 1A Homo sapiens 47-53 35131383-8 2022 These results showed that the ARID1A mutation induced aberrant DNA methylation, and this is likely to be one of the potential mechanisms of CIMP induction. Cyclic IMP 140-144 AT-rich interaction domain 1A Homo sapiens 30-36 2824499-10 1987 Peak 2 holoenzyme, as compared to Peak 1, had enhanced binding in nonequilibrium [3H]cIMP and [3H]cAMP binding assays, as was expected due to the presence of cAMP and to the known positive cooperativity in binding of cyclic nucleotides to the kinase. Cyclic IMP 85-89 pseudopodium enriched atypical kinase 1 Bos taurus 34-40 35134107-9 2022 Among the 19 CIMP-positive cancers, very few shared potential driver events, and those drivers were only IDH1 and SETD2 mutations. Cyclic IMP 13-17 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 105-109 35134107-9 2022 Among the 19 CIMP-positive cancers, very few shared potential driver events, and those drivers were only IDH1 and SETD2 mutations. Cyclic IMP 13-17 SET domain containing 2, histone lysine methyltransferase Homo sapiens 114-119 6288370-9 1982 For type I, of the analogs tested the most efficacious for stimulating [3H]cIMP binding were those containing a nitrogen atom attached to C-8, 8-aminobutylamino-cAMP being the most effective. Cyclic IMP 75-79 homeobox C8 Homo sapiens 138-141 33169529-6 2020 We found that inhibition of PDE1 and PDE5 substantially elevated cIMP content in endothelium-denuded coronary artery supplemented with exogenous purified cIMP. Cyclic IMP 154-158 phosphodiesterase 5A Homo sapiens 37-41 33846524-7 2021 RESULTS: Compared with CIMP-low/negative CRC, CIMP-high CRC was associated with more stage IV disease, BRAF V600E mutation and high body mass index (BMI 27.5 kg/m2) in younger patients (age < 50 y), and more right-sided tumour, BRAF V600E mutation, MSI-high and colorectal polyp in elder patients (age 50 y). Cyclic IMP 46-50 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 103-107 33846524-7 2021 RESULTS: Compared with CIMP-low/negative CRC, CIMP-high CRC was associated with more stage IV disease, BRAF V600E mutation and high body mass index (BMI 27.5 kg/m2) in younger patients (age < 50 y), and more right-sided tumour, BRAF V600E mutation, MSI-high and colorectal polyp in elder patients (age 50 y). Cyclic IMP 46-50 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 230-234 6278942-2 1982 In the present study, we found that derivatives of cAMP and cIMP can also inhibit binding of cholecystokinin as well as its actions on acinar cell function. Cyclic IMP 60-64 cholecystokinin Homo sapiens 93-108 221047-5 1979 Cyclic IMP resembled cyclic AMP in effectiveness in stimulating cyclic GMP-dependent protein kinase but was intermediate between cyclic AMP and cyclic GMP in stimulating cyclic AMP-dependent protein kinase. Cyclic IMP 0-10 5'-nucleotidase, cytosolic II Homo sapiens 71-74 221047-6 1979 The effect of cyclic IMP on cyclic GMP-dependent protein kinase was confirmed in studies of autophosphorylation of cyclic GMP-dependent protein kinase where both cyclic AMP and cyclic IMP enhanced autophosphorylation. Cyclic IMP 14-24 5'-nucleotidase, cytosolic II Homo sapiens 35-38 221047-6 1979 The effect of cyclic IMP on cyclic GMP-dependent protein kinase was confirmed in studies of autophosphorylation of cyclic GMP-dependent protein kinase where both cyclic AMP and cyclic IMP enhanced autophosphorylation. Cyclic IMP 14-24 5'-nucleotidase, cytosolic II Homo sapiens 122-125 221047-6 1979 The effect of cyclic IMP on cyclic GMP-dependent protein kinase was confirmed in studies of autophosphorylation of cyclic GMP-dependent protein kinase where both cyclic AMP and cyclic IMP enhanced autophosphorylation. Cyclic IMP 177-187 5'-nucleotidase, cytosolic II Homo sapiens 35-38 221047-6 1979 The effect of cyclic IMP on cyclic GMP-dependent protein kinase was confirmed in studies of autophosphorylation of cyclic GMP-dependent protein kinase where both cyclic AMP and cyclic IMP enhanced autophosphorylation. Cyclic IMP 177-187 5'-nucleotidase, cytosolic II Homo sapiens 122-125 33169529-6 2020 We found that inhibition of PDE1 and PDE5 substantially elevated cIMP content in endothelium-denuded coronary artery supplemented with exogenous purified cIMP. Cyclic IMP 65-69 phosphodiesterase 5A Homo sapiens 37-41 33169529-8 2020 The increased cIMP levels induced by PDE1 or PDE5 inhibition further led to augmented hypoxic constriction without apparently affecting the relaxation response. Cyclic IMP 14-18 phosphodiesterase 5A Homo sapiens 45-49 33169529-9 2020 In intact coronary artery, PDE1 or PDE5 inhibition up-regulated cIMP levels under hypoxic condition. Cyclic IMP 64-68 phosphodiesterase 5A Homo sapiens 35-39 33169529-12 2020 Taken together, these data suggest that cIMP levels in coronary arteries are regulated by PDE1 and PDE5, whose inhibition at a certain level leads to increased cIMP content and enhanced hypoxic constriction. Cyclic IMP 40-44 phosphodiesterase 5A Homo sapiens 99-103 33169529-12 2020 Taken together, these data suggest that cIMP levels in coronary arteries are regulated by PDE1 and PDE5, whose inhibition at a certain level leads to increased cIMP content and enhanced hypoxic constriction. Cyclic IMP 160-164 phosphodiesterase 5A Homo sapiens 99-103 33229221-5 2021 CIMP was measured using the classical 6-gene methylated-in-tumor (MINT) marker panel (MINT1, MINT2, MINT31, p14, p16, and MLH1) in ATTACC and genome-wide human methylation arrays in Integromics and TCGA, respectively. Cyclic IMP 0-4 amyloid beta precursor protein binding family A member 1 Homo sapiens 86-91 33238621-6 2020 The mutation profiles of CIMP-high tumors were significantly different from those of CIMP-low or CIMP-0 tumors (i.e., higher frequencies of BRAF, POLD1, MSH3, and SMAD4 mutations but lower frequencies of APC, TP53, and KRAS mutations). Cyclic IMP 25-29 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 140-144 33238621-6 2020 The mutation profiles of CIMP-high tumors were significantly different from those of CIMP-low or CIMP-0 tumors (i.e., higher frequencies of BRAF, POLD1, MSH3, and SMAD4 mutations but lower frequencies of APC, TP53, and KRAS mutations). Cyclic IMP 25-29 DNA polymerase delta 1, catalytic subunit Homo sapiens 146-151 33238621-6 2020 The mutation profiles of CIMP-high tumors were significantly different from those of CIMP-low or CIMP-0 tumors (i.e., higher frequencies of BRAF, POLD1, MSH3, and SMAD4 mutations but lower frequencies of APC, TP53, and KRAS mutations). Cyclic IMP 25-29 mutS homolog 3 Homo sapiens 153-157 33238621-6 2020 The mutation profiles of CIMP-high tumors were significantly different from those of CIMP-low or CIMP-0 tumors (i.e., higher frequencies of BRAF, POLD1, MSH3, and SMAD4 mutations but lower frequencies of APC, TP53, and KRAS mutations). Cyclic IMP 25-29 SMAD family member 4 Homo sapiens 163-168 33238621-6 2020 The mutation profiles of CIMP-high tumors were significantly different from those of CIMP-low or CIMP-0 tumors (i.e., higher frequencies of BRAF, POLD1, MSH3, and SMAD4 mutations but lower frequencies of APC, TP53, and KRAS mutations). Cyclic IMP 25-29 tumor protein p53 Homo sapiens 209-213 33238621-6 2020 The mutation profiles of CIMP-high tumors were significantly different from those of CIMP-low or CIMP-0 tumors (i.e., higher frequencies of BRAF, POLD1, MSH3, and SMAD4 mutations but lower frequencies of APC, TP53, and KRAS mutations). Cyclic IMP 25-29 KRAS proto-oncogene, GTPase Homo sapiens 219-223 33229221-5 2021 CIMP was measured using the classical 6-gene methylated-in-tumor (MINT) marker panel (MINT1, MINT2, MINT31, p14, p16, and MLH1) in ATTACC and genome-wide human methylation arrays in Integromics and TCGA, respectively. Cyclic IMP 0-4 amyloid beta precursor protein binding family A member 2 Homo sapiens 93-98 33229221-5 2021 CIMP was measured using the classical 6-gene methylated-in-tumor (MINT) marker panel (MINT1, MINT2, MINT31, p14, p16, and MLH1) in ATTACC and genome-wide human methylation arrays in Integromics and TCGA, respectively. Cyclic IMP 0-4 cyclin dependent kinase inhibitor 2A Homo sapiens 108-111 33229221-5 2021 CIMP was measured using the classical 6-gene methylated-in-tumor (MINT) marker panel (MINT1, MINT2, MINT31, p14, p16, and MLH1) in ATTACC and genome-wide human methylation arrays in Integromics and TCGA, respectively. Cyclic IMP 0-4 cyclin dependent kinase inhibitor 2A Homo sapiens 113-116 33229221-5 2021 CIMP was measured using the classical 6-gene methylated-in-tumor (MINT) marker panel (MINT1, MINT2, MINT31, p14, p16, and MLH1) in ATTACC and genome-wide human methylation arrays in Integromics and TCGA, respectively. Cyclic IMP 0-4 mutL homolog 1 Homo sapiens 122-126 31496795-7 2019 MAPT were preferentially methylated among proximal colon tumors or CIMP high tumors (both P<0.001). Cyclic IMP 67-71 microtubule associated protein tau Homo sapiens 0-4 32821544-12 2020 We then established a CIMP-related prognostic gene signature comprising six genes (CST6, SLC7A2, RAB3B, IGFBP1, VSTM2L and EVX2). Cyclic IMP 22-26 cystatin E/M Homo sapiens 83-87 32821544-12 2020 We then established a CIMP-related prognostic gene signature comprising six genes (CST6, SLC7A2, RAB3B, IGFBP1, VSTM2L and EVX2). Cyclic IMP 22-26 solute carrier family 7 member 2 Homo sapiens 89-95 32821544-12 2020 We then established a CIMP-related prognostic gene signature comprising six genes (CST6, SLC7A2, RAB3B, IGFBP1, VSTM2L and EVX2). Cyclic IMP 22-26 RAB3B, member RAS oncogene family Homo sapiens 97-102 32821544-12 2020 We then established a CIMP-related prognostic gene signature comprising six genes (CST6, SLC7A2, RAB3B, IGFBP1, VSTM2L and EVX2). Cyclic IMP 22-26 insulin like growth factor binding protein 1 Homo sapiens 104-110 32821544-12 2020 We then established a CIMP-related prognostic gene signature comprising six genes (CST6, SLC7A2, RAB3B, IGFBP1, VSTM2L and EVX2). Cyclic IMP 22-26 V-set and transmembrane domain containing 2 like Homo sapiens 112-118 32821544-12 2020 We then established a CIMP-related prognostic gene signature comprising six genes (CST6, SLC7A2, RAB3B, IGFBP1, VSTM2L and EVX2). Cyclic IMP 22-26 even-skipped homeobox 2 Homo sapiens 123-127 30967137-9 2019 Up to 8-fold decrease in the expression of OGDHL gene involved in tricarboxylic acid (TCA) cycle was observed in CIMP-high tumors. Cyclic IMP 113-117 oxoglutarate dehydrogenase L Homo sapiens 43-48 30770352-3 2019 We sought to identify a biomarker that faithfully captures this subgroup.Experimental Design: We analyzed ACC-TCGA data to characterize differentially regulated biological processes, and identify a biomarker that is methylated and silenced exclusively in CIMP-high ACC. Cyclic IMP 255-259 acetyl-CoA carboxylase alpha Homo sapiens 265-268 30770352-6 2019 RESULTS: We show that CIMP-high ACC is characterized by upregulation of cell cycle and DNA damage response programs, and identify that hypermethylation and silencing of G0S2 distinguishes this subgroup. Cyclic IMP 22-26 acetyl-CoA carboxylase alpha Homo sapiens 32-35 30967137-12 2019 Differential methylation of at least nine CpG sites in OGDHL promoter region as well as decreased OGDHL mRNA level can potentially serve as an additional biomarker of the CIMP-high status in COAD. Cyclic IMP 171-175 oxoglutarate dehydrogenase L Homo sapiens 55-60 30967137-12 2019 Differential methylation of at least nine CpG sites in OGDHL promoter region as well as decreased OGDHL mRNA level can potentially serve as an additional biomarker of the CIMP-high status in COAD. Cyclic IMP 171-175 oxoglutarate dehydrogenase L Homo sapiens 98-103 29906313-7 2018 Intra-epithelial CD163+ macrophage densities were associated with perineural invasion, MSI, CIMP and TIL densities (P < 0.001). Cyclic IMP 92-96 CD163 molecule Homo sapiens 17-22 30753821-2 2019 provide compelling evidence that aging-like DNA methylation of multiple CpG islands, the CpG island methylator phenotype (CIMP), produces a cellular context that can tolerate BRAF activation avoiding senescence by dedicating 5-month culture of colon-derived organoids to epigenomic and stemness analysis. Cyclic IMP 122-126 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 175-179 31933925-13 2019 CONCLUSIONS: The BRAF gene mutation is closely related to the two types of CIMP and MSI, which may be an important part of the above two molecular mechanisms, and provide a reference for the treatment of the patients with CIMP-H and MSI-H. Cyclic IMP 75-79 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 17-21 30407260-3 2019 The CIMP pathway is tightly linked with mutations of the oncogene BRAF. Cyclic IMP 4-8 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 66-70 30062552-1 2018 Earlier studies on isolated arteries demonstrated that the para-quinone thymoquinone, like acute hypoxia, induces augmentation of contractions, depending on biased activity of soluble guanylyl cyclase (sGC), generating inosine-3",5"-cyclic monophosphate (cyclic IMP) rather than guanosine-3",5"-cyclic monophosphate (cyclic GMP). Cyclic IMP 255-265 guanylate cyclase 1 soluble subunit alpha 1 Rattus norvegicus 176-200 30062552-1 2018 Earlier studies on isolated arteries demonstrated that the para-quinone thymoquinone, like acute hypoxia, induces augmentation of contractions, depending on biased activity of soluble guanylyl cyclase (sGC), generating inosine-3",5"-cyclic monophosphate (cyclic IMP) rather than guanosine-3",5"-cyclic monophosphate (cyclic GMP). Cyclic IMP 255-265 guanylate cyclase 1 soluble subunit alpha 1 Rattus norvegicus 202-205 29379130-0 2018 DUSP5 is methylated in CIMP-high colorectal cancer but is not a major regulator of intestinal cell proliferation and tumorigenesis. Cyclic IMP 23-27 dual specificity phosphatase 5 Mus musculus 0-5 29642018-3 2018 We previously reported that the IDH mutant G-CIMP-high subtype would be a predecessor to the G-CIMP-low subtype. Cyclic IMP 45-49 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 32-35 29642018-3 2018 We previously reported that the IDH mutant G-CIMP-high subtype would be a predecessor to the G-CIMP-low subtype. Cyclic IMP 95-99 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 32-35 30188916-6 2018 RESULTS: Patients with the combination of microsatellite stable (MSS) tumours, BRAF mutation and CIMP positive exhibited the worst prognosis in univariate (log rank P<0.0001) and multivariate analyses (hazard ratio 1.75, 95% CI 1.05-2.93, P = 0.03) after adjusting for age, sex, chemotherapy, and TNM stage. Cyclic IMP 97-101 teneurin transmembrane protein 1 Homo sapiens 300-303 29505529-5 2018 The lowest EMP3 expression was observed in cluster 5 DNA methylation, which all belong to G-CIMP phenotype. Cyclic IMP 92-96 epithelial membrane protein 3 Homo sapiens 11-15 28752025-5 2017 The endothelium-dependent augmentation it causes counterintuitively depends on biased activation of soluble guanylyl cyclase (sGC) producing inosine 3",5"-cyclic monophosphate (cyclic IMP) rather than guanosine 3",5"-cyclic monophosphate. Cyclic IMP 141-175 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 100-124 28542846-3 2017 CIMP status was determined by analyzing the 5-markers CAGNA1G, IGF2, NEUROG1, RUNX3 and SOCS1 by quantitative methylation specific PCR (qMSP). Cyclic IMP 0-4 insulin like growth factor 2 Homo sapiens 63-67 28542846-3 2017 CIMP status was determined by analyzing the 5-markers CAGNA1G, IGF2, NEUROG1, RUNX3 and SOCS1 by quantitative methylation specific PCR (qMSP). Cyclic IMP 0-4 neurogenin 1 Homo sapiens 69-76 28542846-3 2017 CIMP status was determined by analyzing the 5-markers CAGNA1G, IGF2, NEUROG1, RUNX3 and SOCS1 by quantitative methylation specific PCR (qMSP). Cyclic IMP 0-4 RUNX family transcription factor 3 Homo sapiens 78-83 28542846-3 2017 CIMP status was determined by analyzing the 5-markers CAGNA1G, IGF2, NEUROG1, RUNX3 and SOCS1 by quantitative methylation specific PCR (qMSP). Cyclic IMP 0-4 suppressor of cytokine signaling 1 Homo sapiens 88-93 28542846-7 2017 In stratified analyses, CIMP tumors showed significantly worse outcome among patients with microsatellite stable (MSS, P < 0.001), and MSS BRAF mutated tumors (P < 0.001), a finding that persisted in patients with stage II, III or IV disease, and that remained significant in multivariate analysis (P < 0.01). Cyclic IMP 24-28 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 142-146 28542846-9 2017 To conclude, CIMP is significantly associated with inferior outcome for colorectal cancer patients, and can stratify the poor prognostic patients with MSS BRAF mutated tumors. Cyclic IMP 13-17 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 155-159 28685624-6 2017 CXCR4 expression was significantly lower in CpG island methylation phenotype (CIMP) group than in non CIMP group. Cyclic IMP 78-82 C-X-C motif chemokine receptor 4 Homo sapiens 0-5 28685624-6 2017 CXCR4 expression was significantly lower in CpG island methylation phenotype (CIMP) group than in non CIMP group. Cyclic IMP 102-106 C-X-C motif chemokine receptor 4 Homo sapiens 0-5 28646291-7 2017 We found that QR2 messenger RNA (mRNA) is overexpressed in CRC characterized by CIN, particularly in cells showing a positive KRAS (Kirsten rat sarcoma viral oncogene homolog) mutation, as well as by the MSI but not the CIMP phenotype. Cyclic IMP 220-224 N-ribosyldihydronicotinamide:quinone reductase 2 Rattus norvegicus 14-17 28752025-5 2017 The endothelium-dependent augmentation it causes counterintuitively depends on biased activation of soluble guanylyl cyclase (sGC) producing inosine 3",5"-cyclic monophosphate (cyclic IMP) rather than guanosine 3",5"-cyclic monophosphate. Cyclic IMP 141-175 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 126-129 28752025-5 2017 The endothelium-dependent augmentation it causes counterintuitively depends on biased activation of soluble guanylyl cyclase (sGC) producing inosine 3",5"-cyclic monophosphate (cyclic IMP) rather than guanosine 3",5"-cyclic monophosphate. Cyclic IMP 177-187 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 100-124 28752025-5 2017 The endothelium-dependent augmentation it causes counterintuitively depends on biased activation of soluble guanylyl cyclase (sGC) producing inosine 3",5"-cyclic monophosphate (cyclic IMP) rather than guanosine 3",5"-cyclic monophosphate. Cyclic IMP 177-187 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 126-129 28567185-11 2017 Intermediate CIMP status was significantly associated with KRAS mutation (P = 0.01). Cyclic IMP 13-17 KRAS proto-oncogene, GTPase Homo sapiens 59-63 28422723-7 2017 Multivariate analysis revealed that MACs without both SAC morphology and CIMP-positive status exhibited 3.955 times greater risk of cancer relapse than MACs having both characteristics or either one (P=0.035). Cyclic IMP 73-77 myristoylated alanine rich protein kinase C substrate Homo sapiens 36-40 28440489-0 2017 Genome-wide DNA methylation sequencing reveals miR-663a is a novel epimutation candidate in CIMP-high endometrial cancer. Cyclic IMP 92-96 microRNA 663a Homo sapiens 47-55 28440489-7 2017 Surprisingly, in normal tissues of the CIMP-H patients, promoter region of the miR-663a locus is hypermethylated relative to CIMP(-) samples. Cyclic IMP 39-43 microRNA 663a Homo sapiens 79-87 28440489-7 2017 Surprisingly, in normal tissues of the CIMP-H patients, promoter region of the miR-663a locus is hypermethylated relative to CIMP(-) samples. Cyclic IMP 125-129 microRNA 663a Homo sapiens 79-87 28440489-9 2017 The same region of the miR663a locus is found to be highly methylated in cancer tissues of both CIMP-H and CIMP(-) cases. Cyclic IMP 96-100 microRNA 663a Homo sapiens 23-30 28440489-9 2017 The same region of the miR663a locus is found to be highly methylated in cancer tissues of both CIMP-H and CIMP(-) cases. Cyclic IMP 107-111 microRNA 663a Homo sapiens 23-30 28368388-12 2017 Notably, we observed that methylation of DKK1 is high in BRAF mutant and CIMP (CpG island methylator phenotype)-positive cancers, whereas AXIN2 methylation appears to be associated with CMS4. Cyclic IMP 73-77 dickkopf WNT signaling pathway inhibitor 1 Homo sapiens 41-45 28465358-1 2017 Gliomas harboring mutations in isocitrate dehydrogenase 1/2 (IDH1/2) have the CpG island methylator phenotype (CIMP) and significantly longer patient survival time than wild-type IDH1/2 (wtIDH1/2) tumors. Cyclic IMP 111-115 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 61-67 27988423-10 2017 MTSS1 is down-regulated by DNA methylation in glioblastoma cell lines and is part of the G-CIMP phenotype in primary glioma tissues. Cyclic IMP 91-95 MTSS I-BAR domain containing 1 Homo sapiens 0-5 28314692-6 2017 Further distinguishing features of this "CIMP-Atypical" subtype include an antiviral gene expression profile associated with pro-inflammatory M1 macrophages and CD8+ T cell infiltration, CASP8 mutations, and a well-differentiated state corresponding to normal SOX2 copy number and SOX2OT hypermethylation. Cyclic IMP 41-45 caspase 8 Homo sapiens 187-192 28314692-6 2017 Further distinguishing features of this "CIMP-Atypical" subtype include an antiviral gene expression profile associated with pro-inflammatory M1 macrophages and CD8+ T cell infiltration, CASP8 mutations, and a well-differentiated state corresponding to normal SOX2 copy number and SOX2OT hypermethylation. Cyclic IMP 41-45 SRY-box transcription factor 2 Homo sapiens 260-264 28314692-6 2017 Further distinguishing features of this "CIMP-Atypical" subtype include an antiviral gene expression profile associated with pro-inflammatory M1 macrophages and CD8+ T cell infiltration, CASP8 mutations, and a well-differentiated state corresponding to normal SOX2 copy number and SOX2OT hypermethylation. Cyclic IMP 41-45 SOX2 overlapping transcript Homo sapiens 281-287 28351398-13 2017 Three genes, EYA4, TLX1 and TFPI2 are hypermethylated in >90% of all tumour samples, regardless of CIMP subtype. Cyclic IMP 102-106 EYA transcriptional coactivator and phosphatase 4 Homo sapiens 13-17 28351398-13 2017 Three genes, EYA4, TLX1 and TFPI2 are hypermethylated in >90% of all tumour samples, regardless of CIMP subtype. Cyclic IMP 102-106 tissue factor pathway inhibitor 2 Homo sapiens 28-33 27310704-3 2016 METHODS: Eight CIMP-specific promoters (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1, CDKN2A, CRABP1, and MLH1) were examined. Cyclic IMP 15-19 calcium voltage-gated channel subunit alpha1 G Homo sapiens 40-47 27435270-3 2016 However, the relationship between the effect of standard chemotherapy, including cytotoxic drugs and anti-epidermal growth factor receptor (EGFR) antibodies, and CIMP status has not been elucidated. Cyclic IMP 162-166 epidermal growth factor receptor Homo sapiens 140-144 27435270-7 2016 Furthermore, CIMP-positive tumors showed higher mutation frequencies for the five EGFR-related genes (74.1 %) than the CIMP-negative tumors did (50.0 %). Cyclic IMP 13-17 epidermal growth factor receptor Homo sapiens 82-86 27435270-8 2016 Among the KRAS wild-type tumors, CIMP-positive tumors were associated with a worse clinical outcome than CIMP-negative tumors following anti-EGFR antibody therapy. Cyclic IMP 33-37 KRAS proto-oncogene, GTPase Homo sapiens 10-14 27435270-8 2016 Among the KRAS wild-type tumors, CIMP-positive tumors were associated with a worse clinical outcome than CIMP-negative tumors following anti-EGFR antibody therapy. Cyclic IMP 33-37 epidermal growth factor receptor Homo sapiens 141-145 27435270-10 2016 High frequencies of mutation in EGFR-related genes in CIMP-positive tumors may cause the lower response to anti-EGFR antibody therapy seen in patients with wild-type KRAS and CIMP-positive tumors. Cyclic IMP 54-58 epidermal growth factor receptor Homo sapiens 32-36 27435270-10 2016 High frequencies of mutation in EGFR-related genes in CIMP-positive tumors may cause the lower response to anti-EGFR antibody therapy seen in patients with wild-type KRAS and CIMP-positive tumors. Cyclic IMP 54-58 epidermal growth factor receptor Homo sapiens 112-116 27435270-10 2016 High frequencies of mutation in EGFR-related genes in CIMP-positive tumors may cause the lower response to anti-EGFR antibody therapy seen in patients with wild-type KRAS and CIMP-positive tumors. Cyclic IMP 54-58 KRAS proto-oncogene, GTPase Homo sapiens 166-170 27435270-10 2016 High frequencies of mutation in EGFR-related genes in CIMP-positive tumors may cause the lower response to anti-EGFR antibody therapy seen in patients with wild-type KRAS and CIMP-positive tumors. Cyclic IMP 175-179 epidermal growth factor receptor Homo sapiens 32-36 27435270-10 2016 High frequencies of mutation in EGFR-related genes in CIMP-positive tumors may cause the lower response to anti-EGFR antibody therapy seen in patients with wild-type KRAS and CIMP-positive tumors. Cyclic IMP 175-179 epidermal growth factor receptor Homo sapiens 112-116 27811854-10 2016 Although CIMP status was associated with the presence of MSI-H and BRAF mutation, the prognostic effects of MSI-H (HR=0.49; 95% CI=0.27-0.90) and BRAF mutation (HR=1.78; 95% CI=1.10-2.84) were independent of CIMP status. Cyclic IMP 9-13 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 67-71 26867769-6 2016 Fifty-four patients (28 %, 54/191) were in the CIMP-high (CIMP-H) group associated with high nodal stage (P = 0.007), the presence of micropapillary or solid histology (P = 0.003), and the absence of an epidermal growth factor receptor (EGFR) mutation (P = 0.002). Cyclic IMP 47-51 epidermal growth factor receptor Homo sapiens 203-235 26867769-6 2016 Fifty-four patients (28 %, 54/191) were in the CIMP-high (CIMP-H) group associated with high nodal stage (P = 0.007), the presence of micropapillary or solid histology (P = 0.003), and the absence of an epidermal growth factor receptor (EGFR) mutation (P = 0.002). Cyclic IMP 47-51 epidermal growth factor receptor Homo sapiens 237-241 26867769-6 2016 Fifty-four patients (28 %, 54/191) were in the CIMP-high (CIMP-H) group associated with high nodal stage (P = 0.007), the presence of micropapillary or solid histology (P = 0.003), and the absence of an epidermal growth factor receptor (EGFR) mutation (P = 0.002). Cyclic IMP 58-62 epidermal growth factor receptor Homo sapiens 203-235 26867769-6 2016 Fifty-four patients (28 %, 54/191) were in the CIMP-high (CIMP-H) group associated with high nodal stage (P = 0.007), the presence of micropapillary or solid histology (P = 0.003), and the absence of an epidermal growth factor receptor (EGFR) mutation (P = 0.002). Cyclic IMP 58-62 epidermal growth factor receptor Homo sapiens 237-241 26867769-9 2016 Of the six CIMP markers, ACAN alone was significantly associated with patient survival. Cyclic IMP 11-15 aggrecan Homo sapiens 25-29 27335436-9 2016 Thymoquinone is the first pharmacological agent that causes endothelium-dependent augmentation of contractions of isolated arteries, which requires endothelium-derived NO and biased sGC activation, resulting in the augmented production of cIMP favoring the contractile process. Cyclic IMP 239-243 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 182-185 27310704-3 2016 METHODS: Eight CIMP-specific promoters (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1, CDKN2A, CRABP1, and MLH1) were examined. Cyclic IMP 15-19 neurogenin 1 Homo sapiens 55-62 27272216-5 2016 RESULTS: EREG and AREG expression was highly inversely correlated with methylation and was inversely associated with right-sided primary tumour, BRAF mutation, and CIMP-high status. Cyclic IMP 164-168 epiregulin Homo sapiens 9-13 27272216-5 2016 RESULTS: EREG and AREG expression was highly inversely correlated with methylation and was inversely associated with right-sided primary tumour, BRAF mutation, and CIMP-high status. Cyclic IMP 164-168 amphiregulin Homo sapiens 18-22 27272216-8 2016 Among known BRAF/NRAS wild-type tumours, inferior PFS remained associated with CIMP-high status (median PFS 5.6 vs 9.0 mo, P=0.023). Cyclic IMP 79-83 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 12-16 27272216-9 2016 CONCLUSIONS: EREG and AREG are strongly regulated by methylation, and their expression is associated with CIMP status and primary tumour site, which may explain the association of primary tumour site and EREG/AREG expression with anti-EGFR therapy efficacy. Cyclic IMP 106-110 epiregulin Homo sapiens 13-17 27272216-9 2016 CONCLUSIONS: EREG and AREG are strongly regulated by methylation, and their expression is associated with CIMP status and primary tumour site, which may explain the association of primary tumour site and EREG/AREG expression with anti-EGFR therapy efficacy. Cyclic IMP 106-110 amphiregulin Homo sapiens 22-26 27272216-9 2016 CONCLUSIONS: EREG and AREG are strongly regulated by methylation, and their expression is associated with CIMP status and primary tumour site, which may explain the association of primary tumour site and EREG/AREG expression with anti-EGFR therapy efficacy. Cyclic IMP 106-110 epiregulin Homo sapiens 204-208 27272216-9 2016 CONCLUSIONS: EREG and AREG are strongly regulated by methylation, and their expression is associated with CIMP status and primary tumour site, which may explain the association of primary tumour site and EREG/AREG expression with anti-EGFR therapy efficacy. Cyclic IMP 106-110 amphiregulin Homo sapiens 209-213 27272216-9 2016 CONCLUSIONS: EREG and AREG are strongly regulated by methylation, and their expression is associated with CIMP status and primary tumour site, which may explain the association of primary tumour site and EREG/AREG expression with anti-EGFR therapy efficacy. Cyclic IMP 106-110 epidermal growth factor receptor Homo sapiens 235-239 26061684-4 2015 Genes encoding microtubule-associated proteins, such as DNAH2, DNAH5, DNAH10, RP1 and HAUS8, showed a 10% or higher incidence of genetic aberrations (non-synonymous single-nucleotide mutations and insertions/deletions) in CIMP-positive RCCs, whereas CIMP-negative RCCs lacked distinct genetic characteristics. Cyclic IMP 222-226 dynein axonemal heavy chain 2 Homo sapiens 56-61 26702772-5 2016 CIMP status was determined using the DNA methylation status of CACNA1G, IGF2, NEUROG1, RUNX3, and SOCS1. Cyclic IMP 0-4 calcium voltage-gated channel subunit alpha1 G Homo sapiens 63-70 26702772-5 2016 CIMP status was determined using the DNA methylation status of CACNA1G, IGF2, NEUROG1, RUNX3, and SOCS1. Cyclic IMP 0-4 insulin like growth factor 2 Homo sapiens 72-76 26702772-5 2016 CIMP status was determined using the DNA methylation status of CACNA1G, IGF2, NEUROG1, RUNX3, and SOCS1. Cyclic IMP 0-4 neurogenin 1 Homo sapiens 78-85 26702772-5 2016 CIMP status was determined using the DNA methylation status of CACNA1G, IGF2, NEUROG1, RUNX3, and SOCS1. Cyclic IMP 0-4 RUNX family transcription factor 3 Homo sapiens 87-92 26702772-5 2016 CIMP status was determined using the DNA methylation status of CACNA1G, IGF2, NEUROG1, RUNX3, and SOCS1. Cyclic IMP 0-4 suppressor of cytokine signaling 1 Homo sapiens 98-103 26702772-9 2016 CIMP(+) tumors were more likely to be right-sided and BRAF mutant (chi(2), P < .001). Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 54-58 25943321-5 2016 RESULTS: Hypermethylation of the p16 gene was detected in 14 of 49 patients (28.6%) and showed significant association with KRAS mutation (Fisher exact, p=0.01) and CIMP positivity (Fisher exact, p=0.002). Cyclic IMP 165-169 cyclin dependent kinase inhibitor 2A Homo sapiens 33-36 27404270-7 2016 There were no CIMP-positive tumors in cancers with BRAF D594G mutations, whereas 67.8% of tumors with BRAF V600E mutations were CIMP-positive. Cyclic IMP 128-132 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 102-106 26061684-8 2015 These data suggest that abnormalities of the spindle checkpoint pathway participate in CIMP-positive renal carcinogenesis, and that AURKA and AURKB may be potential therapeutic targets in more aggressive CIMP-positive RCCs. Cyclic IMP 204-208 aurora kinase A Homo sapiens 132-137 27167203-4 2016 We hypothesized that CIMP+ cell lines, which epigenetically silence key regulatory genes would also evidence silencing of RXRalpha and EGCG treatment would restore its expression. Cyclic IMP 21-25 retinoid X receptor alpha Homo sapiens 122-130 26528695-7 2016 EPCAM-PL (n = 50; 6.9%) was also associated with CIMP-high and adverse pathologic factors and was confirmed to be an independent poor prognostic factor in CRC (HR, 1.57; 95% CI, 1.04 to 2.39). Cyclic IMP 49-53 epithelial cell adhesion molecule Homo sapiens 0-5 26963001-7 2016 We observed more BRAF mutations (OR 34.87; 95% CI, 22.49-54.06) and microsatellite instability (MSI) (OR 12.85 95% CI, 8.84-18.68) in CIMP-positive vs. -negative CRCs, whereas KRAS mutations were less frequent (OR 0.47; 95% CI, 0.30-0.75). Cyclic IMP 134-138 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 17-21 26963001-7 2016 We observed more BRAF mutations (OR 34.87; 95% CI, 22.49-54.06) and microsatellite instability (MSI) (OR 12.85 95% CI, 8.84-18.68) in CIMP-positive vs. -negative CRCs, whereas KRAS mutations were less frequent (OR 0.47; 95% CI, 0.30-0.75). Cyclic IMP 134-138 KRAS proto-oncogene, GTPase Homo sapiens 176-180 26963001-11 2016 CONCLUSIONS: The meta-analysis highlights that CIMP-positive CRCs take their own molecular feature, especially overlapping with BRAF mutations, and clinicopathological features and worse prognosis from CIMP-negative CRCs, suggesting CIMP could be used as an independent prognostic marker for CRCs. Cyclic IMP 47-51 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 128-132 26512054-2 2016 Approximately 25% to 60% of CIMP tumors are microsatellite unstable (MSI-H) due to DNA hypermethylation of the MLH1 gene promoter. Cyclic IMP 28-32 mutL homolog 1 Homo sapiens 111-115 26512054-3 2016 Our aim was to determine if the distributions of clinicopathologic factors in CIMP-positive tumors with MLH1 DNA methylation differed from those in CIMP-positive tumors without DNA methylation of MLH1. Cyclic IMP 78-82 mutL homolog 1 Homo sapiens 104-108 26512054-5 2016 RESULTS: Subjects with CIMP-positive tumors without MLH1 methylation were significantly younger, more likely to be male, and more likely to have distal colon or rectal primaries and the MSI-L phenotype. Cyclic IMP 23-27 RB binding protein 4, chromatin remodeling factor Homo sapiens 186-189 26512054-6 2016 CIMP-positive MLH1-unmethylated tumors were significantly less likely than CIMP-positive MLH1-methylated tumors to harbor a BRAF V600E mutation and significantly more likely to harbor a KRAS mutation. Cyclic IMP 0-4 mutL homolog 1 Homo sapiens 14-18 26512054-6 2016 CIMP-positive MLH1-unmethylated tumors were significantly less likely than CIMP-positive MLH1-methylated tumors to harbor a BRAF V600E mutation and significantly more likely to harbor a KRAS mutation. Cyclic IMP 0-4 mutL homolog 1 Homo sapiens 89-93 26512054-6 2016 CIMP-positive MLH1-unmethylated tumors were significantly less likely than CIMP-positive MLH1-methylated tumors to harbor a BRAF V600E mutation and significantly more likely to harbor a KRAS mutation. Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 124-128 26512054-6 2016 CIMP-positive MLH1-unmethylated tumors were significantly less likely than CIMP-positive MLH1-methylated tumors to harbor a BRAF V600E mutation and significantly more likely to harbor a KRAS mutation. Cyclic IMP 0-4 KRAS proto-oncogene, GTPase Homo sapiens 186-190 26512054-6 2016 CIMP-positive MLH1-unmethylated tumors were significantly less likely than CIMP-positive MLH1-methylated tumors to harbor a BRAF V600E mutation and significantly more likely to harbor a KRAS mutation. Cyclic IMP 75-79 mutL homolog 1 Homo sapiens 89-93 26512054-6 2016 CIMP-positive MLH1-unmethylated tumors were significantly less likely than CIMP-positive MLH1-methylated tumors to harbor a BRAF V600E mutation and significantly more likely to harbor a KRAS mutation. Cyclic IMP 75-79 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 124-128 26512054-8 2016 CONCLUSIONS: These data suggest that MLH1 methylation in CIMP-positive tumors is not a completely random event and implies that there are environmental or genetic determinants that modify the probability that MLH1 will become methylated during CIMP pathogenesis. Cyclic IMP 57-61 mutL homolog 1 Homo sapiens 37-41 26512054-8 2016 CONCLUSIONS: These data suggest that MLH1 methylation in CIMP-positive tumors is not a completely random event and implies that there are environmental or genetic determinants that modify the probability that MLH1 will become methylated during CIMP pathogenesis. Cyclic IMP 57-61 mutL homolog 1 Homo sapiens 209-213 26512054-8 2016 CONCLUSIONS: These data suggest that MLH1 methylation in CIMP-positive tumors is not a completely random event and implies that there are environmental or genetic determinants that modify the probability that MLH1 will become methylated during CIMP pathogenesis. Cyclic IMP 244-248 mutL homolog 1 Homo sapiens 37-41 26512054-8 2016 CONCLUSIONS: These data suggest that MLH1 methylation in CIMP-positive tumors is not a completely random event and implies that there are environmental or genetic determinants that modify the probability that MLH1 will become methylated during CIMP pathogenesis. Cyclic IMP 244-248 mutL homolog 1 Homo sapiens 209-213 26061684-8 2015 These data suggest that abnormalities of the spindle checkpoint pathway participate in CIMP-positive renal carcinogenesis, and that AURKA and AURKB may be potential therapeutic targets in more aggressive CIMP-positive RCCs. Cyclic IMP 204-208 aurora kinase B Homo sapiens 142-147 26061684-4 2015 Genes encoding microtubule-associated proteins, such as DNAH2, DNAH5, DNAH10, RP1 and HAUS8, showed a 10% or higher incidence of genetic aberrations (non-synonymous single-nucleotide mutations and insertions/deletions) in CIMP-positive RCCs, whereas CIMP-negative RCCs lacked distinct genetic characteristics. Cyclic IMP 222-226 dynein axonemal heavy chain 5 Homo sapiens 63-68 26061684-4 2015 Genes encoding microtubule-associated proteins, such as DNAH2, DNAH5, DNAH10, RP1 and HAUS8, showed a 10% or higher incidence of genetic aberrations (non-synonymous single-nucleotide mutations and insertions/deletions) in CIMP-positive RCCs, whereas CIMP-negative RCCs lacked distinct genetic characteristics. Cyclic IMP 222-226 dynein axonemal heavy chain 10 Homo sapiens 70-76 26061684-4 2015 Genes encoding microtubule-associated proteins, such as DNAH2, DNAH5, DNAH10, RP1 and HAUS8, showed a 10% or higher incidence of genetic aberrations (non-synonymous single-nucleotide mutations and insertions/deletions) in CIMP-positive RCCs, whereas CIMP-negative RCCs lacked distinct genetic characteristics. Cyclic IMP 222-226 RP1 axonemal microtubule associated Homo sapiens 78-81 26061684-4 2015 Genes encoding microtubule-associated proteins, such as DNAH2, DNAH5, DNAH10, RP1 and HAUS8, showed a 10% or higher incidence of genetic aberrations (non-synonymous single-nucleotide mutations and insertions/deletions) in CIMP-positive RCCs, whereas CIMP-negative RCCs lacked distinct genetic characteristics. Cyclic IMP 222-226 HAUS augmin like complex subunit 8 Homo sapiens 86-91 26061684-4 2015 Genes encoding microtubule-associated proteins, such as DNAH2, DNAH5, DNAH10, RP1 and HAUS8, showed a 10% or higher incidence of genetic aberrations (non-synonymous single-nucleotide mutations and insertions/deletions) in CIMP-positive RCCs, whereas CIMP-negative RCCs lacked distinct genetic characteristics. Cyclic IMP 250-254 dynein axonemal heavy chain 2 Homo sapiens 56-61 26061684-4 2015 Genes encoding microtubule-associated proteins, such as DNAH2, DNAH5, DNAH10, RP1 and HAUS8, showed a 10% or higher incidence of genetic aberrations (non-synonymous single-nucleotide mutations and insertions/deletions) in CIMP-positive RCCs, whereas CIMP-negative RCCs lacked distinct genetic characteristics. Cyclic IMP 250-254 dynein axonemal heavy chain 5 Homo sapiens 63-68 26061684-4 2015 Genes encoding microtubule-associated proteins, such as DNAH2, DNAH5, DNAH10, RP1 and HAUS8, showed a 10% or higher incidence of genetic aberrations (non-synonymous single-nucleotide mutations and insertions/deletions) in CIMP-positive RCCs, whereas CIMP-negative RCCs lacked distinct genetic characteristics. Cyclic IMP 250-254 dynein axonemal heavy chain 10 Homo sapiens 70-76 26061684-4 2015 Genes encoding microtubule-associated proteins, such as DNAH2, DNAH5, DNAH10, RP1 and HAUS8, showed a 10% or higher incidence of genetic aberrations (non-synonymous single-nucleotide mutations and insertions/deletions) in CIMP-positive RCCs, whereas CIMP-negative RCCs lacked distinct genetic characteristics. Cyclic IMP 250-254 RP1 axonemal microtubule associated Homo sapiens 78-81 26061684-4 2015 Genes encoding microtubule-associated proteins, such as DNAH2, DNAH5, DNAH10, RP1 and HAUS8, showed a 10% or higher incidence of genetic aberrations (non-synonymous single-nucleotide mutations and insertions/deletions) in CIMP-positive RCCs, whereas CIMP-negative RCCs lacked distinct genetic characteristics. Cyclic IMP 250-254 HAUS augmin like complex subunit 8 Homo sapiens 86-91 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 188-192 aurora kinase A Homo sapiens 109-114 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 188-192 aurora kinase B Homo sapiens 116-121 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 188-192 baculoviral IAP repeat containing 5 Homo sapiens 123-128 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 188-192 BUB1 mitotic checkpoint serine/threonine kinase Homo sapiens 130-134 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 188-192 cell division cycle 20 Homo sapiens 136-141 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 188-192 NIMA related kinase 2 Homo sapiens 143-147 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 188-192 SPC25 component of NDC80 kinetochore complex Homo sapiens 152-157 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 210-214 aurora kinase A Homo sapiens 109-114 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 210-214 aurora kinase B Homo sapiens 116-121 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 210-214 baculoviral IAP repeat containing 5 Homo sapiens 123-128 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 210-214 BUB1 mitotic checkpoint serine/threonine kinase Homo sapiens 130-134 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 210-214 cell division cycle 20 Homo sapiens 136-141 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 210-214 NIMA related kinase 2 Homo sapiens 143-147 26061684-6 2015 Quantitative RT-PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP-positive than in CIMP-negative RCCs. Cyclic IMP 210-214 SPC25 component of NDC80 kinetochore complex Homo sapiens 152-157 26061684-7 2015 All CIMP-positive RCCs showed overexpression of Aurora kinases, AURKA and AURKB, and this overexpression was mainly attributable to increased copy number. Cyclic IMP 4-8 aurora kinase A Homo sapiens 64-69 26061684-7 2015 All CIMP-positive RCCs showed overexpression of Aurora kinases, AURKA and AURKB, and this overexpression was mainly attributable to increased copy number. Cyclic IMP 4-8 aurora kinase B Homo sapiens 74-79 25418895-7 2015 Hierarchical clustering as well as principal component analysis identified three distinct subgroups of patients having discrete age at onset, clinicopathological, molecular and survival characteristics: (i) a KRAS associated CIMP-high subgroup; (ii) a significantly younger MSS, CIMP low, TP53 mutant group having differential KRAS mutation patterns, and (iii) a CIMP-negative, TP53 mutated group. Cyclic IMP 225-229 KRAS proto-oncogene, GTPase Homo sapiens 209-213 25023548-7 2014 However, in CIMP-high tumors, but not CIMP-low/0 tumors, SMO expression was significantly associated with better colorectal cancer-specific survival (log-rank P = 0.012; multivariate hazard ratio, 0.36; 95 % CI 0.13-0.95; P interaction = 0.035, for SMO and CIMP status). Cyclic IMP 12-16 smoothened, frizzled class receptor Homo sapiens 57-60 26063725-8 2015 This trend was also observed in colon polyps (CIMP-P, 16/40, 40%; CIMP-N, 2/24, 8%; P = 0.002), suggesting that TET1 methylation is an early event in CIMP tumorigenesis. Cyclic IMP 46-50 tet methylcytosine dioxygenase 1 Homo sapiens 112-116 26063725-11 2015 Our data suggest that TET1 methylation may contribute to the establishment of a unique pathway in respect to CIMP-mediated tumorigenesis, which may be incidental to hMLH1 methylation. Cyclic IMP 109-113 tet methylcytosine dioxygenase 1 Homo sapiens 22-26 26063725-11 2015 Our data suggest that TET1 methylation may contribute to the establishment of a unique pathway in respect to CIMP-mediated tumorigenesis, which may be incidental to hMLH1 methylation. Cyclic IMP 109-113 mutL homolog 1 Homo sapiens 165-170 26121593-8 2015 Stratification of CIMP status with regards to MLH1 methylation status further enabled prediction of gastric cancer prognosis. Cyclic IMP 18-22 mutL homolog 1 Homo sapiens 46-50 24838152-8 2015 Interestingly, no CIMP features were found for the weakly methylated samples analyzed in this study but could be seen in 82% of the strongly methylated cases, indicating a possible use for DUSP9 as CIMP marker. Cyclic IMP 198-202 dual specificity phosphatase 9 Homo sapiens 189-194 25468227-5 2015 In the CIMP-negative, mainly IDH wild-type group, MGMT promoter methylation may be used to identify patients who benefit from alkylating chemotherapy. Cyclic IMP 7-11 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 29-32 25468227-5 2015 In the CIMP-negative, mainly IDH wild-type group, MGMT promoter methylation may be used to identify patients who benefit from alkylating chemotherapy. Cyclic IMP 7-11 O-6-methylguanine-DNA methyltransferase Homo sapiens 50-54 25367952-0 2014 MAFG mediates CIMP in BRAF-mutant colorectal cancer. Cyclic IMP 14-18 MAF bZIP transcription factor G Homo sapiens 0-4 24752710-8 2014 In contrast, miR-31 was slightly but insignificantly associated with CIMP status in the cases with wild-type BRAF. Cyclic IMP 69-73 microRNA 31 Homo sapiens 13-19 24752710-11 2014 In conclusion, miR-31 expression was associated with CIMP-high status in serrated lesions with BRAF mutation. Cyclic IMP 53-57 microRNA 31 Homo sapiens 15-21 24752710-11 2014 In conclusion, miR-31 expression was associated with CIMP-high status in serrated lesions with BRAF mutation. Cyclic IMP 53-57 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 95-99 25367952-0 2014 MAFG mediates CIMP in BRAF-mutant colorectal cancer. Cyclic IMP 14-18 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 22-26 25367952-1 2014 An MAFG-containing corepressor complex induces CIMP in BRAF(V600E)-positive colorectal cancer. Cyclic IMP 47-51 MAF bZIP transcription factor G Homo sapiens 3-7 25367952-1 2014 An MAFG-containing corepressor complex induces CIMP in BRAF(V600E)-positive colorectal cancer. Cyclic IMP 47-51 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 55-60 25496513-2 2014 CIMP is associated with microsatellite instability but is also found in BRAF mutant microsatellite stable cancers that are associated with poor prognosis. Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 72-76 25496513-3 2014 The isocitrate dehydrogenase 1 (IDH1) gene causes CIMP in glioma due to an activating mutation that produces the 2-hydroxyglutarate oncometabolite. Cyclic IMP 50-54 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 4-30 25496513-3 2014 The isocitrate dehydrogenase 1 (IDH1) gene causes CIMP in glioma due to an activating mutation that produces the 2-hydroxyglutarate oncometabolite. Cyclic IMP 50-54 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 32-36 25496513-4 2014 We therefore examined IDH1 alteration as a potential cause of CIMP in colorectal cancer. Cyclic IMP 62-66 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 22-26 25496513-5 2014 The IDH1 mutational hotspot was screened in 86 CIMP-positive and 80 CIMP-negative cancers. Cyclic IMP 47-51 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 4-8 25496513-5 2014 The IDH1 mutational hotspot was screened in 86 CIMP-positive and 80 CIMP-negative cancers. Cyclic IMP 68-72 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 4-8 25496513-10 2014 Unsupervised hierarchical cluster analysis identified an IDH1 mutation-like methylation signature in approximately half of the CIMP-positive cancers. Cyclic IMP 127-131 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 57-61 25496513-11 2014 IDH1 mutation appears to cause CIMP in a small proportion of BRAF mutant, microsatellite stable colorectal cancers. Cyclic IMP 31-35 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 0-4 25496513-11 2014 IDH1 mutation appears to cause CIMP in a small proportion of BRAF mutant, microsatellite stable colorectal cancers. Cyclic IMP 31-35 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 61-65 24928946-5 2014 CL3 had the highest methylation index (0.25, 0.49, and 0.69, respectively, P = <0.01) and was strongly associated with CIMP (P < 0.01). Cyclic IMP 122-126 adhesion G protein-coupled receptor L3 Homo sapiens 0-3 26134964-8 2014 Finally, multivariate analysis showed that proximal location and BRAF mutation were significantly associated with an increased risk of CIMP. Cyclic IMP 135-139 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 65-69 25005754-6 2014 BRAF mutations were significantly associated with right sided tumors (p = 0.0019), MSI-H status (p = 0.0144), CIMP (p = 0.0017) and a high proliferative index of Ki67 expression (p = 0.0162). Cyclic IMP 110-114 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 0-4 25332168-5 2014 RESULTS: Receiver operating characteristic curve analysis showed that area under the curve values for the 23 CpG units including the 32 CpG sites in the 7 CIMP-marker genes, i.e. FAM150A, ZNF540, ZNF671, ZNF154, PRAC, TRH and SLC13A5, for discrimination of CIMP-positive from CIMP-negative ccRCCs were larger than 0.95. Cyclic IMP 155-159 ALK and LTK ligand 1 Homo sapiens 179-186 25332168-5 2014 RESULTS: Receiver operating characteristic curve analysis showed that area under the curve values for the 23 CpG units including the 32 CpG sites in the 7 CIMP-marker genes, i.e. FAM150A, ZNF540, ZNF671, ZNF154, PRAC, TRH and SLC13A5, for discrimination of CIMP-positive from CIMP-negative ccRCCs were larger than 0.95. Cyclic IMP 155-159 zinc finger protein 540 Homo sapiens 188-194 25093535-7 2014 In line, independent TCGA data revealed a significant expression loss of ITIH5, particularly in the MSI-high and CIMP-positive phenotype concordant with an increased ITIH5 hypermethylation in CIMP-positive colon tumors (P<0.001). Cyclic IMP 113-117 inter-alpha-trypsin inhibitor heavy chain 5 Homo sapiens 73-78 25093535-7 2014 In line, independent TCGA data revealed a significant expression loss of ITIH5, particularly in the MSI-high and CIMP-positive phenotype concordant with an increased ITIH5 hypermethylation in CIMP-positive colon tumors (P<0.001). Cyclic IMP 192-196 inter-alpha-trypsin inhibitor heavy chain 5 Homo sapiens 166-171 25093535-8 2014 In proximal, i.e., right-sided tumors, abundant ITIH5 expression was associated with longer overall survival (OS, P = 0.049) and the CIMP-positive (P = 0.032) subgroup. Cyclic IMP 133-137 inter-alpha-trypsin inhibitor heavy chain 5 Homo sapiens 48-53 25093535-10 2014 In conclusion, our results indicate that ITIH5 is a novel putative tumor suppressor gene in colon cancer with a potential impact in the CIMP-related pathway. Cyclic IMP 136-140 inter-alpha-trypsin inhibitor heavy chain 5 Homo sapiens 41-46 25093535-11 2014 ITIH5 may serve as a novel epigenetic-based diagnostic biomarker with further clinical impact for risk stratification of CIMP-positive colon cancer patients. Cyclic IMP 121-125 inter-alpha-trypsin inhibitor heavy chain 5 Homo sapiens 0-5 25126956-12 2014 Loss of CDX2 expression is probably correlated to tumor grade, stage, right-sided tumor location, MMR-deficiency, CIMP, and BRAF mutations. Cyclic IMP 114-118 caudal type homeobox 2 Homo sapiens 8-12 24906916-11 2014 The augmentation of contraction caused by hypoxia or cIMP was accompanied by increased phosphorylation of myosin phosphatase target subunit 1 at Thr(853), which was prevented by the ROCK inhibitor Y-27632. Cyclic IMP 53-57 protein phosphatase 1 regulatory subunit 12A Homo sapiens 106-141 24885062-10 2014 Of interest, compared to KRAS-wild-type, overall, KRAS-mutated cancers more frequently exhibited cecal location (24% vs. 12% in KRAS-wild-type; P < 0.0001), CIMP-low (49% vs. 32% in KRAS-wild-type; P < 0.0001), and PIK3CA mutations (24% vs. 11% in KRAS-wild-type; P < 0.0001). Cyclic IMP 160-164 KRAS proto-oncogene, GTPase Homo sapiens 50-54 24885062-10 2014 Of interest, compared to KRAS-wild-type, overall, KRAS-mutated cancers more frequently exhibited cecal location (24% vs. 12% in KRAS-wild-type; P < 0.0001), CIMP-low (49% vs. 32% in KRAS-wild-type; P < 0.0001), and PIK3CA mutations (24% vs. 11% in KRAS-wild-type; P < 0.0001). Cyclic IMP 160-164 KRAS proto-oncogene, GTPase Homo sapiens 50-54 24885062-10 2014 Of interest, compared to KRAS-wild-type, overall, KRAS-mutated cancers more frequently exhibited cecal location (24% vs. 12% in KRAS-wild-type; P < 0.0001), CIMP-low (49% vs. 32% in KRAS-wild-type; P < 0.0001), and PIK3CA mutations (24% vs. 11% in KRAS-wild-type; P < 0.0001). Cyclic IMP 160-164 KRAS proto-oncogene, GTPase Homo sapiens 50-54 24885062-10 2014 Of interest, compared to KRAS-wild-type, overall, KRAS-mutated cancers more frequently exhibited cecal location (24% vs. 12% in KRAS-wild-type; P < 0.0001), CIMP-low (49% vs. 32% in KRAS-wild-type; P < 0.0001), and PIK3CA mutations (24% vs. 11% in KRAS-wild-type; P < 0.0001). Cyclic IMP 160-164 KRAS proto-oncogene, GTPase Homo sapiens 50-54 24778007-7 2014 CIMP is the third most commonly involved event, and is defined by widespread methylation of CpG islands of suppressor promoters, with two phenotypes: CIMP-high and CIMP-low which interact with MSI or CIN status V-raf murine sarcoma viral oncogene homolog B (BRAF) is a serine-threonine protein kinase that acts as a downstream effector of the Kirsten rat sarcoma viral oncogene homolog (KRAS) pathway. Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Rattus norvegicus 211-256 24166180-4 2014 The aim of this study is to determine the specificity of Cdx2 protein expression and CpG promoter hypermethylation for BRAF(V600E) and high-level CIMP in colorectal cancer. Cyclic IMP 146-150 caudal type homeobox 2 Homo sapiens 57-61 24778007-7 2014 CIMP is the third most commonly involved event, and is defined by widespread methylation of CpG islands of suppressor promoters, with two phenotypes: CIMP-high and CIMP-low which interact with MSI or CIN status V-raf murine sarcoma viral oncogene homolog B (BRAF) is a serine-threonine protein kinase that acts as a downstream effector of the Kirsten rat sarcoma viral oncogene homolog (KRAS) pathway. Cyclic IMP 0-4 Braf transforming gene Mus musculus 258-262 24778007-7 2014 CIMP is the third most commonly involved event, and is defined by widespread methylation of CpG islands of suppressor promoters, with two phenotypes: CIMP-high and CIMP-low which interact with MSI or CIN status V-raf murine sarcoma viral oncogene homolog B (BRAF) is a serine-threonine protein kinase that acts as a downstream effector of the Kirsten rat sarcoma viral oncogene homolog (KRAS) pathway. Cyclic IMP 0-4 KRAS proto-oncogene, GTPase Rattus norvegicus 387-391 23801749-3 2013 Recently, it was shown that somatic isocitrate dehydrogenase-1 (IDH1) mutations, frequently observed in gliomas, establish CIMP in primary human astrocytes by remodeling the methylome. Cyclic IMP 123-127 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 36-62 24211491-10 2014 A prevalence screen showed that nonsilencing mutations in CHD7 and CHD8 occurred significantly more frequently in CIMP1 tumors (18 of 42 [43%]) than in CIMP2 (3 of 34 [9%]; P < .01) or CIMP-negative tumors (2 of 34 [6%]; P < .001). Cyclic IMP 114-118 chromodomain helicase DNA binding protein 7 Homo sapiens 58-62 24211491-10 2014 A prevalence screen showed that nonsilencing mutations in CHD7 and CHD8 occurred significantly more frequently in CIMP1 tumors (18 of 42 [43%]) than in CIMP2 (3 of 34 [9%]; P < .01) or CIMP-negative tumors (2 of 34 [6%]; P < .001). Cyclic IMP 114-118 chromodomain helicase DNA binding protein 8 Homo sapiens 67-71 24812557-0 2014 The CIMP Phenotype in BRAF Mutant Serrated Polyps from a Prospective Colonoscopy Patient Cohort. Cyclic IMP 4-8 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 22-26 24812557-3 2014 This study aims to evaluate CIMP status of all the serrated polyp subtypes and its association with functionally important genes such as MLH1, p16, and IGFBP7. Cyclic IMP 28-32 mutL homolog 1 Homo sapiens 137-141 24812557-3 2014 This study aims to evaluate CIMP status of all the serrated polyp subtypes and its association with functionally important genes such as MLH1, p16, and IGFBP7. Cyclic IMP 28-32 cyclin dependent kinase inhibitor 2A Homo sapiens 143-146 24812557-3 2014 This study aims to evaluate CIMP status of all the serrated polyp subtypes and its association with functionally important genes such as MLH1, p16, and IGFBP7. Cyclic IMP 28-32 insulin like growth factor binding protein 7 Homo sapiens 152-158 24812557-5 2014 Results showed that CIMP-high serrated polyps were strongly associated with BRAF mutation and proximal colon. Cyclic IMP 20-24 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 76-80 23794399-7 2014 After stratifying by tumor molecular subtype, SNP associations observed for colon cancer were: VEGFA rs2010963 with CIMP+ colon tumors; FLT1 rs4771249 and rs7987649 with TP53; FLT1 rs3751397, rs7337610, rs7987649, and rs9513008 and KDR rs10020464, rs11941492, and rs12498529 with MSI+ and CIMP+/KRAS2-mutated tumors. Cyclic IMP 116-120 vascular endothelial growth factor A Homo sapiens 95-100 24074367-3 2013 Although CadD is annotated as an adenosine deaminase, the protein specifically deaminates cAMP to cyclic-3",5"-inosine monophosphate (cIMP) with a kcat/Km of 2.7 +- 0.4 x 10(5) M(-1) s(-1) and has no activity on adenosine, adenine, or 5"-adenosine monophosphate (AMP). Cyclic IMP 134-138 adenosine deaminase Homo sapiens 33-52 23948976-9 2013 CIMP+ and MGMT-STP27 methylated tumors showed a clear benefit from adjuvant PCV chemotherapy: the median OS of CIMP+ samples in the RT and RT-PCV arms was 3.27 and 9.51 years, respectively (P = 0.0033); for MGMT-STP27 methylated samples, it was 1.98 and 8.65 years. Cyclic IMP 0-4 O-6-methylguanine-DNA methyltransferase Homo sapiens 207-211 23801749-3 2013 Recently, it was shown that somatic isocitrate dehydrogenase-1 (IDH1) mutations, frequently observed in gliomas, establish CIMP in primary human astrocytes by remodeling the methylome. Cyclic IMP 123-127 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 64-68 23785428-7 2013 High-levels of CIMP were more frequently found in PIK3CA-mutated tumors compared with PIK3CA wild-type tumors (22% vs. 11%; P = 0.004). Cyclic IMP 15-19 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 50-56 23739128-5 2013 Almost all NBLs with MYCN amplification displayed CIMP, and even among NBLs without MYCN amplification, NBLs with CIMP had worse prognosis (HR=12). Cyclic IMP 50-54 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 21-25 23370766-7 2013 The discordant subtypes, CIMP-H MLH1 methylation-negative and CIMP-L/0 MLH1m+, were found in 5 and 7% of microsatellite-unstable colorectal cancers, respectively. Cyclic IMP 25-29 mutL homolog 1 Homo sapiens 32-36 23689617-9 2013 Furthermore, transcriptomic analyses revealed CIMP-specific gene expression signatures, indicating the impact of genetic status (IDH mutation, 1p/19q codeletion, TP53 mutation) on gene expression, and pointing to candidate biomarkers. Cyclic IMP 46-50 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 129-132 23689617-9 2013 Furthermore, transcriptomic analyses revealed CIMP-specific gene expression signatures, indicating the impact of genetic status (IDH mutation, 1p/19q codeletion, TP53 mutation) on gene expression, and pointing to candidate biomarkers. Cyclic IMP 46-50 tumor protein p53 Homo sapiens 162-166 23633456-9 2013 In integrated cohort analysis, PIK3CA exon 9 and 20 mutations were overrepresented in proximal, CIMP-low (CIMP-L), and KRAS-mutated cancers (P <= 0.011). Cyclic IMP 96-100 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 31-37 23785428-11 2013 In summary, PIK3CA-mutated colorectal carcinomas are more likely to develop in the proximal colon, to demonstrate high levels of CIMP, KRAS mutation and loss of MGMT expression. Cyclic IMP 129-133 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 12-18 23341177-3 2013 CIMP-positive CRCs are associated with a proximal location in the colon, microsatellite instability, BRAF mutation and a relatively poor clinical outcome. Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 101-105 23328994-8 2013 However, inclusion of MSI screening status and CIMP status in the multivariate analysis strengthened the risk estimates for high FAP expression in the tumor center (HR = 1.89; 95 % CI 1.13-3.14; p = 0.014), emphasizing the role of FAP as an independent prognostic factor. Cyclic IMP 47-51 fibroblast activation protein alpha Homo sapiens 129-132 22995252-6 2012 Interestingly, a subset of CIMP-positive malignant lesions exhibited frequent copy number gains on chromosomes 7 and 19 and genetic defects in the AKT/PIK3CA pathway genes. Cyclic IMP 27-31 AKT serine/threonine kinase 1 Homo sapiens 147-150 23291739-5 2013 Cluster analysis has shown that a subset of LTS showed a G-CIMP positive phenotype that was tightly associated with IDH1 mutation status and was confirmed by analysis of the G-CIMP signature genes. Cyclic IMP 59-63 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 116-120 22899282-5 2012 We demonstrate that many of these alterations are consistent with those observed in IDH1-mutant and G-CIMP+ primary gliomas and can segregate IDH wild-type and mutated tumors as well as those exhibiting the G-CIMP phenotype in unsupervised analysis of two primary glioma cohorts. Cyclic IMP 102-106 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 84-88 22899282-5 2012 We demonstrate that many of these alterations are consistent with those observed in IDH1-mutant and G-CIMP+ primary gliomas and can segregate IDH wild-type and mutated tumors as well as those exhibiting the G-CIMP phenotype in unsupervised analysis of two primary glioma cohorts. Cyclic IMP 102-106 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 84-87 22899282-5 2012 We demonstrate that many of these alterations are consistent with those observed in IDH1-mutant and G-CIMP+ primary gliomas and can segregate IDH wild-type and mutated tumors as well as those exhibiting the G-CIMP phenotype in unsupervised analysis of two primary glioma cohorts. Cyclic IMP 209-213 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 84-88 22899282-5 2012 We demonstrate that many of these alterations are consistent with those observed in IDH1-mutant and G-CIMP+ primary gliomas and can segregate IDH wild-type and mutated tumors as well as those exhibiting the G-CIMP phenotype in unsupervised analysis of two primary glioma cohorts. Cyclic IMP 209-213 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 84-87 22995252-6 2012 Interestingly, a subset of CIMP-positive malignant lesions exhibited frequent copy number gains on chromosomes 7 and 19 and genetic defects in the AKT/PIK3CA pathway genes. Cyclic IMP 27-31 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 151-157 22825585-6 2012 RESULTS: CIMP(+) was detected in 27 of 99 (27.3%) duodenal adenocarcinomas and was associated with MSI (P = 0.011) and MLH1 methylation (P < 0.001), but not with KRAS mutations (P = 0.114), as compared with CIMP(-) tumors. Cyclic IMP 9-13 RB binding protein 4, chromatin remodeling factor Homo sapiens 99-102 23323463-5 2012 CIMP negative cases have a high rate of p53 mutations and lower rates of MSI or mutations of BRAF or KRAS. Cyclic IMP 0-4 tumor protein p53 Homo sapiens 40-43 23323463-5 2012 CIMP negative cases have a high rate of p53 mutations and lower rates of MSI or mutations of BRAF or KRAS. Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 93-97 23323463-5 2012 CIMP negative cases have a high rate of p53 mutations and lower rates of MSI or mutations of BRAF or KRAS. Cyclic IMP 0-4 KRAS proto-oncogene, GTPase Homo sapiens 101-105 22825585-8 2012 Among the CIMP(+) tumors, 15 (55.6%) were CIMP(+)/MLH1-unmethylated (MLH1-U). Cyclic IMP 10-14 mutL homolog 1 Homo sapiens 50-54 22825585-8 2012 Among the CIMP(+) tumors, 15 (55.6%) were CIMP(+)/MLH1-unmethylated (MLH1-U). Cyclic IMP 10-14 mutL homolog 1 Homo sapiens 69-73 22825585-11 2012 Patients with CIMP(+)/MLH1-U tumors had the worst OS and TTR. Cyclic IMP 14-18 mutL homolog 1 Homo sapiens 22-26 22810491-8 2012 Lower prevalence of MGMT methylation among CpG island methylator phenotype (CIMP) positive tumors was found in glioblastomas from The Cancer Genome Atlas than in low grade and anaplastic glioma cohorts, while in CIMP-negative gliomas MGMT was classified as methylated in approximately 50 % regardless of tumor grade. Cyclic IMP 76-80 O-6-methylguanine-DNA methyltransferase Homo sapiens 20-24 22825585-6 2012 RESULTS: CIMP(+) was detected in 27 of 99 (27.3%) duodenal adenocarcinomas and was associated with MSI (P = 0.011) and MLH1 methylation (P < 0.001), but not with KRAS mutations (P = 0.114), as compared with CIMP(-) tumors. Cyclic IMP 9-13 mutL homolog 1 Homo sapiens 119-123 22825585-6 2012 RESULTS: CIMP(+) was detected in 27 of 99 (27.3%) duodenal adenocarcinomas and was associated with MSI (P = 0.011) and MLH1 methylation (P < 0.001), but not with KRAS mutations (P = 0.114), as compared with CIMP(-) tumors. Cyclic IMP 9-13 KRAS proto-oncogene, GTPase Homo sapiens 165-169 21932420-7 2012 Overall, PIK3CA mutation was positively correlated with KRAS mutation (p < 0.001), MGMT methylation (p = 0.007) and CIMP (p < 0.001). Cyclic IMP 119-123 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 9-15 21557216-11 2012 CIMP was less common in MSS/BRAF mutant (26/47, 55.3%) compared to MSI/BRAF mutant cancers (41/54, 75.9%), but was more common than in MSS/BRAF wild type cancers (3/85, 3.5%) (p < 0.0001). Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 28-32 21964812-6 2012 In this study, we analyze the impact of SMAD4 expression on prognosis in relation to MSI screening status and CIMP status. Cyclic IMP 110-114 SMAD family member 4 Homo sapiens 40-45 22157715-8 2012 We have utilized this assay to compare the methylation levels of the PCDHB cluster between high-risk and very low-risk NB patients, confirming the predictive value of CIMP. Cyclic IMP 167-171 protocadherin beta cluster Homo sapiens 69-74 21791485-7 2012 The promoter regions of subset of genes highly specific to characterize the CIMP status (NEUROG1, IGF2, RUNX3, SOCS1, including MLH1) were hypermethylated, suggesting the presence of CIMP+ and MSI high tumor. Cyclic IMP 76-80 neurogenin 1 Homo sapiens 89-96 21791485-7 2012 The promoter regions of subset of genes highly specific to characterize the CIMP status (NEUROG1, IGF2, RUNX3, SOCS1, including MLH1) were hypermethylated, suggesting the presence of CIMP+ and MSI high tumor. Cyclic IMP 76-80 insulin like growth factor 2 Homo sapiens 98-102 21791485-7 2012 The promoter regions of subset of genes highly specific to characterize the CIMP status (NEUROG1, IGF2, RUNX3, SOCS1, including MLH1) were hypermethylated, suggesting the presence of CIMP+ and MSI high tumor. Cyclic IMP 76-80 RUNX family transcription factor 3 Homo sapiens 104-109 21791485-7 2012 The promoter regions of subset of genes highly specific to characterize the CIMP status (NEUROG1, IGF2, RUNX3, SOCS1, including MLH1) were hypermethylated, suggesting the presence of CIMP+ and MSI high tumor. Cyclic IMP 76-80 suppressor of cytokine signaling 1 Homo sapiens 111-116 21791485-7 2012 The promoter regions of subset of genes highly specific to characterize the CIMP status (NEUROG1, IGF2, RUNX3, SOCS1, including MLH1) were hypermethylated, suggesting the presence of CIMP+ and MSI high tumor. Cyclic IMP 76-80 mutL homolog 1 Homo sapiens 128-132 21659424-8 2012 One non-CIMP subgroup is distinguished by a significantly higher frequency of TP53 mutations and frequent occurrence in the distal colon, while the tumors that belong to the fourth group exhibit a low frequency of both cancer-specific DNA hypermethylation and gene mutations and are significantly enriched for rectal tumors. Cyclic IMP 8-12 tumor protein p53 Homo sapiens 78-82 22343889-6 2012 Examination of the epigenome of a large set of intermediate-grade gliomas demonstrates a distinct G-CIMP phenotype that is highly dependent on the presence of IDH mutation. Cyclic IMP 100-104 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 159-162 22343889-7 2012 Introduction of mutant IDH1 into primary human astrocytes alters specific histone marks, induces extensive DNA hypermethylation, and reshapes the methylome in a fashion that mirrors the changes observed in G-CIMP-positive lower-grade gliomas. Cyclic IMP 208-212 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 23-27 22343889-9 2012 Our findings demonstrate that IDH mutation is the molecular basis of CIMP in gliomas, provide a framework for understanding oncogenesis in these gliomas, and highlight the interplay between genomic and epigenomic changes in human cancers. Cyclic IMP 69-73 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 30-33 21987236-1 2012 In view of recent studies highlighting the prognostic relevance of expression and CpG island methylator phenotype (CIMP) of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (BNIP3) in invasive duct cell carcinoma (IDC), we hypothesized in this article that impaired one-carbon metabolism might influence CIMP phenotype of BNIP3. Cyclic IMP 115-119 BCL2 interacting protein 3 Homo sapiens 124-173 21987236-1 2012 In view of recent studies highlighting the prognostic relevance of expression and CpG island methylator phenotype (CIMP) of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (BNIP3) in invasive duct cell carcinoma (IDC), we hypothesized in this article that impaired one-carbon metabolism might influence CIMP phenotype of BNIP3. Cyclic IMP 115-119 BCL2 interacting protein 3 Homo sapiens 175-180 21987236-1 2012 In view of recent studies highlighting the prognostic relevance of expression and CpG island methylator phenotype (CIMP) of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (BNIP3) in invasive duct cell carcinoma (IDC), we hypothesized in this article that impaired one-carbon metabolism might influence CIMP phenotype of BNIP3. Cyclic IMP 305-309 BCL2 interacting protein 3 Homo sapiens 124-173 21987236-1 2012 In view of recent studies highlighting the prognostic relevance of expression and CpG island methylator phenotype (CIMP) of Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (BNIP3) in invasive duct cell carcinoma (IDC), we hypothesized in this article that impaired one-carbon metabolism might influence CIMP phenotype of BNIP3. Cyclic IMP 305-309 BCL2 interacting protein 3 Homo sapiens 175-180 21914791-6 2011 CIMP status correlated with survival, MGMT promoter methylation, 1p19q LOH, and IDH1 mutation status. Cyclic IMP 0-4 O-6-methylguanine-DNA methyltransferase Homo sapiens 38-42 22122229-6 2012 When Mg(2+) is used, sGC generates cGMP, cAMP, cIMP, and cXMP. Cyclic IMP 47-51 guanylate cyclase 1 soluble subunit beta 2 Rattus norvegicus 21-24 21914791-6 2011 CIMP status correlated with survival, MGMT promoter methylation, 1p19q LOH, and IDH1 mutation status. Cyclic IMP 0-4 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 80-84 21914791-9 2011 CONCLUSION: The strong association between CIMP status and MGMT promoter methylation suggests that the MGMT promoter methylation status is part of a more general, prognostically favorable genome-wide methylation profile. Cyclic IMP 43-47 O-6-methylguanine-DNA methyltransferase Homo sapiens 59-63 21914791-9 2011 CONCLUSION: The strong association between CIMP status and MGMT promoter methylation suggests that the MGMT promoter methylation status is part of a more general, prognostically favorable genome-wide methylation profile. Cyclic IMP 43-47 O-6-methylguanine-DNA methyltransferase Homo sapiens 103-107 21660972-5 2011 CIMP-H was found in 24 cases (7.1%) and linked (p < 0.0001) to more proximal tumour location, BRAF mutation, MSI-H, MGMT methylation (p = 0.022), advanced pT classification (p = 0.03), mucinous histology (p = 0.069), and less frequent KRAS mutation (p = 0.067) compared to CIMP-low or -negative cases. Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 97-101 21660972-5 2011 CIMP-H was found in 24 cases (7.1%) and linked (p < 0.0001) to more proximal tumour location, BRAF mutation, MSI-H, MGMT methylation (p = 0.022), advanced pT classification (p = 0.03), mucinous histology (p = 0.069), and less frequent KRAS mutation (p = 0.067) compared to CIMP-low or -negative cases. Cyclic IMP 0-4 O-6-methylguanine-DNA methyltransferase Homo sapiens 119-123 21660972-5 2011 CIMP-H was found in 24 cases (7.1%) and linked (p < 0.0001) to more proximal tumour location, BRAF mutation, MSI-H, MGMT methylation (p = 0.022), advanced pT classification (p = 0.03), mucinous histology (p = 0.069), and less frequent KRAS mutation (p = 0.067) compared to CIMP-low or -negative cases. Cyclic IMP 0-4 KRAS proto-oncogene, GTPase Homo sapiens 238-242 21427714-6 2011 Furthermore, a significant difference was observed in the frequency of the CpG island methylator phenotype (CIMP), involving the methylation of two or more CIMP-related genes (MINT1, MINT2, MINT31, p16, and MLH1), between SNs with the hyperplastic pattern and those with the mixed/adenomatous patterns (18/32 (56%) vs. 8/28 (29%) or 7/26 (27%); P=0.0309 or P=0.0249, respectively). Cyclic IMP 108-112 amyloid beta precursor protein binding family A member 1 Homo sapiens 176-181 21915661-7 2011 Aberrant CIMP was detected in 16% of chromosomal instable tumors and in 44% of both microsatellite instable and microsatellite and chromosomally stable carcinomas, KRAS was mutated in 55%, 0% and 10% of chromosomal instable, microsatellite instable and microsatellite and chromosomal stable tumors, respectively, while BRAF mutations occurred in 6% of chromosomal instable and 22% of both microsatellite instable and microsatellite and chromosomal stable carcinomas. Cyclic IMP 9-13 KRAS proto-oncogene, GTPase Homo sapiens 164-168 21915661-7 2011 Aberrant CIMP was detected in 16% of chromosomal instable tumors and in 44% of both microsatellite instable and microsatellite and chromosomally stable carcinomas, KRAS was mutated in 55%, 0% and 10% of chromosomal instable, microsatellite instable and microsatellite and chromosomal stable tumors, respectively, while BRAF mutations occurred in 6% of chromosomal instable and 22% of both microsatellite instable and microsatellite and chromosomal stable carcinomas. Cyclic IMP 9-13 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 319-323 21827707-7 2011 RESULTS: CIMP-high CRCs were identified in 34 cases (13.9%), and were significantly associated with proximal tumor location, poorly differentiated carcinoma, mucinous histology, and high frequencies of BRAF mutation, MGMT methylation, and MSI-high compared to CIMP-low/negative carcinomas. Cyclic IMP 9-13 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 202-206 21827707-7 2011 RESULTS: CIMP-high CRCs were identified in 34 cases (13.9%), and were significantly associated with proximal tumor location, poorly differentiated carcinoma, mucinous histology, and high frequencies of BRAF mutation, MGMT methylation, and MSI-high compared to CIMP-low/negative carcinomas. Cyclic IMP 9-13 O-6-methylguanine-DNA methyltransferase Homo sapiens 217-221 21827707-7 2011 RESULTS: CIMP-high CRCs were identified in 34 cases (13.9%), and were significantly associated with proximal tumor location, poorly differentiated carcinoma, mucinous histology, and high frequencies of BRAF mutation, MGMT methylation, and MSI-high compared to CIMP-low/negative carcinomas. Cyclic IMP 9-13 RB binding protein 4, chromatin remodeling factor Homo sapiens 239-242 21427714-6 2011 Furthermore, a significant difference was observed in the frequency of the CpG island methylator phenotype (CIMP), involving the methylation of two or more CIMP-related genes (MINT1, MINT2, MINT31, p16, and MLH1), between SNs with the hyperplastic pattern and those with the mixed/adenomatous patterns (18/32 (56%) vs. 8/28 (29%) or 7/26 (27%); P=0.0309 or P=0.0249, respectively). Cyclic IMP 108-112 amyloid beta precursor protein binding family A member 2 Homo sapiens 183-188 21427714-6 2011 Furthermore, a significant difference was observed in the frequency of the CpG island methylator phenotype (CIMP), involving the methylation of two or more CIMP-related genes (MINT1, MINT2, MINT31, p16, and MLH1), between SNs with the hyperplastic pattern and those with the mixed/adenomatous patterns (18/32 (56%) vs. 8/28 (29%) or 7/26 (27%); P=0.0309 or P=0.0249, respectively). Cyclic IMP 108-112 cyclin dependent kinase inhibitor 2A Homo sapiens 198-201 21427714-6 2011 Furthermore, a significant difference was observed in the frequency of the CpG island methylator phenotype (CIMP), involving the methylation of two or more CIMP-related genes (MINT1, MINT2, MINT31, p16, and MLH1), between SNs with the hyperplastic pattern and those with the mixed/adenomatous patterns (18/32 (56%) vs. 8/28 (29%) or 7/26 (27%); P=0.0309 or P=0.0249, respectively). Cyclic IMP 108-112 mutL homolog 1 Homo sapiens 207-211 21427714-6 2011 Furthermore, a significant difference was observed in the frequency of the CpG island methylator phenotype (CIMP), involving the methylation of two or more CIMP-related genes (MINT1, MINT2, MINT31, p16, and MLH1), between SNs with the hyperplastic pattern and those with the mixed/adenomatous patterns (18/32 (56%) vs. 8/28 (29%) or 7/26 (27%); P=0.0309 or P=0.0249, respectively). Cyclic IMP 156-160 amyloid beta precursor protein binding family A member 1 Homo sapiens 176-181 21423154-6 2011 In particular, colorectal carcinomas with BRAF mutations have been shown to be strongly associated with CIMP. Cyclic IMP 104-108 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 42-46 22977561-12 2011 In MSI cancers with the BRAF mutation, a higher correlation with CIMP (p=0.032) was observed. Cyclic IMP 65-69 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 24-28 21068132-8 2011 The CIMP marker RUNX3 was the earliest CpG island showing significant change, followed by the CIMP markers NEUROG1 and CACNA1G at the hyperplastic polyp stage. Cyclic IMP 4-8 RUNX family transcription factor 3 Homo sapiens 16-21 20949557-7 2011 The CRP rs1205 AA genotype also was associated with an increased risk of CIMP+ rectal tumors (OR 2.5, 95%CI 1.2-5.3); conversely, the rs1417938 A allele was associated with a reduced risk of CIMP+ rectal tumors (OR 0.5, 95%CI 0.3-0.9). Cyclic IMP 73-77 C-reactive protein Homo sapiens 4-7 21068132-12 2011 A subset of the CIMP panel (NEUROG1, CACNA1G and CDKN2A) positively correlated with DNMT3B levels of expression (p < 0.05). Cyclic IMP 16-20 neurogenin 1 Homo sapiens 28-35 21068132-12 2011 A subset of the CIMP panel (NEUROG1, CACNA1G and CDKN2A) positively correlated with DNMT3B levels of expression (p < 0.05). Cyclic IMP 16-20 calcium voltage-gated channel subunit alpha1 G Homo sapiens 37-44 21068132-12 2011 A subset of the CIMP panel (NEUROG1, CACNA1G and CDKN2A) positively correlated with DNMT3B levels of expression (p < 0.05). Cyclic IMP 16-20 cyclin dependent kinase inhibitor 2A Homo sapiens 49-55 21068132-12 2011 A subset of the CIMP panel (NEUROG1, CACNA1G and CDKN2A) positively correlated with DNMT3B levels of expression (p < 0.05). Cyclic IMP 16-20 DNA methyltransferase 3 beta Homo sapiens 84-90 21036793-3 2011 Activation of oncogenes including KRAS, BRAF and PIK3CA affects intracellular signalling pathways and has been associated with CIMP and MSI. Cyclic IMP 127-131 KRAS proto-oncogene, GTPase Homo sapiens 34-38 21036793-3 2011 Activation of oncogenes including KRAS, BRAF and PIK3CA affects intracellular signalling pathways and has been associated with CIMP and MSI. Cyclic IMP 127-131 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 40-44 21036793-3 2011 Activation of oncogenes including KRAS, BRAF and PIK3CA affects intracellular signalling pathways and has been associated with CIMP and MSI. Cyclic IMP 127-131 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 49-55 21949851-9 2011 Among MSI-high tumors, TGFBR2 mononucleotide mutation was associated with CIMP-high independent of other variables [multivariate odds ratio, 3.57; 95% CI, 1.66-7.66; p = 0.0011]. Cyclic IMP 74-78 transforming growth factor beta receptor 2 Homo sapiens 23-29 21347319-3 2011 CIMP is associated with methylation of tumor suppressor genes including regulators of DNA mismatch repair (such as MLH1, MGMT), and negative regulators of Wnt signaling (such as WIF1). Cyclic IMP 0-4 mutL homolog 1 Homo sapiens 115-119 21347319-3 2011 CIMP is associated with methylation of tumor suppressor genes including regulators of DNA mismatch repair (such as MLH1, MGMT), and negative regulators of Wnt signaling (such as WIF1). Cyclic IMP 0-4 O-6-methylguanine-DNA methyltransferase Homo sapiens 121-125 21347319-3 2011 CIMP is associated with methylation of tumor suppressor genes including regulators of DNA mismatch repair (such as MLH1, MGMT), and negative regulators of Wnt signaling (such as WIF1). Cyclic IMP 0-4 WNT inhibitory factor 1 Homo sapiens 178-182 21462086-2 2011 We also examined folate intake and common MTHFR polymorphisms in relation to CIMP. Cyclic IMP 77-81 methylenetetrahydrofolate reductase Homo sapiens 42-47 21462086-7 2011 MTHFR 1298A>C influenced folate in male CIMP+ risk (P interaction < 0.01). Cyclic IMP 43-47 methylenetetrahydrofolate reductase Homo sapiens 0-5 20444249-9 2010 CIMP-high was infrequent and related to BRAF mutations in patients below 50 years. Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 40-44 20077021-9 2010 CONCLUSIONS: The study suggests that specific CIMP markers, such as p16 ( INK4a ) and MINT31, should be further verified as potential epigenetic targets for the design of efficient chemotherapy regimens. Cyclic IMP 46-50 cyclin dependent kinase inhibitor 2A Homo sapiens 68-71 20077021-9 2010 CONCLUSIONS: The study suggests that specific CIMP markers, such as p16 ( INK4a ) and MINT31, should be further verified as potential epigenetic targets for the design of efficient chemotherapy regimens. Cyclic IMP 46-50 cyclin dependent kinase inhibitor 2A Homo sapiens 74-79 20381446-6 2010 The CIMP status of the CRC cases was determined by MS-PCR in tumor tissue by a panel of five markers (CACNA1G, IGF2, NEUROG1, RUNX3 and SOCS1), which was also followed by analyzing hMLH1 methylation and BRAF V600E mutation. Cyclic IMP 4-8 calcium voltage-gated channel subunit alpha1 G Homo sapiens 102-109 20492682-10 2010 This study suggests that both KRAS and BRAF mutations are involved with the CIMP-H pathway of CRC rather than with distinct CIMP subgroups. Cyclic IMP 76-80 KRAS proto-oncogene, GTPase Homo sapiens 30-34 20492682-10 2010 This study suggests that both KRAS and BRAF mutations are involved with the CIMP-H pathway of CRC rather than with distinct CIMP subgroups. Cyclic IMP 76-80 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 39-43 21507361-5 2011 Cancers with CIMP show distinct genetic changes, including microsatellite instability and mutations in the BRAF Ser/Thr kinase gene. Cyclic IMP 13-17 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 107-111 20490964-7 2010 There was a significant association between CIMP and methylation of RASSF1A, BRCA1, p16, CDH1, ER, RARbeta2, APC, and DAPK (P < 0.05); the methylation link profile of CDH1, RASSF1A, BRCA1, and RARbeta2 as breast cancer marker may contribute high sensitivity (90%) and specificity (88%). Cyclic IMP 44-48 Ras association domain family member 1 Homo sapiens 68-75 20490964-7 2010 There was a significant association between CIMP and methylation of RASSF1A, BRCA1, p16, CDH1, ER, RARbeta2, APC, and DAPK (P < 0.05); the methylation link profile of CDH1, RASSF1A, BRCA1, and RARbeta2 as breast cancer marker may contribute high sensitivity (90%) and specificity (88%). Cyclic IMP 44-48 BRCA1 DNA repair associated Homo sapiens 77-82 20490964-7 2010 There was a significant association between CIMP and methylation of RASSF1A, BRCA1, p16, CDH1, ER, RARbeta2, APC, and DAPK (P < 0.05); the methylation link profile of CDH1, RASSF1A, BRCA1, and RARbeta2 as breast cancer marker may contribute high sensitivity (90%) and specificity (88%). Cyclic IMP 44-48 cyclin dependent kinase inhibitor 2A Homo sapiens 84-87 20490964-7 2010 There was a significant association between CIMP and methylation of RASSF1A, BRCA1, p16, CDH1, ER, RARbeta2, APC, and DAPK (P < 0.05); the methylation link profile of CDH1, RASSF1A, BRCA1, and RARbeta2 as breast cancer marker may contribute high sensitivity (90%) and specificity (88%). Cyclic IMP 44-48 cadherin 1 Homo sapiens 89-93 20490964-7 2010 There was a significant association between CIMP and methylation of RASSF1A, BRCA1, p16, CDH1, ER, RARbeta2, APC, and DAPK (P < 0.05); the methylation link profile of CDH1, RASSF1A, BRCA1, and RARbeta2 as breast cancer marker may contribute high sensitivity (90%) and specificity (88%). Cyclic IMP 44-48 death associated protein kinase 1 Homo sapiens 118-122 20490964-7 2010 There was a significant association between CIMP and methylation of RASSF1A, BRCA1, p16, CDH1, ER, RARbeta2, APC, and DAPK (P < 0.05); the methylation link profile of CDH1, RASSF1A, BRCA1, and RARbeta2 as breast cancer marker may contribute high sensitivity (90%) and specificity (88%). Cyclic IMP 44-48 cadherin 1 Homo sapiens 170-174 20490964-7 2010 There was a significant association between CIMP and methylation of RASSF1A, BRCA1, p16, CDH1, ER, RARbeta2, APC, and DAPK (P < 0.05); the methylation link profile of CDH1, RASSF1A, BRCA1, and RARbeta2 as breast cancer marker may contribute high sensitivity (90%) and specificity (88%). Cyclic IMP 44-48 Ras association domain family member 1 Homo sapiens 176-183 20490964-7 2010 There was a significant association between CIMP and methylation of RASSF1A, BRCA1, p16, CDH1, ER, RARbeta2, APC, and DAPK (P < 0.05); the methylation link profile of CDH1, RASSF1A, BRCA1, and RARbeta2 as breast cancer marker may contribute high sensitivity (90%) and specificity (88%). Cyclic IMP 44-48 BRCA1 DNA repair associated Homo sapiens 185-190 19790197-7 2010 Among colon cancer patients, CDK8 expression significantly increased colon cancer-specific mortality in both univariate analysis [HR 1.70; 95% confidence interval (CI), 1.03-2.83; p = 0.039] and multivariate analysis (adjusted HR 2.05; 95% CI, 1.18-3.56; p = 0.011) that was adjusted for potential confounders including beta-catenin, COX-2, FASN, LINE-1 hypomethylation, CIMP and MSI. Cyclic IMP 371-375 cyclin dependent kinase 8 Homo sapiens 29-33 19841986-7 2010 In the COPD group, unmethylated SPARC and sFRP-2 genes or a negative CpG island methylator phenotype (CIMP) was a negative prognostic factor, while methylation of p16(INK4A) and WNT antagonist genes was a negative prognostic factor in the non-COPD group. Cyclic IMP 102-106 COPD Homo sapiens 7-11 20388775-8 2010 The mean methylation scores at CIMP-related markers were significantly higher in Lynch syndrome tumors with MSH2 methylation than MSH2-unmethylated CRCs. Cyclic IMP 31-35 mutS homolog 2 Homo sapiens 108-112 20388775-8 2010 The mean methylation scores at CIMP-related markers were significantly higher in Lynch syndrome tumors with MSH2 methylation than MSH2-unmethylated CRCs. Cyclic IMP 31-35 mutS homolog 2 Homo sapiens 130-134 20388775-11 2010 High levels of aberrant methylation at CIMP-related markers in MSH2-methylated tumors raise the possibility that MSH2 is a target susceptible to aberrant methylation in Lynch syndrome. Cyclic IMP 39-43 mutS homolog 2 Homo sapiens 63-67 20388775-11 2010 High levels of aberrant methylation at CIMP-related markers in MSH2-methylated tumors raise the possibility that MSH2 is a target susceptible to aberrant methylation in Lynch syndrome. Cyclic IMP 39-43 mutS homolog 2 Homo sapiens 113-117 20012180-6 2010 For CIMP-negative CRC, only the MTHFR polymorphisms were statistically significantly related to risk, inversely for 677C>T and positively for 1298A>C, but a tendency toward a reduced risk was observed in subjects with an adequate methyl availability, combining the plasma variables [multivariate odds ratio 0.61 (95% CI 0.32-1.15)]. Cyclic IMP 4-8 methylenetetrahydrofolate reductase Homo sapiens 32-37 20200425-7 2010 RESULTS: PTGER2 overexpression was positively associated with the mucinous component (P = 0.0016), signet ring cells (P = 0.0024), CIMP-high (P = 0.0023), and MSI-high (P < 0.0001). Cyclic IMP 131-135 prostaglandin E receptor 2 Homo sapiens 9-15 19936946-8 2010 Collectively, these exploratory data provide suggestive evidence for the association of MTHFR 429 Ala/ Ala and TCN2 259 Arg/Arg and CIMP status in colorectal cancer. Cyclic IMP 132-136 methylenetetrahydrofolate reductase Homo sapiens 88-93 19936946-8 2010 Collectively, these exploratory data provide suggestive evidence for the association of MTHFR 429 Ala/ Ala and TCN2 259 Arg/Arg and CIMP status in colorectal cancer. Cyclic IMP 132-136 transcobalamin 2 Homo sapiens 111-115 19911194-8 2009 However, poor prognosis of CIMP+/MSI- subtype was found to be attributed to BRAF mutation. Cyclic IMP 27-31 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 76-80 20028768-10 2010 The high-methylation epigenotype correlated significantly with MSI-high and BRAF-mutation(+) in concordance with reported CIMP. Cyclic IMP 122-126 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 76-80 19638426-2 2010 CRCs with CIMP show a specific pattern of genetic alterations, including a high frequency of BRAF mutations and a low frequency of p53 mutations. Cyclic IMP 10-14 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 93-97 19638426-2 2010 CRCs with CIMP show a specific pattern of genetic alterations, including a high frequency of BRAF mutations and a low frequency of p53 mutations. Cyclic IMP 10-14 tumor protein p53 Homo sapiens 131-134 19638426-9 2010 Methylation of IGFBP7 was correlated with BRAF mutations, an absence of p53 mutations and the presence of CIMP. Cyclic IMP 106-110 insulin like growth factor binding protein 7 Homo sapiens 15-21 19638426-10 2010 Thus, epigenetic inactivation of IGFBP7 appears to play a key role in tumorigenesis of CRCs with CIMP by enabling escape from p53-induced senescence. Cyclic IMP 97-101 insulin like growth factor binding protein 7 Homo sapiens 33-39 19879258-5 2010 We found metastasis, gamma-glutamyl transpeptidase (GGT) and tumor node metastasis (TNM) stage were significantly different among patients with different CIMP status. Cyclic IMP 154-158 inactive glutathione hydrolase 2 Homo sapiens 21-50 19787768-9 2009 MSI-H/CIMP-H tumours had a high frequency of BRAF mutation and a low rate of KRAS mutation; the opposite was true for MSS/CIMP-neg tumours (P < 0.001). Cyclic IMP 6-10 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 45-49 19582761-5 2009 CIMP was determined by methylation-specific polymerase chain reaction (PCR) of CpG islands in MLH1, methylated in tumors (MINT)1, MINT2, MINT31, and CDKN2A. Cyclic IMP 0-4 mutL homolog 1 Homo sapiens 94-98 19582761-5 2009 CIMP was determined by methylation-specific polymerase chain reaction (PCR) of CpG islands in MLH1, methylated in tumors (MINT)1, MINT2, MINT31, and CDKN2A. Cyclic IMP 0-4 amyloid beta precursor protein binding family A member 1 Homo sapiens 122-128 19582761-5 2009 CIMP was determined by methylation-specific polymerase chain reaction (PCR) of CpG islands in MLH1, methylated in tumors (MINT)1, MINT2, MINT31, and CDKN2A. Cyclic IMP 0-4 amyloid beta precursor protein binding family A member 2 Homo sapiens 130-135 19582761-5 2009 CIMP was determined by methylation-specific polymerase chain reaction (PCR) of CpG islands in MLH1, methylated in tumors (MINT)1, MINT2, MINT31, and CDKN2A. Cyclic IMP 0-4 cyclin dependent kinase inhibitor 2A Homo sapiens 149-155 19787768-9 2009 MSI-H/CIMP-H tumours had a high frequency of BRAF mutation and a low rate of KRAS mutation; the opposite was true for MSS/CIMP-neg tumours (P < 0.001). Cyclic IMP 6-10 KRAS proto-oncogene, GTPase Homo sapiens 77-81 18832519-6 2009 RESULTS: After adjustment for other predictors of patient survival, patients with CIMP-high cancers (126 (19%) tumours with >or=6/8 methylated CIMP-specific promoters) experienced a significantly low colon cancer-specific mortality (multivariate HR 0.44, 95% confidence interval (CI) 0.22 to 0.88), whereas the BRAF mutation was significantly associated with a high cancer-specific mortality (multivariate HR 1.97, 95% CI 1.13 to 3.42). Cyclic IMP 82-86 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 314-318 19430421-8 2009 SIRT1 overexpression was associated with CIMP-high (> or =6 of 8 methylated CIMP-specific promoters, P=0.002) and microsatellite instability (MSI)-high phenotype (P<0.0001). Cyclic IMP 41-45 sirtuin 1 Homo sapiens 0-5 19430421-8 2009 SIRT1 overexpression was associated with CIMP-high (> or =6 of 8 methylated CIMP-specific promoters, P=0.002) and microsatellite instability (MSI)-high phenotype (P<0.0001). Cyclic IMP 79-83 sirtuin 1 Homo sapiens 0-5 19430421-12 2009 In conclusion, SIRT1 expression is associated with CIMP-high MSI-high colon cancer, suggesting involvement of SIRT1 in gene silencing in this unique tumor subtype. Cyclic IMP 51-55 sirtuin 1 Homo sapiens 15-20 18992263-3 2009 Insulin-related genes were associated with CIMP-positive and MSI tumors, with the strongest associations among aspirin users. Cyclic IMP 43-47 insulin Homo sapiens 0-7 18992263-4 2009 The Fok1 vitamin D receptor (VDR) polymorphism was associated with CIMP-positive/Ki-ras-mutated tumors; the Poly A and CDX2 VDR polymorphisms were associated only with Ki-ras-mutated tumors. Cyclic IMP 67-71 vitamin D receptor Homo sapiens 29-32 18992263-5 2009 NAT2 was associated with CIMP-positive/Ki-ras-mutated tumors but not with MSI tumors. Cyclic IMP 25-29 N-acetyltransferase 2 Homo sapiens 0-4 19723919-6 2009 p21 Loss was independently associated with low colon cancer-specific mortality [HR, 0.58; 95% confidence interval (95% CI), 0.38-0.89; adjusted for the covariates including MSI, CIMP, and LINE-1 methylation]. Cyclic IMP 178-182 cyclin dependent kinase inhibitor 1A Homo sapiens 0-3 19505918-6 2009 Compared with p27-nuclear+ patients, p27-altered patients experienced low colon cancer-specific [adjusted HR, 0.63; 95% confidence interval (95% CI), 0.42-0.94] and overall mortality (adjusted HR, 0.70; 95% CI, 0.51-0.95), independent of FASN, MSI, CIMP, LINE-1 methylation, and other potential confounders. Cyclic IMP 249-253 interferon alpha inducible protein 27 Homo sapiens 37-40 19470733-3 2009 We hypothesized that cellular DNMT3B level might influence the occurrence of widespread CpG island methylation (i.e., the CpG island methylator phenotype, CIMP) in colon cancer. Cyclic IMP 155-159 DNA methyltransferase 3 beta Homo sapiens 30-36 19470733-11 2009 CONCLUSIONS: Tumoral DNMT3B overexpression is associated with CIMP-high in colorectal cancer. Cyclic IMP 62-66 DNA methyltransferase 3 beta Homo sapiens 21-27 19117505-5 2008 Possible CIMP tumors were identified by comparing the methylation profile with microsatellite instability (MSI), BRAF-, KRAS-, and TP53 mutation status. Cyclic IMP 9-13 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 113-117 19117505-5 2008 Possible CIMP tumors were identified by comparing the methylation profile with microsatellite instability (MSI), BRAF-, KRAS-, and TP53 mutation status. Cyclic IMP 9-13 KRAS proto-oncogene, GTPase Homo sapiens 120-124 19117505-5 2008 Possible CIMP tumors were identified by comparing the methylation profile with microsatellite instability (MSI), BRAF-, KRAS-, and TP53 mutation status. Cyclic IMP 9-13 tumor protein p53 Homo sapiens 131-135 18782444-18 2008 Further, we show that BRAF mutations occur in association with CIMP phenotype in colorectal serrated polyps and verified that colorectal serrated polyps and MSI CRC show a similar frequency of BRAF mutations. Cyclic IMP 63-67 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 22-26 18829479-7 2008 RESULTS: The identified CIMP-positive cancers correlate with microsatellite instability (P = 0.075) and the BRAF mutation V600E (P = 0.00005). Cyclic IMP 24-28 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 108-112 18615680-5 2008 CIMP was determined previously by methylation-specific PCR of CpG islands in MLH1, methylated in tumors (MINT)1, MINT2, MINT31, and CDKN2A (p16). Cyclic IMP 0-4 mutL homolog 1 Homo sapiens 77-81 18615680-5 2008 CIMP was determined previously by methylation-specific PCR of CpG islands in MLH1, methylated in tumors (MINT)1, MINT2, MINT31, and CDKN2A (p16). Cyclic IMP 0-4 amyloid beta precursor protein binding family A member 1 Homo sapiens 105-111 18615680-5 2008 CIMP was determined previously by methylation-specific PCR of CpG islands in MLH1, methylated in tumors (MINT)1, MINT2, MINT31, and CDKN2A (p16). Cyclic IMP 0-4 amyloid beta precursor protein binding family A member 2 Homo sapiens 113-118 18615680-5 2008 CIMP was determined previously by methylation-specific PCR of CpG islands in MLH1, methylated in tumors (MINT)1, MINT2, MINT31, and CDKN2A (p16). Cyclic IMP 0-4 cyclin dependent kinase inhibitor 2A Homo sapiens 132-138 18615680-5 2008 CIMP was determined previously by methylation-specific PCR of CpG islands in MLH1, methylated in tumors (MINT)1, MINT2, MINT31, and CDKN2A (p16). Cyclic IMP 0-4 cyclin dependent kinase inhibitor 2A Homo sapiens 140-143 18922929-9 2008 KRAS mutations were more associated with CIMP-High and CIMP-Low status (P = 0.008). Cyclic IMP 41-45 KRAS proto-oncogene, GTPase Homo sapiens 0-4 18922929-9 2008 KRAS mutations were more associated with CIMP-High and CIMP-Low status (P = 0.008). Cyclic IMP 55-59 KRAS proto-oncogene, GTPase Homo sapiens 0-4 18834226-3 2008 OBJECTIVE: To investigate and compare the molecular and clinicopathologic features of CIMP-positive colorectal cancers defined by classic (p16, hMLH1, MINT1, MINT2, MINT31) and new (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1) CIMP panels. Cyclic IMP 86-90 cyclin dependent kinase inhibitor 2A Homo sapiens 139-142 18834226-3 2008 OBJECTIVE: To investigate and compare the molecular and clinicopathologic features of CIMP-positive colorectal cancers defined by classic (p16, hMLH1, MINT1, MINT2, MINT31) and new (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1) CIMP panels. Cyclic IMP 86-90 mutL homolog 1 Homo sapiens 144-149 18834226-3 2008 OBJECTIVE: To investigate and compare the molecular and clinicopathologic features of CIMP-positive colorectal cancers defined by classic (p16, hMLH1, MINT1, MINT2, MINT31) and new (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1) CIMP panels. Cyclic IMP 86-90 amyloid beta precursor protein binding family A member 1 Homo sapiens 151-156 18834226-3 2008 OBJECTIVE: To investigate and compare the molecular and clinicopathologic features of CIMP-positive colorectal cancers defined by classic (p16, hMLH1, MINT1, MINT2, MINT31) and new (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1) CIMP panels. Cyclic IMP 86-90 amyloid beta precursor protein binding family A member 2 Homo sapiens 158-163 18834226-3 2008 OBJECTIVE: To investigate and compare the molecular and clinicopathologic features of CIMP-positive colorectal cancers defined by classic (p16, hMLH1, MINT1, MINT2, MINT31) and new (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1) CIMP panels. Cyclic IMP 86-90 calcium voltage-gated channel subunit alpha1 G Homo sapiens 182-189 18834226-3 2008 OBJECTIVE: To investigate and compare the molecular and clinicopathologic features of CIMP-positive colorectal cancers defined by classic (p16, hMLH1, MINT1, MINT2, MINT31) and new (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1) CIMP panels. Cyclic IMP 86-90 insulin like growth factor 2 Homo sapiens 191-195 18834226-3 2008 OBJECTIVE: To investigate and compare the molecular and clinicopathologic features of CIMP-positive colorectal cancers defined by classic (p16, hMLH1, MINT1, MINT2, MINT31) and new (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1) CIMP panels. Cyclic IMP 86-90 neurogenin 1 Homo sapiens 197-204 18834226-3 2008 OBJECTIVE: To investigate and compare the molecular and clinicopathologic features of CIMP-positive colorectal cancers defined by classic (p16, hMLH1, MINT1, MINT2, MINT31) and new (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1) CIMP panels. Cyclic IMP 86-90 RUNX family transcription factor 3 Homo sapiens 206-211 18834226-3 2008 OBJECTIVE: To investigate and compare the molecular and clinicopathologic features of CIMP-positive colorectal cancers defined by classic (p16, hMLH1, MINT1, MINT2, MINT31) and new (CACNA1G, IGF2, NEUROG1, RUNX3, SOCS1) CIMP panels. Cyclic IMP 86-90 suppressor of cytokine signaling 1 Homo sapiens 213-218 18834226-7 2008 With at least 3 markers methylated, new CIMP-positive colorectal cancers (16.9%) were closely associated with proximal tumor location, low frequency of KRAS mutation, and high frequency of BRAF mutation (all P values were less than .05), whereas classic CIMP-positive colorectal cancers (18.5%) were closely associated with proximal tumor location, frequent microsatellite instability, and frequent BRAF mutation (all P values were less than .05). Cyclic IMP 40-44 KRAS proto-oncogene, GTPase Homo sapiens 152-156 18834226-7 2008 With at least 3 markers methylated, new CIMP-positive colorectal cancers (16.9%) were closely associated with proximal tumor location, low frequency of KRAS mutation, and high frequency of BRAF mutation (all P values were less than .05), whereas classic CIMP-positive colorectal cancers (18.5%) were closely associated with proximal tumor location, frequent microsatellite instability, and frequent BRAF mutation (all P values were less than .05). Cyclic IMP 40-44 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 189-193 18834226-7 2008 With at least 3 markers methylated, new CIMP-positive colorectal cancers (16.9%) were closely associated with proximal tumor location, low frequency of KRAS mutation, and high frequency of BRAF mutation (all P values were less than .05), whereas classic CIMP-positive colorectal cancers (18.5%) were closely associated with proximal tumor location, frequent microsatellite instability, and frequent BRAF mutation (all P values were less than .05). Cyclic IMP 40-44 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 399-403 18068703-3 2008 Positive CIMP is associated with BRAF mutations. Cyclic IMP 9-13 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 33-37 18517279-2 2008 OBJECTIVE: To determine whether the CpG island methylator phenotype (CIMP) pathway, characterized by simultaneous methylation of several known tumor suppressor genes, is the principal underlying mechanism in cases without chromosomal or microsatellite instability, and to determine the significance of CIMP pathway and BRAF mutations in microsatellite-stable (MSS) cases. Cyclic IMP 69-73 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 319-323 18435933-1 2008 BACKGROUND & AIMS: Colorectal cancers (CRCs) with the CpG island methylator phenotype (CIMP) often associate with epigenetic silencing of hMLH1 and an activating mutation in the BRAF gene. Cyclic IMP 91-95 mutL homolog 1 Homo sapiens 142-147 18435933-1 2008 BACKGROUND & AIMS: Colorectal cancers (CRCs) with the CpG island methylator phenotype (CIMP) often associate with epigenetic silencing of hMLH1 and an activating mutation in the BRAF gene. Cyclic IMP 91-95 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 182-186 18435933-3 2008 Because BRAF and KRAS belong to same signaling pathway, we hypothesized that not only mutations in BRAF but mutant KRAS may also associate with CIMP in CRC. Cyclic IMP 144-148 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 8-12 18435933-3 2008 Because BRAF and KRAS belong to same signaling pathway, we hypothesized that not only mutations in BRAF but mutant KRAS may also associate with CIMP in CRC. Cyclic IMP 144-148 KRAS proto-oncogene, GTPase Homo sapiens 17-21 18435933-3 2008 Because BRAF and KRAS belong to same signaling pathway, we hypothesized that not only mutations in BRAF but mutant KRAS may also associate with CIMP in CRC. Cyclic IMP 144-148 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 99-103 18435933-3 2008 Because BRAF and KRAS belong to same signaling pathway, we hypothesized that not only mutations in BRAF but mutant KRAS may also associate with CIMP in CRC. Cyclic IMP 144-148 KRAS proto-oncogene, GTPase Homo sapiens 115-119 18435933-5 2008 RESULTS: Methylation analysis of 7 CIMP-related markers revealed that the mean number of methylated loci was highest in BRAF-mutated CRCs (3.6) vs KRAS-mutated (1.2, P < .0001) or BRAF/KRAS wild-type tumors (0.7, P < .0001). Cyclic IMP 35-39 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 120-124 18435933-8 2008 CONCLUSIONS: CIMP in CRC may result from activating mutations in either BRAF or KRAS, and the inclusion of additional methylation markers that correlate with mutant KRAS may help clarify CIMP in future studies. Cyclic IMP 13-17 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 72-76 18435933-8 2008 CONCLUSIONS: CIMP in CRC may result from activating mutations in either BRAF or KRAS, and the inclusion of additional methylation markers that correlate with mutant KRAS may help clarify CIMP in future studies. Cyclic IMP 13-17 KRAS proto-oncogene, GTPase Homo sapiens 80-84 18403637-10 2008 Given that the number of hypermethylated loci at 2q14.2 likely affects the range of silenced flanking genes, high frequency of simultaneous hypermethylation of three CpG islands (EN1, SCTR, and INHBB) may have potential influence on specific characteristics of CIMP+ colorectal cancers. Cyclic IMP 261-265 engrailed homeobox 1 Homo sapiens 179-182 18403637-10 2008 Given that the number of hypermethylated loci at 2q14.2 likely affects the range of silenced flanking genes, high frequency of simultaneous hypermethylation of three CpG islands (EN1, SCTR, and INHBB) may have potential influence on specific characteristics of CIMP+ colorectal cancers. Cyclic IMP 261-265 inhibin subunit beta B Homo sapiens 194-199 18628431-6 2008 Tumors were classified as CIMP positive when at least three of five markers (RUNX3, CACNA1G, SOCS1, NEUROG1, and IGF2) were methylated according to MethyLight analysis. Cyclic IMP 26-30 RUNX family transcription factor 3 Homo sapiens 77-82 18628431-6 2008 Tumors were classified as CIMP positive when at least three of five markers (RUNX3, CACNA1G, SOCS1, NEUROG1, and IGF2) were methylated according to MethyLight analysis. Cyclic IMP 26-30 calcium voltage-gated channel subunit alpha1 G Homo sapiens 84-91 18628431-6 2008 Tumors were classified as CIMP positive when at least three of five markers (RUNX3, CACNA1G, SOCS1, NEUROG1, and IGF2) were methylated according to MethyLight analysis. Cyclic IMP 26-30 insulin like growth factor 2 Homo sapiens 113-117 18451217-7 2008 CIMP with MSI-H due to hMLH1 hypermethylation, or CIMP with loss of MGMT expression in non-MSI-H tumors, was associated with BRAF mutation (OR, 4.5; P < 0.0002). Cyclic IMP 0-4 mutL homolog 1 Homo sapiens 23-28 18451217-7 2008 CIMP with MSI-H due to hMLH1 hypermethylation, or CIMP with loss of MGMT expression in non-MSI-H tumors, was associated with BRAF mutation (OR, 4.5; P < 0.0002). Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 125-129 18451217-7 2008 CIMP with MSI-H due to hMLH1 hypermethylation, or CIMP with loss of MGMT expression in non-MSI-H tumors, was associated with BRAF mutation (OR, 4.5; P < 0.0002). Cyclic IMP 50-54 O-6-methylguanine-DNA methyltransferase Homo sapiens 68-72 18451217-7 2008 CIMP with MSI-H due to hMLH1 hypermethylation, or CIMP with loss of MGMT expression in non-MSI-H tumors, was associated with BRAF mutation (OR, 4.5; P < 0.0002). Cyclic IMP 50-54 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 125-129 18451217-8 2008 CIMP was also associated with BRAF V600E T-to-A transversion (OR, 48.5; P < 0.0002). Cyclic IMP 0-4 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 30-34 18607505-5 2008 CDH1 methylation occurred in 48.9% (23/47) of cancer, in 23.8% (5/21) of premalignant, and in 25% (4/16) of noncancerous tissues and was correlated with patients" age (P = .01), lymph node metastasis, and CIMP severity (P = .000-.028). Cyclic IMP 205-209 cadherin 1 Homo sapiens 0-4 18607505-7 2008 The close correlation between CDH1 methylation and CIMP severity suggests the necessity of their combination in GC prevention and earlier diagnosis. Cyclic IMP 51-55 cadherin 1 Homo sapiens 30-34 18199160-7 2008 High CIMP was closely associated with MSI and BRAF mutation but not with KRAS mutation. Cyclic IMP 5-9 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 46-50 18199160-9 2008 A worse clinical outcome was found for CIMP-high, MSS CRC with KRAS/BRAF mutation but not for those lacking KRAS/BRAF mutation. Cyclic IMP 39-43 KRAS proto-oncogene, GTPase Homo sapiens 63-67 18199160-9 2008 A worse clinical outcome was found for CIMP-high, MSS CRC with KRAS/BRAF mutation but not for those lacking KRAS/BRAF mutation. Cyclic IMP 39-43 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 68-72