PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 26963001-11 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 26512054-6 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 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 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 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 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 25496513-11 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 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 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 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 24812557-5 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 99-103 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 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 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 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 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 68-72 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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