PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23821658-0 2013 NOTCH1, SF3B1, and TP53 mutations in fludarabine-refractory CLL patients treated with alemtuzumab: results from the CLL2H trial of the GCLLSG. fludarabine 37-48 tumor protein p53 Homo sapiens 19-23 25119920-9 2014 Among 20 patients who received fludarabine therapy, the overall remission rate for those with p53 gene deletion (20%) was lower than those without (75%) (P<0.05). fludarabine 31-42 tumor protein p53 Homo sapiens 94-97 25119920-14 2014 High-level ZAP-70 expression and the presence of p53 deletion are associated with shorter survival and poor response to fludarabine containing therapy. fludarabine 120-131 tumor protein p53 Homo sapiens 49-52 24144307-5 2014 [Flu + Clo + Bu + SAHA] resulted in synergistic cytotoxicity, which can be attributed to (1) activated DNA-damage response and cell cycle checkpoint activation through the ATM-CHK2-P53 (or P73) pathway or ATM-CHK2-cdc25-cdc2 pathway, (2) histone modifications and (3) activated apoptosis pathway. fludarabine 1-4 tumor protein p53 Homo sapiens 181-184 23821658-1 2013 We studied the incidences, associations, and prognostic roles of NOTCH1 and SF3B1 mutations (NOTCH1(mut), SF3B1(mut)) as compared with TP53(mut) in fludarabine-refractory chronic lymphocytic leukemia (CLL) patients treated with alemtuzumab in the CLL2H trial. fludarabine 148-159 tumor protein p53 Homo sapiens 135-139 22937789-6 2012 Both S-MDM4 and MDM2 expressions were significantly increased after fludarabine treatment of CLL cells without p53 aberrations (P = 0.013 and P = 0.030). fludarabine 68-79 tumor protein p53 Homo sapiens 111-114 22641291-1 2012 PURPOSE: Human Raji cells treated with fludarabine nucleoside (2-FaraA, 3 muM) undergo apoptosis with accumulation of p53 in the nuclei as multiple phosphorylated isoforms and C-terminal truncated derivatives. fludarabine 63-70 tumor protein p53 Homo sapiens 118-121 23052131-0 2012 Expression level of DEK in chronic lymphocytic leukemia is regulated by fludarabine and Nutlin-3 depending on p53 status. fludarabine 72-83 tumor protein p53 Homo sapiens 110-113 23052131-6 2012 Both fludarabine and Nutlin-3 significantly downregulated DEK in the primary CLL cells which were with normal function of p53, or without deletion or mutation of p53 (p = 0.042, p = 0.038; p = 0.021, p = 0.017; p = 0.037, p = 0.017). fludarabine 5-16 tumor protein p53 Homo sapiens 122-125 23052131-8 2012 These data show that DEK might be applied for the assessment of prognosis in patients with CLL, and fludarabine and Nutlin-3 regulate DEK expression depended on p53 status. fludarabine 100-111 tumor protein p53 Homo sapiens 161-164 22149137-0 2012 The Hsp90 inhibitor SNX-7081 synergizes with and restores sensitivity to fludarabine in chronic lymphocytic leukemia cells with lesions in the TP53 pathway: a potential treatment strategy for fludarabine refractory disease. fludarabine 73-84 tumor protein p53 Homo sapiens 143-147 22149137-0 2012 The Hsp90 inhibitor SNX-7081 synergizes with and restores sensitivity to fludarabine in chronic lymphocytic leukemia cells with lesions in the TP53 pathway: a potential treatment strategy for fludarabine refractory disease. fludarabine 192-203 tumor protein p53 Homo sapiens 143-147 22149137-4 2012 In seven cell lines and 23 patient samples synergy between SNX-7081 and fludarabine (2-FaraA) was apparent in the three TP53 mutated cell lines and at significantly lower concentrations in TP53 or ATM dysfunctional patient cells. fludarabine 72-83 tumor protein p53 Homo sapiens 120-124 22149137-4 2012 In seven cell lines and 23 patient samples synergy between SNX-7081 and fludarabine (2-FaraA) was apparent in the three TP53 mutated cell lines and at significantly lower concentrations in TP53 or ATM dysfunctional patient cells. fludarabine 85-92 tumor protein p53 Homo sapiens 120-124 22641291-8 2012 CONCLUSIONS AND CLINICAL RELEVANCE: Comprehensive information on the subcellular distributions and responses of p53, p63 and p73 to 2-FaraA provides additional insight into mechanisms for induction of apoptosis in the treatment of B-lymphoproliferative disorders with fludarabine. fludarabine 132-139 tumor protein p53 Homo sapiens 112-115 23556086-11 2011 The only group that can be clearly identified pretreatment for whom conventional fludarabine-based therapies produce significantly inferior response rates, PFS and overall survival are the patients who harbour a genetic fault; deletion or mutation or a combination of deletion and mutation of tumour protein p53 (TP53). fludarabine 81-92 tumor protein p53 Homo sapiens 308-311 22308293-0 2012 Disruption of BIRC3 associates with fludarabine chemorefractoriness in TP53 wild-type chronic lymphocytic leukemia. fludarabine 36-47 tumor protein p53 Homo sapiens 71-75 22962562-4 2012 In this pilot study, changes in p53 and its transcriptional targets, p21/waf1 and MDM2 were analyzed by immunoblotting and densitometry in CLL cells from 10 patients immediately prior to the start of chemotherapy, and after culture for 24 hours (h) with fludarabine (n=7) or chlorambucil (n=3). fludarabine 254-265 tumor protein p53 Homo sapiens 32-35 22039264-4 2011 In fludarabine-refractory CLL, SF3B1 mutations and TP53 disruption distributed in a mutually exclusive fashion (P = .046). fludarabine 3-14 tumor protein p53 Homo sapiens 51-55 21521181-0 2011 A pilot monocentric analysis of efficacy and safety of Fludarabine-Campath combination (Flucam) as first line treatment in elderly patients with chronic lymphocytic leukaemia and Tp53 disfunction. fludarabine 55-66 tumor protein p53 Homo sapiens 179-183 23556086-11 2011 The only group that can be clearly identified pretreatment for whom conventional fludarabine-based therapies produce significantly inferior response rates, PFS and overall survival are the patients who harbour a genetic fault; deletion or mutation or a combination of deletion and mutation of tumour protein p53 (TP53). fludarabine 81-92 tumor protein p53 Homo sapiens 313-317 23556086-12 2011 TP53 inactivation is a less common finding at first treatment but becomes much more common in fludarabine-refractory patients. fludarabine 94-105 tumor protein p53 Homo sapiens 0-4 20504344-7 2010 After performing messenger RNA expression profile of the same patients, the activation of p53-responsive genes was detected in fludarabine responsive cases only, therefore suggesting a possible mechanism linked to microRNA deregulation in non-responder patients. fludarabine 127-138 tumor protein p53 Homo sapiens 90-93 20504344-8 2010 Importantly, inhibition of miR-21 and miR-222 by anti-miRNA oligonucleotides induced a significant increase in caspase activity in fludarabine-treated p53-mutant MEG-01 cells, suggesting that miR-21 and miR-222 up-regulation may be involved in the establishment of fludarabine resistance. fludarabine 131-142 tumor protein p53 Homo sapiens 151-154 20504344-8 2010 Importantly, inhibition of miR-21 and miR-222 by anti-miRNA oligonucleotides induced a significant increase in caspase activity in fludarabine-treated p53-mutant MEG-01 cells, suggesting that miR-21 and miR-222 up-regulation may be involved in the establishment of fludarabine resistance. fludarabine 265-276 tumor protein p53 Homo sapiens 151-154 19778838-2 2009 Dysfunction of p53 leads to resistance to fludarabine-based therapies. fludarabine 42-53 tumor protein p53 Homo sapiens 15-18 19643983-0 2009 Detailed analysis of p53 pathway defects in fludarabine-refractory chronic lymphocytic leukemia (CLL): dissecting the contribution of 17p deletion, TP53 mutation, p53-p21 dysfunction, and miR34a in a prospective clinical trial. fludarabine 44-55 tumor protein p53 Homo sapiens 21-24 19018867-6 2009 RESULTS AND CONCLUSIONS: At the clinically relevant concentration of fludarabine, TP53-abnormal samples exhibited markedly higher resistance to fludarabine than the remaining CLL samples (P = 0.012); cohort with ATM deletion was not more resistant than wt cells. fludarabine 69-80 tumor protein p53 Homo sapiens 82-86 19018867-6 2009 RESULTS AND CONCLUSIONS: At the clinically relevant concentration of fludarabine, TP53-abnormal samples exhibited markedly higher resistance to fludarabine than the remaining CLL samples (P = 0.012); cohort with ATM deletion was not more resistant than wt cells. fludarabine 144-155 tumor protein p53 Homo sapiens 82-86 19062342-4 2008 In contrast, chlorambucil and fludarabine resistance correlated with basal p53 protein levels. fludarabine 30-41 tumor protein p53 Homo sapiens 75-78 18945750-8 2008 CONCLUSIONS: We demonstrate a correlation between the recently described p53-inducible apoptosis gene TIGAR and both sensitivity to fludarabine and hENT2 expression in chronic lymphocytic leukemia cells. fludarabine 132-143 tumor protein p53 Homo sapiens 73-76 17325891-8 2007 In conclusion, 17p deletion, which causes loss of p53 gene, is associated with resistance to fludarabine-induced apoptosis in vitro. fludarabine 93-104 tumor protein p53 Homo sapiens 50-53 18092340-2 2008 Exposure to chlorambucil, fludarabine, and Nutlin-3 induced p53 accumulation and variably affected cell cycle progression in SKW6.4 lymphoblastoid cells. fludarabine 26-37 tumor protein p53 Homo sapiens 60-63 18092340-5 2008 Analysis of the gene expression profile of the p53-transcriptional targets showed distinct features between chlorambucil, Nutlin-3 and fludarabine, which likely account for their differential effect on cell cycle in SKW6.4 cells. fludarabine 135-146 tumor protein p53 Homo sapiens 47-50 17728781-0 2008 Multiple forms of nuclear p53 formed in human Raji and MEC1 cells treated with fludarabine. fludarabine 79-90 tumor protein p53 Homo sapiens 26-29 17226861-5 2007 In vitro resistance to fludarabine was greatest in B-CLL cells with deletions of p53, a cytogenetic abnormality that is almost invariably associated with a poor therapeutic response clinically. fludarabine 23-34 tumor protein p53 Homo sapiens 81-84 16741250-5 2006 Transduction of CLL cells with an adenovirus encoding p73 also induced Bid and CD95 and enhanced the sensitivity to F-ara-A of p53-deficient CLL cells. fludarabine 116-123 tumor protein p53 Homo sapiens 127-130 16543464-7 2006 Combination treatment of Nutlin-3a and fludarabine synergistically increased p53 levels, and induced conformational change of Bax and apoptosis in wild-type p53 cells but not in cells with mutant p53. fludarabine 39-50 tumor protein p53 Homo sapiens 77-80 16543464-7 2006 Combination treatment of Nutlin-3a and fludarabine synergistically increased p53 levels, and induced conformational change of Bax and apoptosis in wild-type p53 cells but not in cells with mutant p53. fludarabine 39-50 tumor protein p53 Homo sapiens 157-160 16543464-7 2006 Combination treatment of Nutlin-3a and fludarabine synergistically increased p53 levels, and induced conformational change of Bax and apoptosis in wild-type p53 cells but not in cells with mutant p53. fludarabine 39-50 tumor protein p53 Homo sapiens 157-160 15217838-8 2004 Nuclear translocation of p53 after fludarabine treatment was decreased when STAT1beta was overexpressed, and it was increased when STAT1alpha was induced. fludarabine 35-46 tumor protein p53 Homo sapiens 25-28 16501812-0 2006 Fludarabine induces apoptosis in chronic lymphocytic leukemia--the role of P53, Bcl-2, Bax, Mcl-1, and Bag-1 proteins. fludarabine 0-11 tumor protein p53 Homo sapiens 75-78 15217838-10 2004 Our results show that imbalance between the antiproliferative/proapoptotic isoform STAT1alpha and the proliferative isoform STAT1beta is likely to play a crucial role in the regulation of proliferation and apoptosis and that STAT1alpha may regulate p53 activity and sensitize B cells to fludarabine-induced apoptosis. fludarabine 287-298 tumor protein p53 Homo sapiens 249-252 14623330-0 2003 Involvement of p53 in alpha4beta1 integrin-mediated resistance of B-CLL cells to fludarabine. fludarabine 81-92 tumor protein p53 Homo sapiens 15-18 15138159-0 2004 Fludarabine treatment of patients with chronic lymphocytic leukemia induces a p53-dependent gene expression response. fludarabine 0-11 tumor protein p53 Homo sapiens 78-81 15138159-4 2004 Many of the fludarabine signature genes were known p53 target genes and genes involved in DNA repair. fludarabine 12-23 tumor protein p53 Homo sapiens 51-54 15138159-6 2004 Using isogenic p53 wild-type and null lymphoblastoid cell lines, we confirmed that many of the fludarabine signature genes were also p53 target genes. fludarabine 95-106 tumor protein p53 Homo sapiens 15-18 15138159-6 2004 Using isogenic p53 wild-type and null lymphoblastoid cell lines, we confirmed that many of the fludarabine signature genes were also p53 target genes. fludarabine 95-106 tumor protein p53 Homo sapiens 133-136 15138159-7 2004 Because in vivo treatment with fludarabine induces a p53-dependent gene expression response, fludarabine treatment has the potential to select p53-mutant CLL cells, which are more drug resistant and associated with an aggressive clinical course. fludarabine 31-42 tumor protein p53 Homo sapiens 53-56 15138159-7 2004 Because in vivo treatment with fludarabine induces a p53-dependent gene expression response, fludarabine treatment has the potential to select p53-mutant CLL cells, which are more drug resistant and associated with an aggressive clinical course. fludarabine 31-42 tumor protein p53 Homo sapiens 143-146 15138159-7 2004 Because in vivo treatment with fludarabine induces a p53-dependent gene expression response, fludarabine treatment has the potential to select p53-mutant CLL cells, which are more drug resistant and associated with an aggressive clinical course. fludarabine 93-104 tumor protein p53 Homo sapiens 53-56 15138159-7 2004 Because in vivo treatment with fludarabine induces a p53-dependent gene expression response, fludarabine treatment has the potential to select p53-mutant CLL cells, which are more drug resistant and associated with an aggressive clinical course. fludarabine 93-104 tumor protein p53 Homo sapiens 143-146 14623330-4 2003 Parallel to this different viability, fludarabine increased p53 expression on pLys-cultured cells and this increase was significantly reduced (P<or=0.05) on cells cultured on H/89. fludarabine 38-49 tumor protein p53 Homo sapiens 60-63 12912974-0 2003 Activation of a p53-mediated apoptotic pathway in quiescent lymphocytes after the inhibition of DNA repair by fludarabine. fludarabine 110-121 tumor protein p53 Homo sapiens 16-19 12912974-11 2003 CONCLUSIONS: These results suggest that inhibition of UV-induced DNA repair by F-ara-A is critical for cytotoxicity and that induction of apoptosis may be conducted by a p53-mediated signaling mechanism to the Fas death pathway. fludarabine 79-86 tumor protein p53 Homo sapiens 170-173 11526536-4 2001 PNP/fludarabine induced strong p53 accumulation and a more rapid onset of apoptosis in p53-positive HepG2 cells as compared with p53-negative Hep3B cells, but efficiency of tumor cell killing was similar in both cell lines. fludarabine 4-15 tumor protein p53 Homo sapiens 31-34 12176904-6 2002 Fludarabine and FCM induce p53 stabilization, but do not seem to be essential in inducing Bax and Bak conformational changes, as they are also observed in dexamethasone-treated CLL cells. fludarabine 0-11 tumor protein p53 Homo sapiens 27-30 12719725-4 2003 p53 mutations resulted not only in a shorter survival but, notably also in selective resistance to alkylating agents, fludarabine and gamma-irradiation. fludarabine 118-129 tumor protein p53 Homo sapiens 0-3 12085225-8 2002 In the PRI cells fludarabine activated p53, but not in the BL2.B95.8 cells in which the p53 pathway is inactivated. fludarabine 17-28 tumor protein p53 Homo sapiens 39-42 11526536-4 2001 PNP/fludarabine induced strong p53 accumulation and a more rapid onset of apoptosis in p53-positive HepG2 cells as compared with p53-negative Hep3B cells, but efficiency of tumor cell killing was similar in both cell lines. fludarabine 4-15 tumor protein p53 Homo sapiens 87-90 11526536-4 2001 PNP/fludarabine induced strong p53 accumulation and a more rapid onset of apoptosis in p53-positive HepG2 cells as compared with p53-negative Hep3B cells, but efficiency of tumor cell killing was similar in both cell lines. fludarabine 4-15 tumor protein p53 Homo sapiens 87-90 31226417-0 2019 Entinostat combined with Fludarabine synergistically enhances the induction of apoptosis in TP53 mutated CLL cells via the HDAC1/HO-1 pathway. fludarabine 25-36 tumor protein p53 Homo sapiens 92-96 9703875-0 1998 Increased p21/WAF-1 and p53 protein levels following sequential three drug combination regimen of fludarabine, cytarabine and docetaxel induces apoptosis in human leukemia cells. fludarabine 98-109 tumor protein p53 Homo sapiens 24-27 9499672-17 1997 Finally, p53 tumor suppressor gene has been associated with resistance to therapy with fludarabine. fludarabine 87-98 tumor protein p53 Homo sapiens 9-12 9389352-8 1997 Treatment of CLL cells having wild type p53 with CdA, F-ara-A or CLB produced an increase in p53 protein and mdm-2 mRNA. fludarabine 54-61 tumor protein p53 Homo sapiens 40-43 9389352-8 1997 Treatment of CLL cells having wild type p53 with CdA, F-ara-A or CLB produced an increase in p53 protein and mdm-2 mRNA. fludarabine 54-61 tumor protein p53 Homo sapiens 93-96 34886743-2 2022 Results from our laboratory indicate that 2-FaraAMP (fludarabine) has multiple mechanisms of cytotoxicity that include accumulation of isoforms and phosphorylated derivatives of p53, and induction of the unfolded protein response (UPR). fludarabine 53-64 tumor protein p53 Homo sapiens 178-181 34886743-3 2022 Using protein pull-downs with Dynabeads coated with p53 antibody, we have found that 2-FaraA (fludarabine nucleoside) induces major changes in the p53 interactome in human Raji lymphoma and IM9 multiple myeloma cells. fludarabine 85-92 tumor protein p53 Homo sapiens 52-55 34886743-3 2022 Using protein pull-downs with Dynabeads coated with p53 antibody, we have found that 2-FaraA (fludarabine nucleoside) induces major changes in the p53 interactome in human Raji lymphoma and IM9 multiple myeloma cells. fludarabine 85-92 tumor protein p53 Homo sapiens 147-150 31289209-6 2020 Interestingly, we observed that higher levels of HIF-1A mRNA correlate with a lower susceptibility of leukemic cells to spontaneous apoptosis, and associate with the fludarabine resistance that mainly characterizes TP53dis tumour cells. fludarabine 166-177 tumor protein p53 Homo sapiens 215-219 31289209-8 2020 BAY87-2243 also overcomes the constitutive fludarabine resistance of TP53dis leukemic cells and elicits a strongly synergistic cytotoxic effect in combination with ibrutinib, thus providing preclinical evidences for its further investigation as a potential new drug in chronic lymphocytic leukemia. fludarabine 43-54 tumor protein p53 Homo sapiens 69-73 35211418-4 2022 Longitudinal analysis before and after fludarabine based on NGS sequencing demonstrated that low-burden TP53 mutations were present before the onset of treatment and expanded at relapse to become the predominant clone. fludarabine 39-50 tumor protein p53 Homo sapiens 104-108 32253666-3 2020 The aim of therapy for CLL patients has been to control the disease; however, FCR (fludarabine, cyclophosphamide, rituximab) has improved outcomes and reduced the high incidence of undetectable minimum/measurable residual disease (MRD) in previously untreated CLL patients with no 17p deletion/TP53 disruption and mutated immunoglobulin heavy chain gene (IGHV). fludarabine 83-94 tumor protein p53 Homo sapiens 294-298 31226417-2 2019 Worse still, CLL patients with TP53 mutation are associated with poor efficacy to current chemotherapeutic, such as Fludarabine. fludarabine 116-127 tumor protein p53 Homo sapiens 31-35 31226417-4 2019 Subsequently, we demonstrated Entinostat (HDAC1 inhibitor) combination with Fludarabine significantly induced apoptosis in TP53 mutations CLL cells. fludarabine 76-87 tumor protein p53 Homo sapiens 123-127 31226417-8 2019 Finally, combining vitro and vivo experiments, we presented the first demonstration that Entinostat combination with Fludarabine had a synergistic effect on the induction of apoptosis in TP53 mutations CLL cells. fludarabine 117-128 tumor protein p53 Homo sapiens 187-191