PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34791836-12 2022 While nonresponder-associated genes included well-known TP53 and CARD11, genetic classifiers developed using nonresponder-associated genes included ATP6AP1, EP400, ARID1A, SOCS1, and TBL1XR1, suggesting resistance to ibrutinib may be related to broad biological functions connected to epigenetic modification, telomere maintenance, and cancer-associated signaling pathways (mTOR, JAK/STAT, NF-kappaB). ibrutinib 217-226 tumor protein p53 Homo sapiens 56-60 34521099-0 2021 Ibrutinib induces durable remissions in treatment-naive patients with CLL and 17p deletion/TP53 mutations. ibrutinib 0-9 tumor protein p53 Homo sapiens 91-95 34521099-3 2021 Here, we report the long-term outcome of 27 patients with CLL treatment naive with 17p deletion and/or TP53 mutation treated with ibrutinib alone or in combination with rituximab on a Phase-2 clinical study. ibrutinib 130-139 tumor protein p53 Homo sapiens 103-107 34521099-5 2021 These data corroborate that ibrutinib therapy, induces durable remissions in patients with 17p deletion and/or TP53 mutations, and suggest that BTK inhibitor therapy should be a preferred treatment for these patients outside of clinical trials. ibrutinib 28-37 tumor protein p53 Homo sapiens 111-115 34865212-0 2022 Long-term efficacy of first-line ibrutinib treatment for chronic lymphocytic leukaemia in patients with TP53 aberrations: a pooled analysis from four clinical trials. ibrutinib 33-42 tumor protein p53 Homo sapiens 104-108 34865212-3 2022 The pooled analysis included 89 patients with TP53 aberrations receiving first-line treatment with single-agent ibrutinib (n = 45) or ibrutinib in combination with an anti-CD20 antibody (n = 44). ibrutinib 112-121 tumor protein p53 Homo sapiens 46-50 34127506-0 2021 TP53 disruption in chronic lymphocytic leukemia under ibrutinib: more is worse? ibrutinib 54-63 tumor protein p53 Homo sapiens 0-4 34127506-1 2021 Chronic lymphocytic leukemia patients carrying a single TP53 hit (chromosome 17p deletion or single TP53 mutation) demonstrate excellent progression-free and overall survival on ibrutinib compared to cases harboring multiple TP53 hits. ibrutinib 178-187 tumor protein p53 Homo sapiens 56-60 34127506-1 2021 Chronic lymphocytic leukemia patients carrying a single TP53 hit (chromosome 17p deletion or single TP53 mutation) demonstrate excellent progression-free and overall survival on ibrutinib compared to cases harboring multiple TP53 hits. ibrutinib 178-187 tumor protein p53 Homo sapiens 100-104 33963002-0 2021 Clinical Outcomes in Patients with Multi-Hit TP53 Chronic Lymphocytic Leukemia Treated with Ibrutinib. ibrutinib 92-101 tumor protein p53 Homo sapiens 45-49 33963002-10 2021 Conclusions: In this study, single-hit TP53 defines a distinct subgroup of patients with an excellent long-term response to single-agent ibrutinib, while multi-hit TP53 is independently associated with shorter PFS. ibrutinib 137-146 tumor protein p53 Homo sapiens 39-43 33735664-9 2021 Ibrutinib/BTKi showed potential benefit in relapsed/refractory patients and patients without CXCR4NS/MS including those with TP53 mutations. ibrutinib 0-9 tumor protein p53 Homo sapiens 125-129 32833105-1 2020 Ibrutinib-based therapy represents a recent success in managing high-risk CLL patients with 17p/TP53 deletion. ibrutinib 0-9 tumor protein p53 Homo sapiens 96-100 32833105-10 2020 In summary, the data presented establish an association between LPL deletion, resistance to ibrutinib-based therapy, and poorer overall survival in TP53-deleted CLL patients. ibrutinib 92-101 tumor protein p53 Homo sapiens 148-152 31965420-4 2020 The efficacy of ibrutinib, a B cell receptor inhibitor, for B-PLL with the TP53 abnormality as second-line therapy was recently demonstrated. ibrutinib 16-25 tumor protein p53 Homo sapiens 75-79 31965420-5 2020 We herein report that low-dose ibrutinib as upfront therapy induced a complete response in a B-PLL patient with the TP53 abnormality, whose condition has since remained stable with no recurrence for 12 months. ibrutinib 31-40 tumor protein p53 Homo sapiens 116-120 32994268-2 2020 Ibrutinib, a tyrosine kinase inhibitor, is the treatment of choice on relapse or p53-dysfunction. ibrutinib 0-9 tumor protein p53 Homo sapiens 81-84 32791549-7 2020 Patients with the high-risk parameters deletion 17p or TP53mutation are known to poorly respond to chemo(immuno)therapy and should receive either ibrutinib or venetoclax/obinutuzumab.Thus, a choice has to be made between a continuous monotherapy with ibrutinib or a time-limited combination with either venetoclax/obinutuzumab (12 months) or chemoimmunotherapy (usually 6 months). ibrutinib 146-155 tumor protein p53 Homo sapiens 55-59 32791549-7 2020 Patients with the high-risk parameters deletion 17p or TP53mutation are known to poorly respond to chemo(immuno)therapy and should receive either ibrutinib or venetoclax/obinutuzumab.Thus, a choice has to be made between a continuous monotherapy with ibrutinib or a time-limited combination with either venetoclax/obinutuzumab (12 months) or chemoimmunotherapy (usually 6 months). ibrutinib 251-260 tumor protein p53 Homo sapiens 55-59 32726539-0 2020 Ibrutinib for Chronic Lymphocytic Leukemia with TP53 Alterations. ibrutinib 0-9 tumor protein p53 Homo sapiens 48-52 32187452-6 2020 On multivariable analyses, temporary ibrutinib interruption (hazard ratio [HR]: 2.37, P = .006) and TP53 disruption at ibrutinib initiation (HR: 1.81, P = .048) were associated with shorter EFS, whereas only TP53 disruption (HR: 2.38, P = .015) was associated with shorter OS. ibrutinib 119-128 tumor protein p53 Homo sapiens 100-104 31732977-1 2020 A major revolution in the treatment of chronic lymphocytic leukemia (CLL) began with the approval of ibrutinib, a first-in-class oral inhibitor of Bruton tyrosine kinase (BTK), for the treatment of relapsed/refractory (R/R) and/or TP53 mutated patients with CLL. ibrutinib 101-110 tumor protein p53 Homo sapiens 231-235 31732977-5 2020 A possible strategy to overcome some of these obstacles is to combine ibrutinib with other targeted agents especially in high-risk disease, such as previously treated refractory patients or those with TP53 aberrations or complex karyotypes, in whom rapid eradication of disease is most desirable. ibrutinib 70-79 tumor protein p53 Homo sapiens 201-205 32172299-4 2020 However, 17p-deleted, p53-mutated or IGHV-UM subgroups are generally resistant to FCR, and much better responses are seen with ibrutinib and venetoclax, frequently inducing MRD negativity that hopefully will be translated into durable remissions. ibrutinib 127-136 tumor protein p53 Homo sapiens 22-25 31628428-4 2020 Ibrutinib benefit was also consistent in patients with high prognostic risk (TP53 mutation, 11q deletion, and/or unmutated IGHV) (PFS: HR [95% CI]: 0.083 [0.047-0.145]; OS: HR [95% CI]: 0.366 [0.181-0.736]). ibrutinib 0-9 tumor protein p53 Homo sapiens 77-81 31924585-2 2020 Although recently introduced small-molecule B-cell receptor signalling inhibitors have revolutionized CLL treatment, data for ibrutinib still point to impaired prognosis for TP53-affected patients. ibrutinib 126-135 tumor protein p53 Homo sapiens 174-178 31180577-1 2020 The Bruton"s tyrosine kinase (BTK) inhibitor ibrutinib is inducing durable responses in chronic lymphocytic leukemia (CLL) patients with refractory/relapsed disease or with TP53 defect, with BTK and phospholipase C gamma 2 (PLCG2) mutations representing the predominant mechanisms conferring secondary ibrutinib resistance. ibrutinib 45-54 tumor protein p53 Homo sapiens 173-177 31648477-1 2019 Objective: To improve the knowledge and experience of ibrutinib combined with CAR-T cells in the treatment of high-risk chronic lymphoblastic leukemia (CLL) patients or small lymphocytic lymphoma (SLL) with TP53 gene aberration. ibrutinib 54-63 tumor protein p53 Homo sapiens 207-211 31555576-7 2019 The continuous administration of ibrutinib single agent has led to prolonged PFS and OS in relapsed/refractory and treatment naive CLL, including those with TP53 deletion/mutation or unmutated IGHV genes, though the clinical responses are rarely complete. ibrutinib 33-42 tumor protein p53 Homo sapiens 157-161 31363127-5 2019 Although the detailed molecular mechanisms are still to be defined, our work shows for the first time that in primary B cells, metabolic stressors enhance BTK signaling and suggest that metabolic rewiring to hyperglycemia affects ibrutinib resistance in TP53 deficient chronic lymphocytic leukemia (CLL) lymphocytes. ibrutinib 230-239 tumor protein p53 Homo sapiens 254-258 30842083-6 2019 The PFS benefit with ibrutinib was independent of baseline risk factors, although patients with >=2 prior therapies had shorter PFS than those with <2 prior therapies, and the presence of TP53 or SF3B1 mutations showed a trend toward shorter PFS vs without these factors. ibrutinib 21-30 tumor protein p53 Homo sapiens 188-192 30988561-1 2019 Ibrutinib is the only approved novel agent that is available for the treatment of relapsed-refractory and treatment-naive chronic lymphocytic leukemia patients with deletion 17p or TP53 mutation in India. ibrutinib 0-9 tumor protein p53 Homo sapiens 181-185 30338509-0 2019 Unravelling the suboptimal response of TP53-mutated chronic lymphocytic leukaemia to ibrutinib. ibrutinib 85-94 tumor protein p53 Homo sapiens 39-43 30338509-1 2019 TP53-disrupted chronic lymphocytic leukaemia (CLL) patients show a suboptimal long-term response to ibrutinib. ibrutinib 100-109 tumor protein p53 Homo sapiens 0-4 30338509-2 2019 We hereby report that ibrutinib-induced in vitro apoptosis and proliferation inhibition were significantly lower in TP53-mutated (TP53-M) CLL cells compared to TP53 wild-type cells. ibrutinib 22-31 tumor protein p53 Homo sapiens 116-120 30338509-2 2019 We hereby report that ibrutinib-induced in vitro apoptosis and proliferation inhibition were significantly lower in TP53-mutated (TP53-M) CLL cells compared to TP53 wild-type cells. ibrutinib 22-31 tumor protein p53 Homo sapiens 130-134 30338509-2 2019 We hereby report that ibrutinib-induced in vitro apoptosis and proliferation inhibition were significantly lower in TP53-mutated (TP53-M) CLL cells compared to TP53 wild-type cells. ibrutinib 22-31 tumor protein p53 Homo sapiens 130-134 30559058-0 2019 Aggressive Leukemic Non-Nodal Mantle Cell Lymphoma With P53 Gene Rearrangement/Mutation is Highly Responsive to Rituximab/Ibrutinib Combination Therapy. ibrutinib 122-131 tumor protein p53 Homo sapiens 56-59 30183082-8 2019 WM patients with TP53 mutations show response to ibrutinib. ibrutinib 49-58 tumor protein p53 Homo sapiens 17-21 30175400-12 2018 Demonstration of TP53 and NSD2 mutations in patients who developed blastoid transformation and ATM and TP53 mutations in patients who progressed, opens the door for future investigations in ibrutinib-refractory MCL. ibrutinib 190-199 tumor protein p53 Homo sapiens 17-21 30175400-12 2018 Demonstration of TP53 and NSD2 mutations in patients who developed blastoid transformation and ATM and TP53 mutations in patients who progressed, opens the door for future investigations in ibrutinib-refractory MCL. ibrutinib 190-199 tumor protein p53 Homo sapiens 103-107 29480432-3 2018 RECENT FINDINGS: Ibrutinib was FDA-approved for the upfront treatment of CLL in 2016 after being studied in older patients and those with 17p deletions or TP53 mutations. ibrutinib 17-26 tumor protein p53 Homo sapiens 155-159 28549767-2 2018 Ibrutinib, an inhibitor of Bruton"s tyrosine kinase, has demonstrated impressive response rates in the relapsed/refractory setting, including in the setting of Del17p and/or TP53 mutations. ibrutinib 0-9 tumor protein p53 Homo sapiens 174-178 29484684-3 2018 Recently, ibrutinib was approved for patients with relapsed/refractory CLL or for untreated CLL patients with del 17p or TP53 mutation. ibrutinib 10-19 tumor protein p53 Homo sapiens 121-125 29222275-7 2017 TP53 disruption by gene mutation and/or deletion associates with chemoimmunotherapy failure and mandates treatment with innovative drugs, including ibrutinib, idelalisib, or venetoclax. ibrutinib 148-157 tumor protein p53 Homo sapiens 0-4 29082795-7 2017 Because patients with a TP53 deletion/mutation are resistant to chemo-immunotherapy, treatment with the BTK inhibitor ibrutinib is recommended in this setting. ibrutinib 118-127 tumor protein p53 Homo sapiens 24-28 29250930-7 2017 In the relapsed or refractory setting, patients with del(17p) or TP53 aberrations should be offered treatment with a novel agent, such as ibrutinib, idelalisib-rituximab or venetoclax. ibrutinib 138-147 tumor protein p53 Homo sapiens 65-69 29234595-4 2017 Here we present a case of relapsed TP53 mutated CLL treated with ibrutinib as a bridge to alloHCT, discussing risks and benefits of different treatment options in a "real life" situation. ibrutinib 65-74 tumor protein p53 Homo sapiens 35-39 28782884-14 2017 Patients with a del(17p) or TP53 mutation can be treated with ibrutinib, venetoclax, or a combination of idelalisib and rituximab. ibrutinib 62-71 tumor protein p53 Homo sapiens 28-32 27797975-1 2017 Background: Ibrutinib is an active therapy with an acceptable safety profile for patients with chronic lymphocytic leukemia (CLL), including high-risk patients with del17p or with TP53 mutations. ibrutinib 12-21 tumor protein p53 Homo sapiens 180-184 28130034-0 2017 NICE guidance on ibrutinib for previously treated chronic lymphocytic leukaemia and untreated chronic lymphocytic leukaemia in the presence of 17p deletion or TP53 mutation. ibrutinib 17-26 tumor protein p53 Homo sapiens 159-163 27535981-8 2017 A validation sample of 15 CLL carrying TP53 mutations, of which 13 carried both del17p and a TP53 mutation, confirmed substantially less sensitivity to ibrutinib-induced apoptosis.Conclusions: This study identifies that CLL harboring del17p/TP53-mutated cells are substantially less sensitive to ibrutinib-induced apoptosis than del17p/TP53 wild-type cells. ibrutinib 152-161 tumor protein p53 Homo sapiens 39-43 27535981-8 2017 A validation sample of 15 CLL carrying TP53 mutations, of which 13 carried both del17p and a TP53 mutation, confirmed substantially less sensitivity to ibrutinib-induced apoptosis.Conclusions: This study identifies that CLL harboring del17p/TP53-mutated cells are substantially less sensitive to ibrutinib-induced apoptosis than del17p/TP53 wild-type cells. ibrutinib 152-161 tumor protein p53 Homo sapiens 93-97 27535981-8 2017 A validation sample of 15 CLL carrying TP53 mutations, of which 13 carried both del17p and a TP53 mutation, confirmed substantially less sensitivity to ibrutinib-induced apoptosis.Conclusions: This study identifies that CLL harboring del17p/TP53-mutated cells are substantially less sensitive to ibrutinib-induced apoptosis than del17p/TP53 wild-type cells. ibrutinib 152-161 tumor protein p53 Homo sapiens 93-97 27535981-8 2017 A validation sample of 15 CLL carrying TP53 mutations, of which 13 carried both del17p and a TP53 mutation, confirmed substantially less sensitivity to ibrutinib-induced apoptosis.Conclusions: This study identifies that CLL harboring del17p/TP53-mutated cells are substantially less sensitive to ibrutinib-induced apoptosis than del17p/TP53 wild-type cells. ibrutinib 152-161 tumor protein p53 Homo sapiens 93-97 28185174-3 2017 Ibrutinib was proven as a primary choice for patients with the TP53 gene deletion/mutation, who otherwise have no active treatment available. ibrutinib 0-9 tumor protein p53 Homo sapiens 63-67 27913471-7 2016 These recently approved drugs (ibrutinib, idelalisib, and venetoclax) are reporting excellent outcomes, including patients with high-risk disease such as 17p deletion (17p-) or TP53 mutations (TP53mut). ibrutinib 31-40 tumor protein p53 Homo sapiens 177-181 27198718-2 2016 Ibrutinib, a Bruton"s tyrosine kinase inhibitor is approved for relapsed/refractory and del(17p)/TP53 mutated chronic lymphocytic leukemia. ibrutinib 0-9 tumor protein p53 Homo sapiens 97-101 27284738-6 2016 We show that ibrutinib was effective in increasing survival, activating cellular programs outside the p53 pathway and did not place selective pressure on the remaining wild-type Trp53 allele. ibrutinib 13-22 tumor protein p53 Homo sapiens 102-105 27284738-7 2016 These data provide evidence that ibrutinib acts as an effective treatment for aggressive forms of CLL with TP53 mutations. ibrutinib 33-42 tumor protein p53 Homo sapiens 107-111 27040702-5 2016 Patients with a del(17p) or TP53 mutation should be treated with the kinase inhibitors ibrutinib or a combination of idelalisib and rituximab. ibrutinib 87-96 tumor protein p53 Homo sapiens 28-32 26628631-7 2015 Ibrutinib and idelalisib are active in patients with high-risk features, achieving superior disease control in difficult-to-treat patients than prior best therapy, making them the preferred agents for chronic lymphocytic leukemia with TP53 aberrations and for patients resistant to chemoimmunotherapy. ibrutinib 0-9 tumor protein p53 Homo sapiens 235-239 26118882-2 2015 Ibrutinib has been approved in USA in February 2014 and in France in October 2014 for the treatment of patients with relapsed/refractory mantle cell lymphoma (MCL) or chronic lymphocytic leukaemia (CLL) and for the treatment of patients with CLL and a chromosome 17 deletion (del 17p) or TP53 mutation. ibrutinib 0-9 tumor protein p53 Homo sapiens 288-292 25908509-14 2015 Patients with a del(17p) or TP53 mutation can be treated with ibrutinib or a combination of idelalisib and rituximab. ibrutinib 62-71 tumor protein p53 Homo sapiens 28-32 25802231-2 2015 Oral ibrutinib is indicated for the treatment of patients with relapsed/refractory mantle cell lymphoma (MCL) or chronic lymphocytic leukaemia (CLL) and for the treatment of patients with CLL and a chromosome 17 deletion (del 17p) or TP53 mutation. ibrutinib 5-14 tumor protein p53 Homo sapiens 234-238 25802231-7 2015 Given its efficacy and tolerability, once-daily, oral ibrutinib is an emerging treatment option for patients with relapsed/refractory MCL or CLL and CLL patients with del 17p or TP53 mutation. ibrutinib 54-63 tumor protein p53 Homo sapiens 178-182 25555420-0 2015 Ibrutinib for previously untreated and relapsed or refractory chronic lymphocytic leukaemia with TP53 aberrations: a phase 2, single-arm trial. ibrutinib 0-9 tumor protein p53 Homo sapiens 97-101 25555420-2 2015 We investigated the safety and activity of ibrutinib in previously untreated and relapsed or refractory CLL with TP53 aberrations. ibrutinib 43-52 tumor protein p53 Homo sapiens 113-117 25555420-17 2015 INTERPRETATION: The activity and safety profile of single-agent ibrutinib in CLL with TP53 aberrations is encouraging and supports its consideration as a novel treatment option for patients with this high-risk disease in both first-line and second-line settings. ibrutinib 64-73 tumor protein p53 Homo sapiens 86-90 26637744-5 2015 New B-cell receptor inhibitors, such as ibrutinib and idelalisib, may have a role in the management of B-PLL, especially for the patients harboring abnormalities of TP53. ibrutinib 40-49 tumor protein p53 Homo sapiens 165-169 26637745-6 2015 Ibrutinib and idelalisib are currently approved for the treatment of relapsed or refractory CLL or frontline treatment of 17p-/TP53mut CLL regardless of fitness. ibrutinib 0-9 tumor protein p53 Homo sapiens 127-131 26062943-6 2015 Fortunately, significant progress in the understanding of CLL biology has enabled the development of new molecular drugs targeting the B-cell receptor signaling pathway, such as ibrutinib and idelalisib, which have shown impressive results in patients with relapsed/refractory disease or with TP53 mutation/deletion. ibrutinib 178-187 tumor protein p53 Homo sapiens 293-297 25392275-7 2014 In 2014, several new compounds were approved for patients with ultrahigh risk genetic factors (17p-, TP53mut) and for relapsed/refractory CLL: both idelalisib and ibrutinib are orally bioavailable kinase inhibitors that block key regulators of central pathways. ibrutinib 163-172 tumor protein p53 Homo sapiens 101-105