PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8706243-3 1996 Sublines that were resistant to melphalan, pyrazafurin, mitoxantrone, etoposide and PALA all retained expression of wild-type p53. Melphalan 32-41 tumor protein p53 Homo sapiens 126-129 34530900-12 2021 Moreover, we provide evidences that myeloma cells are dependent on SETD8 activity and its pharmacological inhibition synergizes with melphalan, which could be beneficial to improve MM treatment in high-risk patients whatever their status for p53. Melphalan 133-142 tumor protein p53 Homo sapiens 242-245 34832966-10 2021 Treatment with cisplatin, melphalan, or 9-cis RA decreased p53 expression levels in SK-N-FI cells but not in SK-N-Be (2). Melphalan 26-35 tumor protein p53 Homo sapiens 59-62 25051404-6 2014 Moreover, we found that melphalan-induced apoptosis inversely correlated with the repair efficiency of the TS, with the duration of the inhibition of mRNA synthesis, phosphorylation of p53 at serine 15 and apoptosis rates being higher in responders than in non-responders (all P<0.001). Melphalan 24-33 tumor protein p53 Homo sapiens 185-188 29295500-0 2017 Decitabine and Melphalan Fail to Reactivate p73 in p53 Deficient Myeloma Cells. Melphalan 15-24 tumor protein p53 Homo sapiens 51-54 27693638-0 2016 DNA-PKcs, a novel functional target of acriflavine, mediates acriflavine"s p53-dependent synergistic anti-tumor efficiency with melphalan. Melphalan 128-137 tumor protein p53 Homo sapiens 75-78 33153480-9 2020 In addition, several other signaling pathways including the p53 and transforming growth factor-beta signaling pathways were also implicated in melphalan-induced cardiotoxicity according to the proteomic and transcriptomic analyses. Melphalan 143-152 tumor protein p53 Homo sapiens 60-63 26414189-0 2016 Single nucleotide polymorphisms in TP53 but not KRAS or MDM2 are predictive of clinical outcome in multiple myeloma treated with high-dose melphalan and autologous stem cell support. Melphalan 139-148 tumor protein p53 Homo sapiens 35-39 24308434-3 2014 Sensitivity of HMCLs to both drugs was correlated to p53: the BDM and melphalan median LD50 values of TP53(wild-type) HMCLs were more than two-fold lower than those of TP53(abnormal) HMCLs (p < 0.001), and p53 silencing in TP53(wt) NCI-H929 cells inhibited BDM- and melphalan-induced cell death. Melphalan 70-79 tumor protein p53 Homo sapiens 53-56 24308434-3 2014 Sensitivity of HMCLs to both drugs was correlated to p53: the BDM and melphalan median LD50 values of TP53(wild-type) HMCLs were more than two-fold lower than those of TP53(abnormal) HMCLs (p < 0.001), and p53 silencing in TP53(wt) NCI-H929 cells inhibited BDM- and melphalan-induced cell death. Melphalan 70-79 tumor protein p53 Homo sapiens 102-106 24913980-3 2014 Our findings indicate that sublethal doses of doxorubicin and melphalan initiate a DNA damage response (DDR) controlling ligand upregulation on MM cell lines and patient-derived malignant plasma cells in Chk1/2-dependent and p53-independent manner. Melphalan 62-71 tumor protein p53 Homo sapiens 225-228 24089038-4 2014 Following ex vivo treatment with melphalan, a gradual suppression of the apoptotic pathway occurred in samples collected at different stages of myelomagenesis, with the severity and duration of the inhibition of RNA synthesis, p53 phosphorylation at serine15 and induction of apoptosis being higher in MGUS than SMM and lowest in MM patients (all P<0.0103). Melphalan 33-42 tumor protein p53 Homo sapiens 227-230 18095870-6 2008 Cells expressing the p53 mutants were either more sensitive to cisplatin and melphalan or more resistant than the untransfected cells, depending on the mutation. Melphalan 77-86 tumor protein p53 Homo sapiens 21-24 19417135-1 2009 The repair of melphalan-induced N-alkylpurine monoadducts and interstrand cross-links was examined in different repair backgrounds, focusing on four genes (beta-actin, p53, N-ras, and delta-globin) with dissimilar transcription activities. Melphalan 14-23 tumor protein p53 Homo sapiens 168-171 22653969-8 2012 In summary, the cytotoxic effects of bendamustine, melphalan and doxorubicin on p53-deficient multiple myeloma cell lines were enhanced by the coadministration of AZD7762. Melphalan 51-60 tumor protein p53 Homo sapiens 80-83 11507071-3 2001 We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines. Melphalan 93-102 tumor protein p53 Homo sapiens 14-17 18024399-2 2007 DESIGN AND METHODS: Melphalan-induced damage formation and repair of monoadducts and interstrand cross-links in the p53 gene were studied in peripheral blood mononuclear cells obtained from 32 patients prior to therapy. Melphalan 20-29 tumor protein p53 Homo sapiens 116-119 18024399-9 2007 INTERPRETATION AND CONCLUSIONS: An in vitro assay to quantify melphalan-induced p53-specific damage formation/repair can be used to select those patients with MM who are more likely to benefit from HDM supported by ASCT. Melphalan 62-71 tumor protein p53 Homo sapiens 80-83 15883412-0 2005 Extent of damage and repair in the p53 tumor-suppressor gene after treatment of myeloma patients with high-dose melphalan and autologous blood stem-cell transplantation is individualized and may predict clinical outcome. Melphalan 112-121 tumor protein p53 Homo sapiens 35-38 15883412-2 2005 PATIENTS AND METHODS: The formation and subsequent repair of DNA damage (monoadducts and interstrand cross-links) in the p53 tumor-suppressor gene, the proto-oncogene N-ras, and the housekeeping gene beta-actin during the first 24 hours after treatment with high-dose melphalan (HDM; 200 mg/m2) supported by autologous blood stem-cell transplantation (ABSCT) was measured in blood leukocytes of 26 patients with MM. Melphalan 268-277 tumor protein p53 Homo sapiens 121-124 15308759-7 2004 Levels of p53 were quantified by sensitive fluorogenic enzyme-linked immunosorbent assay at intervals up to 24 h after exposure of cells to various concentrations of melphalan and monohydroxymelphalan. Melphalan 166-175 tumor protein p53 Homo sapiens 10-13 14555520-4 2003 RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links. Melphalan 84-93 tumor protein p53 Homo sapiens 135-138 14555520-4 2003 RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links. Melphalan 84-93 tumor protein p53 Homo sapiens 338-341 14555520-4 2003 RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links. Melphalan 84-93 tumor protein p53 Homo sapiens 338-341 15308759-8 2004 The level of initially formed DNA adducts needed to cause elevation of p53 from a baseline level of 0.5 ng/mg total protein to 2 ng/mg was 5- to 8-fold higher for monohydroxymelphalan than melphalan. Melphalan 174-183 tumor protein p53 Homo sapiens 71-74 11507071-3 2001 We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines. Melphalan 120-125 tumor protein p53 Homo sapiens 14-17 11507071-3 2001 We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines. Melphalan 120-125 tumor protein p53 Homo sapiens 14-17 11507071-9 2001 Loss of p53 function was selectively achieved by transduction of human papillomavirus 16 E6 (which degrades p53) into two drug-sensitive neuroblastoma cell lines with intact p53, causing high-level drug resistance to L-PAM, carboplatin, and etoposide. Melphalan 217-222 tumor protein p53 Homo sapiens 8-11 11507071-3 2001 We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines. Melphalan 104-109 tumor protein p53 Homo sapiens 14-17 11107118-4 2000 RESULTS: Loss of p53 function (p53-LOF), defined as a failure to induce p21 and/or MDM2 in response to melphalan, was seen in 1/8 drug-sensitive and 6/10 drug-resistant cell lines. Melphalan 103-112 tumor protein p53 Homo sapiens 17-20 11107118-4 2000 RESULTS: Loss of p53 function (p53-LOF), defined as a failure to induce p21 and/or MDM2 in response to melphalan, was seen in 1/8 drug-sensitive and 6/10 drug-resistant cell lines. Melphalan 103-112 tumor protein p53 Homo sapiens 31-34 11096420-0 2000 Abrogation of G(2)/M-phase block enhances the cytotoxicity of daunorubicin, melphalan and cisplatin in TP53 mutant human tumor cells. Melphalan 76-85 tumor protein p53 Homo sapiens 103-107 11096420-3 2000 In the TP53-mutated cell lines MeWo and 4451, the survival ratio at 7 Gy measured by colony formation was 2.3-2.8, 8.6-85 and 52-74 for daunorubicin, melphalan and cisplatin, respectively. Melphalan 150-159 tumor protein p53 Homo sapiens 7-11 11050000-5 2000 Expression of wt p53 also leads to cell cycle arrest and protection from doxorubicin (Dox)- and melphalan (Mel)-induced apoptosis. Melphalan 96-105 tumor protein p53 Homo sapiens 17-20 11050000-5 2000 Expression of wt p53 also leads to cell cycle arrest and protection from doxorubicin (Dox)- and melphalan (Mel)-induced apoptosis. Melphalan 107-110 tumor protein p53 Homo sapiens 17-20