PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29731965-10 2018 In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens. Cyclophosphamide 191-207 tumor protein p53 Homo sapiens 36-40 29445054-8 2018 Finally, toxicogenomics analysis of HepG2 and HepaRG cells after exposure to AFB1 and CPA revealed that numerous p53-related genes were upregulated- and the expression of these genes was greater in HepaRG than in HepG2 cells. Cyclophosphamide 86-89 tumor protein p53 Homo sapiens 113-116 29731965-10 2018 In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens. Cyclophosphamide 191-207 tumor protein p53 Homo sapiens 58-62 23131146-4 2012 In contrast, while TP53 mutations have shown to predict response to cyclophosphamide high dose therapy, mutations in general have been associated with anthracycline resistance in human breast cancers. Cyclophosphamide 68-84 tumor protein p53 Homo sapiens 19-23 24244905-3 2013 In particular, we found that cyclophosphamide stimulates anticancer immune responses upon the perception by the immune system of inflammatory danger signals associated with the death of leukocytes, via p53 and type I interferon-related mechanisms. Cyclophosphamide 29-45 tumor protein p53 Homo sapiens 202-205 23759676-7 2013 CONCLUSIONS: Altogether, these data identify the cyclophosphamide-induced immunomodulatory factors in humans and indicate that preconditioning chemotherapy may stimulate immunity as a consequence of danger perception associated with blood cell death, through p53 and IFN-I-related mechanisms. Cyclophosphamide 49-65 tumor protein p53 Homo sapiens 259-262 28791403-10 2017 Among DLBCL cases, the TP53 mutations shortened both OS and PFS of patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and decreased both OS and PFS of patients with secondary DLBCL disease. Cyclophosphamide 108-124 tumor protein p53 Homo sapiens 23-27 26238069-0 2016 TP53 mutations are associated with higher rates of pathologic complete response to anthracycline/cyclophosphamide-based neoadjuvant chemotherapy in operable primary breast cancer. Cyclophosphamide 97-113 tumor protein p53 Homo sapiens 0-4 26238069-7 2016 Our results suggested that patients with TP53 mutations are more likely to respond to anthracycline/ cyclophosphamide-based neoadjuvant chemotherapy and have a favorable survival. Cyclophosphamide 101-117 tumor protein p53 Homo sapiens 41-45 25430047-1 2015 This study aimed to clarify the association between the TP53 rs1625895 polymorphism and the efficiency of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) therapy in 106 patients with diffuse large B cell lymphoma (DLBCL). Cyclophosphamide 125-141 tumor protein p53 Homo sapiens 56-60 24074787-8 2013 We reported that TP53 mutated non inflammatory locally advanced breast carcinomas had a high rate of complete pathological response to dose-dense doxorubicin-cyclophosphamide chemotherapy, while TP53 wild-type (WT) tumors never achieved complete response. Cyclophosphamide 158-174 tumor protein p53 Homo sapiens 17-21 22955915-1 2012 TP53 mutation is an independent marker of poor prognosis in patients with diffuse large B-cell lymphoma (DLBCL) treated with cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP) therapy. Cyclophosphamide 125-141 tumor protein p53 Homo sapiens 0-4 21514041-0 2011 Gene expression signature of TP53 but not its mutation status predicts response to sequential paclitaxel and 5-FU/epirubicin/cyclophosphamide in human breast cancer. Cyclophosphamide 125-141 tumor protein p53 Homo sapiens 29-33 22139992-0 2012 Potentiation of a p53-SLP vaccine by cyclophosphamide in ovarian cancer: a single-arm phase II study. Cyclophosphamide 37-53 tumor protein p53 Homo sapiens 18-21 22139992-1 2012 The purpose of the current phase II single-arm clinical trial was to evaluate whether pretreatment with low-dose cyclophosphamide improves immunogenicity of a p53-synthetic long peptide (SLP) vaccine in patients with recurrent ovarian cancer. Cyclophosphamide 113-129 tumor protein p53 Homo sapiens 159-162 22139992-10 2012 The outcome of this phase II trial warrants new studies on the use of low-dose cyclophosphamide to potentiate the immunogenicity of the p53-SLP vaccine or other antitumor vaccines. Cyclophosphamide 79-95 tumor protein p53 Homo sapiens 136-139 21706156-0 2012 MDM2 SNP309 and TP53 R72P associated with severe and febrile neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide. Cyclophosphamide 128-144 tumor protein p53 Homo sapiens 16-20 20228131-0 2010 Cyclophosphamide dose intensification may circumvent anthracycline resistance of p53 mutant breast cancers. Cyclophosphamide 0-16 tumor protein p53 Homo sapiens 81-84 20655369-7 2010 While cyclophosphamide showed an elevation of activated P53 in the presence of S9, 7,12-dimethylbenz[a]anthracene and aflatoxin B(1) responded without the MAS. Cyclophosphamide 6-22 tumor protein p53 Homo sapiens 56-59 20638924-4 2010 CONCLUSION: We introduced new data related to the contribution of p53 codon 72 to toxicity due to 5-fluorouracil and cyclophosphamide-based neoadjuvant chemotherapy in patients with breast cancer. Cyclophosphamide 117-133 tumor protein p53 Homo sapiens 66-69 20435884-3 2010 Losses of TP53 and CDKN2A, observed in 8% and 35% of patients, respectively, were significantly associated with a shorter survival after rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treatment, independently of the International Prognostic Index and of the cell of origin. Cyclophosphamide 148-164 tumor protein p53 Homo sapiens 10-14 21693655-3 2011 PATIENTS AND METHODS: Epithelial p53 expression was evaluated using two immunohistochemical antibodies (DO7 and 1801) in formalin-fixed, paraffin-embedded tissue from patients with node-positive breast cancer who were randomized to four cycles of cyclophosphamide and one of three doses of doxorubicin (60, 75, or 90 mg/m(2); AC) and to receive four subsequent cycles of paclitaxel (T) or not. Cyclophosphamide 247-263 tumor protein p53 Homo sapiens 33-36 20228131-7 2010 A sharp statistical interaction was detected between p53 status and cyclophosphamide dose intensity. Cyclophosphamide 68-84 tumor protein p53 Homo sapiens 53-56 20228131-10 2010 Thus, our data strongly suggest that cyclophosphamide dose intensification in ER(-) p53-mutated breast cancer patients could significantly improve their response. Cyclophosphamide 37-53 tumor protein p53 Homo sapiens 84-87 19731257-3 2009 The dependence of p53-mediated chemosensitivity on pRb status was first investigated in a prospective study on the prognostic relevance of p53 in breast cancer patients treated with adjuvant chemotherapy (5-fluorouracil, methotrexate and cyclophosphamide). Cyclophosphamide 238-254 tumor protein p53 Homo sapiens 18-21 10472362-1 1999 Expression of mutant p53 in 19 patients with stage III moderately differentiated serous cystadenocarcinoma of the ovary, who all had optimal primary cytoreductive surgery and six cycles of cisplatin and cyclophosphamide was analyzed to determine its prognostic significance. Cyclophosphamide 203-219 tumor protein p53 Homo sapiens 21-24 19372630-8 2009 Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA. Cyclophosphamide 165-168 tumor protein p53 Homo sapiens 92-95 19372630-8 2009 Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA. Cyclophosphamide 165-168 tumor protein p53 Homo sapiens 100-103 19372630-8 2009 Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA. Cyclophosphamide 271-274 tumor protein p53 Homo sapiens 92-95 19372630-8 2009 Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA. Cyclophosphamide 271-274 tumor protein p53 Homo sapiens 100-103 18325917-2 2008 We analysed the efficacy of a preoperative combination between 5-fluorouracil, anthracyclines and cyclophosphamide according to both p53 status and molecular classification. Cyclophosphamide 98-114 tumor protein p53 Homo sapiens 133-136 17876337-1 2007 In advanced breast cancers, TP53 mutation is highly predictive of complete response to high-dose epirubicin/cyclophosphamide chemotherapy. Cyclophosphamide 108-124 tumor protein p53 Homo sapiens 28-32 17388661-0 2007 Exquisite sensitivity of TP53 mutant and basal breast cancers to a dose-dense epirubicin-cyclophosphamide regimen. Cyclophosphamide 89-105 tumor protein p53 Homo sapiens 25-29 17388661-16 2007 CONCLUSIONS: This study demonstrates that, in noninflammatory breast cancers, TP53 status is a key predictive factor for response to this dose-dense epirubicin-cyclophosphamide regimen and further suggests that the basal subtype is exquisitely sensitive to this association. Cyclophosphamide 160-176 tumor protein p53 Homo sapiens 78-82 11935300-6 2002 RESULTS: Ex vivo chemosensitivity testing showed that tumors with p53 mutations were significantly more resistant to the cyclophosphamide/etoposide/epirubicin regimen than with normal p53 gene ( P = 0.012). Cyclophosphamide 121-137 tumor protein p53 Homo sapiens 66-69 11332152-2 2001 The in situ bioactivation of cyclophosphamide by cytochrome p450-2B1 and subsequent p53 delivery were examined. Cyclophosphamide 29-45 tumor protein p53 Homo sapiens 84-87 15182437-9 2004 In the p53 wild-type group, we found a positive correlation for the following drugs: ADM (P < 0.02), ACNU (P < 0.007), CPA (P < 0.011), UFT (P < 0.012), and FT-207 (P < 0.02). Cyclophosphamide 125-128 tumor protein p53 Homo sapiens 7-10 15182437-10 2004 In the p53 mutant group, only CPA (P < 0.003) showed a positive correlation. Cyclophosphamide 30-33 tumor protein p53 Homo sapiens 7-10 9951689-4 1998 Chemosensitivity data, according to a short-term assay (FMCA), indicated that tumours with p53 mutation were more resistant to cisplatin and cyclophosphamide. Cyclophosphamide 141-157 tumor protein p53 Homo sapiens 91-94 9703286-0 1998 Therapy effect of either paclitaxel or cyclophosphamide combination treatment in patients with epithelial ovarian cancer and relation to TP53 gene status. Cyclophosphamide 39-55 tumor protein p53 Homo sapiens 137-141 9291435-6 1997 Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair. Cyclophosphamide 117-133 tumor protein p53 Homo sapiens 58-61 9291435-6 1997 Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair. Cyclophosphamide 117-133 tumor protein p53 Homo sapiens 161-164 9291435-6 1997 Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair. Cyclophosphamide 117-133 tumor protein p53 Homo sapiens 161-164 9610789-0 1998 p53 mutations in cyclophosphamide-associated bladder cancer. Cyclophosphamide 17-33 tumor protein p53 Homo sapiens 0-3 9610789-3 1998 We examined 19 cyclophosphamide-related bladder tumors to test the hypothesis that they might contain somatic mutations in the p53 tumor suppressor gene that could link a specific metabolite to the etiology of these cancers. Cyclophosphamide 15-31 tumor protein p53 Homo sapiens 127-130 9610789-5 1998 The p53 mutation spectrum of these cyclophosphamide-associated bladder cancers differed significantly from patterns reported for sporadic (P = 0.020), smoking-related (0.043), and schistosomiasis-linked (P = 0.002) tumors but not arylamine-associated neoplasms (P = 0.860). Cyclophosphamide 35-51 tumor protein p53 Homo sapiens 4-7 7563172-0 1995 Accumulation of p53 protein as a possible predictor of response to adjuvant combination chemotherapy with cyclophosphamide, methotrexate, fluorouracil, and prednisone for breast cancer. Cyclophosphamide 106-122 tumor protein p53 Homo sapiens 16-19