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We began analyzing https://link.springer.com/article/10.1007/s004410051072, but it redirected us to https://link.springer.com/article/10.1007/s004410051072. The analysis below is for the second page.

Title[redir]:
Predicting response to cancer chemotherapy: the role of p53 | Cell and Tissue Research
Description:
Loss of wild-type p53 activity is thought to be a major predictor of failure to respond to radiotherapy and chemotherapy in various human cancers. This assumption is largely based on some cell-death studies in p53-knockout mice and on correlations of p53 status assessed by immunochemistry or single-strand conformational polymorphism (SSCP) analysis, and responses to therapy in human cancers in vivo. In principle, p53 may enhance chemosensitivity by promoting apoptosis via transcription-independent mechanisms as well as transcriptional activation of proapoptotic genes such as bax and transcriptional repression of antiapoptotic genes such as bcl-2. Drug-induced suicide mediated by the CD95/CD95 ligand system may also involve a p53-controlled pathway. Yet, p53 may decrease chemosensitivity by promoting p21-mediated and p21-independent growth arrest, DNA repair, and differentiation, and by enhancing the transcription of antiapoptotic genes such as bcl-x. Cell-culture work indicates that the effects of altering the p53 status on chemosensitivity depend very much on the cellular context. Disruption of p53 function in otherwise normal, nonneoplastic cells may enhance rather than decrease chemosensitivity. However, targeted p53 gene disruption in some cell types obtained from p53-knockout mice results in enhanced rather than decreased sensitivity, e.g., to irradiation. Transformed cells that have retained wild-type p53 function tend to acquire chemoresistance when p53 function is disabled, with few exceptions. Thus, preexisting molecular alterations or consecutive accumulation of molecular alterations after loss of p53 rather than the loss of wild-type p53 activity per se may confer chemoresistence to tumor cells. Moreover, p53 accumulation resulting from the increased half-life of mutant p53 proteins can act as a gain-of-function mutation, presumably as a consequence of multiple protein-protein interactions. Finally, significant tumor cell-type- and drug-specific patterns of modulation of chemosensitivity by p53 are beginning to emerge. Transfer of wild-type p53 genes into tumor cells commonly induces growth arrest but may render these cells relatively more resistant to most chemotherapeutic drugs. Therefore, careful experimental in vitro and in vivo studies are required before chemotherapy-supported p53 gene therapy for human cancer is introduced into clinical practice.

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article, cancer, access, privacy, cookies, content, research, cell, chemosensitivity, cells, function, information, publish, search, chemotherapy, wildtype, human, genes, tumor, data, log, journal, tissue, response, weller, loss, cancers, therapy, molecular, open, discover, springer, optional, analysis, personal, parties, policy, find, track, predicting, role, cite, michael, explore, activity, studies, pknockout, mice, status, vivo,

Topics {✒️}

mutant p53 proteins p21-independent growth arrest wild-type p53 activity significant tumor cell-type single-strand conformational polymorphism cd95/cd95 ligand system multiple protein-protein interactions month download article/chapter drug-induced suicide mediated wild-type p53 genes molecular neuro-oncology p53-knockout mice results human cancer cancer chemotherapy related subjects tissue research aims privacy choices/manage cookies full article pdf predicting response dna repair therapeutic strategies p53-knockout mice article weller cell-culture work cell types obtained human cancers cell-death studies promoting p21-mediated drug-specific patterns p53 review published p53-controlled pathway check access instant access european economic area increased half-life canonical functions p53 status assessed p53 accumulation resulting conditions privacy policy article cell promoting apoptosis transcription-independent mechanisms preexisting molecular alterations accepting optional cookies main content log journal finder publish article log tumor cells p53 function article cite

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