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Therefore, p may prove to be a better prognostic factor if stable disease is grouped with the responders.The relationship between stable disease and survival is not well documented, and we have not been able to find any report investigating p status in relation to stable disease.However, one of the few reports that have split the nonresponders in stable and progressive disease found that there was no significant difference with regard to survival between patients with regression of the tumor and stable disease. Furthermore, the prognostic role of p seems much less well defined after resection compared with resection and adjuvant chemotherapy. Our data suggest that tumor cells expressing wildtype p prevent proliferation when under stress by inducing either apoptosis or accelerated cellular senescence.Our data are the first showing that senescence may be a normal cellular response to DNA damage in tumor cells.We believe that our observations could have profound clinical implications and explain some of the controversy concerning p as a prognostic factor.In the clinic, replicative senescence appears to be a relevant factor in determining treatment outcome and warrants further investigation, especially regarding p as a prognostic factor and of stable disease in relation to survival after chemotherapy.Such information could be of great value in choosing an appropriate chemotherapeutic strategy.Tumor sections of untreated patients were stained as controls.Tumors had been resected between and days after the last cycle of CAF.Moreover, tetracyclineregulated p expression was capable of inducing senescence, but was not required to maintain it after h. DNA DAMAGE INDUCES SENESCENCE IN TUMOR CELLS. . StanulisPraeger, B.Blood. Cell. Cell. Nature. Cell. Oncogene. Oncogene. Oncogene. Oncogene. Nature. Science. Nature. Science. Science. Oncogene. Nature. Cell. Oncogene. Click on Request Permissions which will take you to the Copyright Clearance Centers Downloaded from cancerres.aacrjournals.org on September. American Association for Cancer Research. Studies of the processes which correct such damage in mammalian cells are, however, still in their early stages.Here we have summarized our recent work which demonstrates new features of mammalian oxidative UNA damage repair, such as the detective repair of oxidative DNA damage in xeroderma pigmentosum cells.Thus, mammalian cells frequently may encoun ter oxidative DNA damage induced by these reactive species.The lesions are heterogeneous and include single and double strand DNA breaks, AP sites, and oxidized purines and pyrimidines. Repair of these forms of damage occurs intracellularly by base excision repair, but as shown below, nucleotide excision repair also may be involved.Defective repair of oxygen free radicalinduced DNA lesions leads to a variety of biological consequences, such as mutation induction, blocking of transcription and replication, and chromosomal aberra tions.Furthermore, recent studies indicate that persistence of DNA damage may transmit signals to other cellular components, including p which may be involved in a G,S cell cycle checkpoint. These observations suggest that DNA damage is processed not only by DNA repair enzymes but also by other nuclear factors involved in a variety of cellular functions.The delineation of cellular responses to oxidative DNA damage in mam malian cells is still at a preliminary stage.We have investigated two specific problems in the repair of oxidative DNA damage by using gently prepared human cellfree extracts together with plasmid DNA containing oxidative lesions as substrate.

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