Restoration of the G1 Checkpoint and the Apoptotic Pathway Mediated by Wild-type p53 Sensitizes Squamous Cell Carcinoma of the Head and Neck to Radiotherapy

Human Endothelial Cell Life Extension by Telomerase Expression

“…To our knowledge, this study is also the first to report EC apoptosis as a function of PDL, and our results indicate that senescent ECs were resistant to apoptosis relative only to midpassage primary ECs, not early passage cells, as reported previously in fibroblasts (54,55). We used only confluent, growth-arrested cells for our apoptosis analyses as it is known that proliferating cells are more susceptable to apoptosis than are quiescent cells; however, unrepaired DNA and chromosomal damage are also known to trigger apoptotic induction (62-64, 74, 75).…”

“…Clarification of EC apoptotic mechanisms thus represents an important therapeutic strategy in the management of acute, chronic, and neoplastic diseases (51)(52)(53). Previous studies of human dermal fibroblasts showed that senescent cells are more resistant to apoptosis relative to young cells in vitro (54,55). Therefore, we monitored the basal apoptotic rate in HDMECs and found that both early and late passage parental HDMECs showed lower nuclear fragmentation relative to mid passage HDMECs (Fig.…”

Enhanced radiosensitivity of malignant glioma cells after adenoviral p53 transduction

“…1,3,4,12,15,19 Our results are distinguished from those of other studies because the enhanced radiosensitivity is accomplished in cells that express wild-type rat p53 themselves. If disruption of p53-mediated mechanisms is essential for development of the neoplastic phenotype, this would argue that cells expressing wild-type p53, such as the RT2 cell, must harbor defects elsewhere in the p53-mediated processes, which would normally protect against the cell proliferation and genomic instability characteristic of neoplastic cells.…”

ADENOVIRUS-MEDIATED p53 GENE TRANSFER TO RAT TESTIS IMPAIRS SPERMATOGENESIS

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