p53-dependent apoptosis modulates the cytotoxicity of anticancer agents

@article{Lowe1993p53dependentAM,
  title={p53-dependent apoptosis modulates the cytotoxicity of anticancer agents},
  author={Scott W. Lowe and H. Earl Ruley and Tyler Jacks and David E. Housman},
  journal={Cell},
  year={1993},
  volume={74},
  pages={957-967}
}
p53-independent apoptosis induced by paclitaxel through an indirect mechanism.
TLDR
The results suggest that the efficacy of paclitaxel in vivo may be due not only to its microtubule-stabilizing activity, but its ability to activate local release of an apoptosis-inducing cytokine.
Determine the effect of p53 on chemosensitivity.
TLDR
Tumors treated with DNA-damaging drugs often undergo alternate forms of cell death, such as senescence or mitotic catastrophe, in addition to apoptosis that may ultimately lead to regression, which is a predictor of chemotherapy response in patients per se.
Analysis of p53 function in cellular responses to microtubule-acting drugs
TLDR
The experiments have addressed two distinct aspects of p53 function relating to its effect on chemotherapeutic resistance and its role as a cell cycle checkpoint, which suggest that the p53-dependent checkpoint following spindle disruption functionally overlaps with the p 53- dependent checkpoint following DNA damage.
Apoptosis and cancer chemotherapy
TLDR
The expanding Bcl-2 family of proteins also play an important role in the cell death program, and evidence suggests that these proteins may function as integrators of damage signals, and may be the final decision point as to whether a cell lives or dies.
Apoptosis, p53, and tumor cell sensitivity to anticancer agents.
TLDR
Because wild-type p53 predisposes cells to a more rapid rate of cell death after DNA damage, that short-term assays have led to the conclusion that mutations in p53 confer resistance to genotoxic agents, this tenet may need to be reexamined for human tumors of nonhematological origin.
Identification and Characterization of Distinct Apoptotic Pathways in Cancer Cells Activated in Response to Treatment with Different Anti-Cancer Agents
TLDR
The ability of E1A to induce pro-caspases and p53 may synergize to promote apoptosis and provide a direct connection between a pro-apoptotic oncogene (E1A) and the cell death machinery.
2 Resistance to Apoptosis in Cancer Therapy
TLDR
A major challenge for the immediate future is to validate the concept that apoptosis plays a crucial role in tumor response to therapy in patients receiving conventional and “designer” drugs, and more specifically, to confirm that the latter effectively hit their targets and produce the desired biological responses.
Resistance to Apoptosis in Cancer Therapy
TLDR
A major challenge for the immediate future is to validate the concept that apoptosis plays a crucial role in tumor response to therapy in patients receiving conventional and “designer” drugs, and more specifically, to confirm that the latter effectively hit their targets and produce the desired biological responses.
Biological significance and molecular mechanisms of p53-induced apoptosis
TLDR
Key insights are offered into the molecular mechanisms employed by p53 to induce cell death that provide an exhilarating array of possible therapeutic interventions against p53-deficient human cancers that may pay enormous dividends in the not-too-distant future.
Cell death pathways in response to antitumor therapy.
TLDR
It is critically reviewed here how antitumor therapy may elicit the response of human cancers through different cell pathways leading to cell death.
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    Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
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TLDR
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