The RB and p53 pathways in cancer
Charles J. Sherr,Frank McCormick +1 more
TLDR
Interconnecting signaling pathways controlled by RB and p53 are discussed, attempting to explain their potentially universal involvement in the etiology of cancer.About:
This article is published in Cancer Cell.The article was published on 2002-08-01 and is currently open access. It has received 1653 citations till now. The article focuses on the topics: Cancer cell & Cancer.read more
Citations
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Hallmarks of cancer: the next generation.
TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
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Cellular senescence: when bad things happen to good cells
TL;DR: Understanding the causes and consequences of cellular senescence has provided novel insights into how cells react to stress, especially genotoxic stress, and how this cellular response can affect complex organismal processes such as the development of cancer and ageing.
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Cell-cycle checkpoints and cancer
Michael B. Kastan,Jiri Bartek +1 more
TL;DR: All life on earth must cope with constant exposure to DNA-damaging agents such as the Sun's radiation, and how cells respond to DNA damage are critical determinants of whether that individual will develop cancer.
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Malignant astrocytic glioma: genetics, biology, and paths to treatment.
Frank B. Furnari,Tim R. Fenton,Robert M. Bachoo,Akitake Mukasa,Jayne M. Stommel,Alexander H. Stegh,William C. Hahn,Keith L. Ligon,David N. Louis,Cameron Brennan,Lynda Chin,Ronald A. DePinho,Webster K. Cavenee +12 more
TL;DR: The recent confluence of advances in stem cell biology, cell signaling, genome and computational science and genetic model systems have revolutionized understanding of the mechanisms underlying the genetics, biology and clinical behavior of glioblastoma.
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Senescent Cells, Tumor Suppression, and Organismal Aging: Good Citizens, Bad Neighbors
Judith Campisi,Judith Campisi +1 more
TL;DR: The senescence response may be antagonistically pleiotropic, promoting early-life survival by curtailing the development of cancer but eventually limiting longevity as dysfunctional senescent cells accumulate.
References
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The hallmarks of cancer.
TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
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p53, the Cellular Gatekeeper for Growth and Division
TL;DR: The author regrets the lack of citations for many important observations mentioned in the text, but their omission is made necessary by restrictions in the preparation of review manuscripts.
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CDK inhibitors: positive and negative regulators of G1-phase progression
TL;DR: This work challenges previous assumptions about how the G1/S transition of the mammalian cell cycle is governed, helps explain some enigmatic features of cell cycle control that also involve the functions of the retinoblastoma protein (Rb) and the INK4 proteins, and changes the thinking about how either p16 loss or overexpression of cyclin D-dependent kinases contribute to cancer.
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Cancer Cell Cycles
TL;DR: Genetic alterations affecting p16INK4a and cyclin D1, proteins that govern phosphorylation of the retinoblastoma protein and control exit from the G1 phase of the cell cycle, are so frequent in human cancers that inactivation of this pathway may well be necessary for tumor development.
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Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a
TL;DR: It is shown that expression of oncogenic ras in primary human or rodent cells results in a permanent G1 arrest, and that the onset of cellular senescence does not simply reflect the accumulation of cell divisions, but can be prematurely activated in response to an onCogenic stimulus.