Literature DB >> 15549092

Intrinsic tumour suppression.

Scott W Lowe1, Enrique Cepero, Gerard Evan.   

Abstract

Mutations that drive uncontrolled cell-cycle progression are requisite events in tumorigenesis. But evolution has installed in the proliferative programmes of mammalian cells a variety of innate tumour-suppressive mechanisms that trigger apoptosis or senescence, should proliferation become aberrant. These contingent processes rely on a series of sensors and transducers that act in a coordinated network to target the machinery responsible for apoptosis and cell-cycle arrest at different points. Although oncogenic mutations that disable such networks can have profound and varied effects on tumour evolution, they may leave intact latent tumour-suppressive potential that can be harnessed therapeutically.

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Year:  2004        PMID: 15549092     DOI: 10.1038/nature03098

Source DB:  PubMed          Journal:  Nature        ISSN: 0028-0836            Impact factor:   49.962


  483 in total

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Review 2.  Using mice to examine p53 functions in cancer, aging, and longevity.

Authors:  Lawrence A Donehower
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Review 3.  Stress and the epigenetic landscape: a link to the pathobiology of human diseases?

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Review 4.  Pancreatic ductal adenocarcinoma and transcription factors: role of c-Myc.

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Review 5.  c-Myc induction of programmed cell death may contribute to carcinogenesis: a perspective inspired by several concepts of chemical carcinogenesis.

Authors:  Chenguang Wang; Yanhong Tai; Michael P Lisanti; D Joshua Liao
Journal:  Cancer Biol Ther       Date:  2011-04-01       Impact factor: 4.742

6.  Ionizing radiation and hematopoietic malignancies: altering the adaptive landscape.

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Journal:  Cell Cycle       Date:  2010-08-07       Impact factor: 4.534

Review 7.  The essence of senescence.

Authors:  Thomas Kuilman; Chrysiis Michaloglou; Wolter J Mooi; Daniel S Peeper
Journal:  Genes Dev       Date:  2010-11-15       Impact factor: 11.361

8.  Oncogenic KRas suppresses inflammation-associated senescence of pancreatic ductal cells.

Authors:  Kyoung Eun Lee; Dafna Bar-Sagi
Journal:  Cancer Cell       Date:  2010-11-16       Impact factor: 31.743

9.  Loss of p53 impedes the antileukemic response to BCR-ABL inhibition.

Authors:  Hans-Guido Wendel; Elisa de Stanchina; Enriqué Cepero; Sagarika Ray; Michael Emig; Jordan S Fridman; Darren R Veach; William G Bornmann; Bayard Clarkson; W Richard McCombie; Scott C Kogan; Andreas Hochhaus; Scott W Lowe
Journal:  Proc Natl Acad Sci U S A       Date:  2006-05-01       Impact factor: 11.205

10.  Bridged Analogues for p53-Dependent Cancer Therapy Obtained by S-Alkylation.

Authors:  Ewa D Micewicz; Shantanu Sharma; Alan J Waring; Hai T Luong; William H McBride; Piotr Ruchala
Journal:  Int J Pept Res Ther       Date:  2015-08-19       Impact factor: 1.931

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