Literature DB >> 12829013

Recent advances in understanding apoptosis: new therapeutic opportunities in cancer chemotherapy.

Guy Makin1, Caroline Dive.   

Abstract

Major advances have been made in our understanding of the regulation of the molecular machinery of apoptosis in vitro. Molecules linking proliferation and apoptosis in healthy cells are being identified and here apoptotic cell death provides the 'fail-safe' mechanism to counteract excess proliferation. More recently, pioneering work on the regulation of apoptosis, in animal models of tumour development, has shown that suppression of apoptosis in the presence of a proliferative stimulus is sufficient for tumour development. Progress has also been made towards clarifying the contribution of drug-induced apoptosis to tumour response. With increasing evidence that failure to engage apoptosis after drug treatment contributes to drug resistance in vivo comes renewed confidence that new therapeutic approaches based on drug targets in apoptotic pathways will improve the treatment of cancer patients. As ever, tumour specificity is the major issue to be resolved.

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Year:  2003        PMID: 12829013     DOI: 10.1016/s1471-4914(03)00084-4

Source DB:  PubMed          Journal:  Trends Mol Med        ISSN: 1471-4914            Impact factor:   11.951


  5 in total

1.  Apoptosis in cancer: archaeology, functional relevance and exploitation in novel treatment strategies.

Authors:  E F Gaffney
Journal:  Ir J Med Sci       Date:  2004 Jan-Mar       Impact factor: 1.568

2.  Alteration of the mitochondrial apoptotic pathway is key to acquired paclitaxel resistance and can be reversed by ABT-737.

Authors:  Ozgur Kutuk; Anthony Letai
Journal:  Cancer Res       Date:  2008-10-01       Impact factor: 12.701

3.  Lowering the apoptotic threshold in colorectal cancer cells by targeting mitochondria.

Authors:  Kevin Sales; Jan-Willem Taanman; Sas Dijk; Marc Winslet; Jayesh Sagar
Journal:  Cancer Cell Int       Date:  2010-09-06       Impact factor: 5.722

4.  DNA damage stress and inhibition of Jak2-V617F cause its degradation and synergistically induce apoptosis through activation of GSK3β.

Authors:  Toshikage Nagao; Gaku Oshikawa; Nan Wu; Tetsuya Kurosu; Osamu Miura
Journal:  PLoS One       Date:  2011-11-08       Impact factor: 3.240

5.  Reciprocal relationship between expression of hypoxia inducible factor 1alpha (HIF-1alpha) and the pro-apoptotic protein bid in ex vivo colorectal cancer.

Authors:  M M Seenath; D Roberts; C Cawthorne; M P Saunders; G R Armstrong; S T O'Dwyer; I J Stratford; C Dive; A G Renehan
Journal:  Br J Cancer       Date:  2008-07-22       Impact factor: 7.640

  5 in total

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