Journal Article

Apoptosis in cancer

Scott W. Lowe and Athena W. Lin

in Carcinogenesis

Volume 21, issue 3, pages 485-495
Published in print March 2000 | ISSN: 0143-3334
Published online March 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.3.485
Apoptosis in cancer

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In the last decade, basic cancer research has produced remarkable advances in our understanding of cancer biology and cancer genetics. Among the most important of these advances is the realization that apoptosis and the genes that control it have a profound effect on the malignant phenotype. For example, it is now clear that some oncogenic mutations disrupt apoptosis, leading to tumor initiation, progression or metastasis. Conversely, compelling evidence indicates that other oncogenic changes promote apoptosis, thereby producing selective pressure to override apoptosis during multistage carcinogenesis. Finally, it is now well documented that most cytotoxic anticancer agents induce apoptosis, raising the intriguing possibility that defects in apoptotic programs contribute to treatment failure. Because the same mutations that suppress apoptosis during tumor development also reduce treatment sensitivity, apoptosis provides a conceptual framework to link cancer genetics with cancer therapy. An intense research effort is uncovering the underlying mechanisms of apoptosis such that, in the next decade, one envisions that this information will produce new strategies to exploit apoptosis for therapeutic benefit.

Keywords: IGF, insulin-like growth factor; NF-κB, nuclear factor κB; PTP, permeability transition pore; TNF-α, tumor necrosis factor α; TRAF-2, TNF receptor-associated factor.

Journal Article.  10687 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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