DNA Damage and Repair in Cancer Therapy
López-González A, Ibeas Millán P and Provencio M*
Servicio de Oncología Médica, Hospital Universitario Puerta de Hierro Majadahonda, Calle Manuel de Falla, s/n, Madajahonda, 28020, Madrid, Spain
- *Corresponding Author:
- Dr. Provencio M
Servicio de Oncología Médica
Hospital Universitario Puerta de Hierro Majadahonda
Calle Manuel de Falla, s/n, Madajahonda
28020, Madrid, Spain
E-mail: [email protected]
Received Date: January 24, 2012; Accepted Date: February 27, 2012; Published Date: February 29, 2012
Citation: López-González A, Ibeas Millán P, Provencio M (2012) DNA Damage and Repair in Cancer Therapy. J Cancer Sci Ther S8:002. doi: 10.4172/1948-5956.S8-002
Copyright: © 2012 López-González A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Most cancer therapies have their main mechanism of action DNA damage. Tumor cells have several ways to respond to this DNA damage: removal of the damaged area and reconstruction of the strand of DNA, activation of DNA damage checkpoint, changes in transcription profile of benefit to the cell and apoptosis in the case in which the DNA is seriously damaged. We summarize in this article the most important cellular responses to DNA damage caused by chemotherapy.
Bcl-2 family, other than in the follicular B-cell lymphoma, is involved in a number of cancers, including melanoma and breast carcinoma, prostate and lung. Its expression was associated with good prognosis in non-small-cell lung cancer. Cytotoxicity of many chemotherapeutic agents is induced through the Bcl-2 apoptotic pathway; overexpression of BCL2 is associated with increased resistance to these agents.