Gene therapy for carcinoma of the breast: Pro-apoptotic gene therapy
Open Access
- 1 February 1999
- journal article
- review article
- Published by Springer Nature in Breast Cancer Research
- Vol. 2 (1) , 32-44
- https://doi.org/10.1186/bcr27
Abstract
The dysregulation of apoptosis contributes in a variety of ways to the malignant phenotype. It is increasingly recognized that the alteration of pro-apoptotic and anti-apoptotic molecules determines not only escape from mechanisms that control cell cycle and DNA damage, but also endows the cancer cells with the capacity to survive in the presence of a metabolically adverse milieu, to resist the attack of the immune system, to locally invade and survive despite a lack of tissue anchorage, and to evade the otherwise lethal insults induced by drugs and radiotherapy. A multitude of apoptosis mediators has been identified in the past decade, and the roles of several of them in breast cancer have been delineated by studying the clinical correlates of pathologically documented abnormalities. Using this information, attempts are being made to correct the fundamental anomalies at the genetic level. Fundamental to this end are the design of more efficient and selective gene transfer systems, and the employment of complex interventions that are tailored to breast cancer and that are aimed concomitantly towards different components of the redundant regulatory pathways. The combination of such genetic modifications is most likely to be effective when combined with conventional treatments, thus robustly activating several pro-apoptotic pathways.Keywords
This publication has 130 references indexed in Scilit:
- In Vivo Protein Transduction: Delivery of a Biologically Active Protein into the MouseScience, 1999
- A novel adenoviral vector expressing human Fas/CD95/APO-1 enhances p53-mediated apoptosisCell Death & Differentiation, 1999
- TUMOR NECROSIS FACTOR RECEPTOR AND Fas SIGNALING MECHANISMSAnnual Review of Immunology, 1999
- Failure of wild-type p53 gene therapy in human cancer cells expressing a mutant p53 proteinGene Therapy, 1999
- Radiosensitization and apoptosisOncogene, 1998
- Bax and Adenine Nucleotide Translocator Cooperate in the Mitochondrial Control of ApoptosisScience, 1998
- Combination Therapy with Interleukin-2 and Wild-Type p53 Expressed by Adenoviral Vectors Potentiates Tumor Regression in a Murine Model of Breast CancerHuman Gene Therapy, 1998
- Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell deathCell, 1993
- Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53Published by Elsevier ,1992
- Programmed cell death: Apoptosis and oncogenesisCell, 1991