Genetic Pathway of Breast Cancer Research Paper

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, 2006). He visualized and described the malignancy process. He suggested that early that "cells of tumors with unlimited growth" would develop with the elimination of chromosomes, which inhibit the growth. The multiple genetic alterations in these inhibiting chromosomes are today known as TSGs. The theory supposes that cancer arises from functional defect or absence of one or more TSGs. Clinical trials of TSG gene replacement therapy for breast cancer include the viral wild-type p53, Rb, and mda7. Molecular chemotherapy involves the introduction of suicide genes. The concept evolved from the assumption that cancer cells could be made more sensitive to chemotherapeutics or toxins by introducing "suicide genes." It was a concept initiated in the late 80s. Suicide gene therapy is categorized into toxin gene therapy and enzyme-activating pro-drug therapy. Suicide gene therapy is also called gene-directed enzyme pro-drug therapy or GDEPT. GDEPT treatment consists of the delivery of the gene for the enzyme to the breast cancer cell and the infusion of a non-toxic pro-drug. The enzymes are categorized into foreign enzymes from non-mammals and from human sources. Proapoptotic complimentary gene therapy introduces genes, which cause apoptotic cell death and transit death signals to adjacent tumor cells as the "bystander effect." Proapoptotic strategies include suicide gene therapy, functional replacement of TSGs BCL-2 family proteins, death receptor and ligand systems and pathways. Antiangiogenic gene therapy inhibits angiogenesis in breast cancer but can yield better results if combined with other conventional and gene transfer-based strategies, such as hormonal and chemotherapy approaches. Genetic immunotherapy evolved from an old concept that the immune response could be used to eliminate cancerous cells. Cancer immunotherapy strategies target the tumor "escape" mechanism. Immunotherapy is either passive or active. The genetic modulation of resistance/sensitivity approach addresses the replacement of gene function leading to the restoration of drug sensitivity. This therapy, like previous ones, has demonstrated vivo and in vitro tumoricidal effects of chemotherapy and radiotherapy in many tumors, including breast tumors (Stoff-Khalili et al.).

This study uses the descriptive-normative method in recording, describing, interpreting, analyzing and comparing data gathered from various and updated peer-reviewed sources.

Findings and Conclusion

A new method of pathway analysis exceeded existing ones in assessing breast gene profiling studies (Ma & Kosorok, 2010). It identified 96 pathways with predictive power, rather than estimation accuracy, in the prognosis of breast cancer.

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In the meantime, many multi-gene prognostic and predictive tests have been developed. Diagnostic kits and centralized laboratory assays are now available (Ross, 2009). But these have yet to be fully evaluated for their effect in a sufficient number of clinical trials for their scientific validity, true use and cost-benefit ratios (Ross). MiRNAs function as regulators of tumor behavior and progression (Lowery et al., 2009). Using ANN, predictive miRNA signatures were identified that corresponded with estrogen, progesterone and HER2/neu in specific breast cancer phenotypes. This discovery will update current knowledge on molecular targets and in identifying pathways that predict response and resistance to therapy as well as to more reliable breast cancer therapy (Lowery et al.).

Gene therapy delivers genes to cancer cells in the body to directly or indirectly induce therapeutic effect (Abaab & Criss, 2002). Viral or non-viral vectors are used, such as retroviruses and adenoviruses. Strategies are the delivery of suicide genes, the delivery of tumor suppression genes, inhibition of angiogenesis, immunotherapy, the use of oncolytic viruses and ribozyme or antisense targeting (Abaab & Criss). TSG cells' loss of function triggers malignancy. Gene therapy approaches are mutation compensation, molecular chemotherapy, proapoptotic gene therapy, genetic immunotherapy, and genetic modulation of resistance/sensitivity (Stoff-Khalili et al., 2006).

New pathways have been successfully identified as predictors of the prognosis of Gene therapy offers strong promise in directly or indirectly treating beast cancer alone or in combination with existing modes of therapy. #

BIBLIOGRAPHY

Abaan, O. D and Criss, Wayne E (2002). Gene therapy in human 32

(2002): 283-291 Turkey Journal of Medical Science: Tubitak. Retrieved on April 15,

2010 from http://journals.tubitak.gov.tr/medical/issues/sag-02-32-4-1-0204.pdf

Lowery, A.J., et al. (2009). MicroRNA signatures predict oestrogen receptor,

progesterone receptor and HER2/neu receptor status in 11 (3) Breast

Cancer Research: BioMed Central, Ltd. Retrieved on April 15, 2010 from http://www.medscape.com/viewarticle/707625

Ma, S. And Kosorok, M.R. (2010). Detection of gene pathways with predictive power for breast cancer prognosis. 11:1 BMC Bioinformatics: BioMed Central. Retrieved on April 16, 2010 from http://www.biomedcentral.com/1471-2105/11/1

Ross, J.S. (2008). Multigene predictors in early-stage breast cancer: moving in or moving out? 8 (2): 129-135 Expert Review of Molecular Diagnostics: Expert

Reviews, Ltd. Retrieved on April 16, 2010 from http://www.medscape.com/viewarticle/575861

Stoff-Khalili M., et al. (2006). Gene therapy for carcinoma of the breast. 13 (7): 33-47….....

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