Note: Sample below may appear distorted but all corresponding word document files contain proper formattingExcerpt from Research Paper:
, 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. 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 breast cancer. Gene therapy offers strong promise in directly or indirectly treating beast cancer alone or in combination with existing modes of therapy. #
Abaan, O. D and Criss, Wayne E (2002). Gene therapy in human breast cancer. 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 breast cancer. 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…[continue]
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women living in Western society will develop breast cancer during her lifetime. Germline mutations in BRCA1, a breast cancer tumor suppressor gene, are responsible for 50% of inherited breast cancers and 90% of combined inherited breast and ovarian cancers. The BRCA1 protein, BRCA1p, is involved in many important cellular pathways, including regulation of the cell cycle, DNA repair, transcription, and cell proliferation. It has been shown to bind over
In the tissue culture, they usually proliferate indefinitely. The normal constraints which limit the growth of the cells absent in the cancerous state and are also characterized by the division ability for number of generations which is unlimited. Cell cycle and cancer With millions of chemical reactions taking place concurrently and in specific areas, the human body can be thought of as a small laboratory. It is the only "machine" with
Cancer nurses with sufficient knowledge of the biological basis of these therapies would be better equipped to deal with the practical clinical implications and provide better symptoms management. The technical understanding of the nurses is also crucial in educating and in enabling the patients to take care of themselves. Further, it also goes without saying that nurses, as the primary caregivers are responsible for the emotional well being of
This then leads to the activation of a number of genes whose products trigger cell-cycle arrest, apoptosis, or DNA repair" (Lakin 1999, p. 7644). In research led by Hussain, he investigated the targets of free radicals, which are DNA, proteins, RNA, and lipids. He noted that, "mutations in cancer-related genes or post-translational modifications of proteins by nitration, nitrosation, phosphorylation, acetylation or polyADP-ribosylation-by free radiacals or lipid peroxidation byproducts…are some of
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particularly focuses on the impact of Vitamin D on Breast Cancer. Since health concerns have become a widespread issue, thus researcher on a constant basis are carrying out investigations that can determine the exact causes of diseases like breast cancer. One particular study has come under focus in this dissertation that lay key emphasis on African and European-American descents and how these races are vulnerable to breast cancer. Moreover,
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