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• W1543944384 abstract "Since the declaration of the "e;war on cancer"e; three decades ago, an improved understanding of molecular mechanisms behind malignant disease has led to the discovery of novel targets for cancer therapy. Despite such great efforts, many compounds that have performed well in the preclinical setting have failed in clinical trials. This may be because of the dynamic nature of cancer, where cells continuously acquire a series of genetic alterations that allow them to escape the constraints of normal cell proliferation and to develop resistance to various drug therapies. Therefore, it is crucial to understand how these genetic changes are involved in the etiology of cancer development and progression, and to identify the molecular mechanisms responsible for resistance to chemotherapeutic drugs. In recent years, the emergence of new genomic technologies has allowed us to address these fundamental issues. Because cellular and molecular heterogeneity of breast tumors involve many genes in pathways that control cell growth, death, and differentiation, the utility of microarray technology for genomic profiling of human breast cancer has provided remarkable insights into the multiple genetic alterations that are involved in the disease that may dictate clinical outcome. Examination of gene expression patterns are being correlated with tumor sensitivities or resistance to particular pharmacological agents. Taken together, microarray technology has led to more definitive classification of breast cancer, identification of signature markers for diagnosis and prognosis, and potential predictive response to clinical treatments that should greatly improve and individualize patient therapies." @default.
• W1543944384 created "2016-06-24" @default.
• W1543944384 creator A5045298314 @default.
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• W1543944384 date "2007-11-08" @default.
• W1543944384 modified "2023-09-25" @default.
• W1543944384 title "Molecular Profiling in Breast Cancer" @default.
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• W1543944384 doi "https://doi.org/10.1007/978-1-59745-035-5_30" @default.
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