Titlebook: Cancer Therapeutic Targets; John L. Marshall Living reference work 20200th edition Anti-angiogenic Targets.HER2/EGFR Targets.Nuclear Rece

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B7.1,id tumors (Lenschow et al. 1996). Nevertheless, B7-1 has been shown to be essential for the induction of T-cell responses, which play a central role in mediating tumor immunosurveillance and immune-mediated tumor regression (Ward and Kaufman 2007). B7-1 consequently plays an important role in cancer

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Bacterial Vaccines,rplay, as well as the recent advances in genetic engineering. Safe, targeted therapies are being developed, in which genetically-modified pathogens are designed to trigger effective anti-tumor immune response. Here we describe the bacterial strains intended for cancer immunotherapies, the genetic mo

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BH3-Only Mimetics,specific groove of anti-apoptotic Bcl-2 family survival factors in a similar manner to native proteins within the cell that regulate these factors. This primes the cell for apoptosis. Several small molecule BH3 mimetics are currently undergoing evaluation in clinical trials.

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BRCA1 and 2,ion to breast cancer, and BRCA2 additionally predisposes to ovarian cancer. Women who carry high-risk BRCA1 mutant alleles have a 50–85 % chance of developing breast cancer by age 70 years. Differences in cancer risk estimates appear to be due to the extent of family history, with a strong family hi

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GRAIN

CCL21, tumors of low immunogenicity. CCL21 mediates the recruitment and co-localization of naive lymphocytes and antigen-stimulated DC into T-cell zones of secondary lymphoid organs, facilitating T-cell activation. In this chapter, we discuss CCL21 as a novel agent to boost immune responses against cancer

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CD4+ T Cells, cytokines and expression of distinct intracellular transcription factors and surface chemokine receptors. The functional diversity of T cells is demonstrated by the association of certain CD4+ T cell types (including Th1 CD4+ T cells) with positive cancer prognosis and other CD4+ T cell types (incl

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S. Roussos,C. R. Soccol,C. AugurUpon reactivation of AR-FL and expression of AR-Vs, traditional methods of treatment targeting the ligand binding domain are ineffective. Targeting the evolutionarily conserved N-terminal domain, DNA binding domain (DBD) or using transcription factors that interact with AR will be key in developing new treatments for PCa.