Anticancer therapy

Fulda S (2007) Inhibitor of apoptosis proteins as targets for anticancer therapy. Expert Rev Anticancer Ther 7 1255-1264... 

Faivre S, Djelloul S, Raymond E (2006) New paradigms in anticancer therapy targeting multiple signaling pathways with kinase inhibitors. Semin Oncol 33 407-420... 

The primary goal of treatment for hypercalcemia is to control the underlying malignancy. Therapies directed at lowering the calcium level are temporary measures that are useful until anticancer therapy begins to work. 

Johnstone, P. 2002. The epidermal growth factor receptor a new target for anticancer therapy - introduction. Current Problems in Cancer 26(3), 114-164. 

Inhibition of the lipid modification cascade provides an alternative way to block aberrant signaling pathways and that opportunity can be exploited in anticancer therapy. As part of the growth factor, signaling of the false activation is transmitted by the mutated ras gene encoded proteins (Ras) and ultimately leads to uncontrolled cell growth. These typical GTP binding proteins are also subject to membrane anchoring and the biosynthesis of those Ras proteins can be blocked at the posttranslational prenylation step. 

Di Paolo A (2004) Liposomal anticancer therapy pharmacokinetic and clinical aspects. J. Chemotherap. 16 90-93. 

Allen TM. Ligand-targeted therapeutics in anticancer therapy. Nat Rev Cancer 2002 2 750. 

L. Single, N. J. Brown, and C. E. Lewis, The role of tumour-associated macrophages in tumour progression implications for new anticancer therapies, J.Pathol. 196(3), 254-265 (2002). 

Stewart ZA, Westfall MD, Pietenpol JA. Cell-cycle dysregulation and anticancer therapy. Trends Pharmacol Sci 2003 24 139 5. 

Mukhopadhyay, N.K., Weisberg, E., Gilchrist, D., Bueno, R., Sugarbaker, D.J. and Jaklitsch, M.T. (2006) Effectiveness of trichostatin A as a potential candidate for anticancer therapy in non-small-cell lung cancer. The Annals of Thoracic Surgery, 81, 1034-1042. 

The structure and function of histone deacetylases The target for anticancer therapy. Current Medicinal Chemistry, 15, 2840-2849. 

Inhibition of HDACs has become an interesting approach for anticancer therapy. Therefore, two approaches, gene knockdown in cells and knockout in animals, have been developed and widely used for functional studies of specific HDAC isoforms. 

Contrary to the other major components of the PI3K/PKB survival pathway, the development of PDKl inhibitors would be, to a certain extent, simpler as only a single PDKl isoform exists in human cells. Moreover, the observation that PDKl hypomorphic mice expressing only approximately 10% of the normal level of PDKl display no obvious harmful phenotype—they are 40-50% smaller than control animals — [100], indicates that a PDKl inhibitor may provide effective anticancer therapy at an acceptable therapeutic index. 

Historically, histone deacetylases (HDACs) were considered as promising drug targets in anticancer therapy due to their regulating role in the histone acetylation status implicated in the epigenetic chromatin control. As a consequence, the potential of HDAC inhibitors was initially attributed to their capacity as chromatin-modulating drugs. 

HDAC inhibition holds particular promise in anticancer therapy, where the concerted effects on multiple pathways involved in growth inhibition, differentiation and apoptosis may prove to be advantageous in the treatment of a heterogeneous pathology such as tiunor formation and growth. 

Raymond E, Faivre S, Armand JP. Epidermal growth factor receptor tyrosine kinase as a target for anticancer therapy. Drugs 2000 60 Suppl 1 15-23. 

Mendelsohn J. Epidermal growth factor receptor inhibition by a monoclonal antibody as anticancer therapy. Clin Cancer Res 1997 3 2703-2707. 

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