Download Drugs for HER-2-positive Breast Cancer (Milestones in Drug by Maria Sibilia, Christoph C. Zielinski, Rupert Bartsch, PDF

Download Drugs for HER-2-positive Breast Cancer (Milestones in Drug by Maria Sibilia, Christoph C. Zielinski, Rupert Bartsch, PDF

By Maria Sibilia, Christoph C. Zielinski, Rupert Bartsch, Thomas W. Grunt

Development issue receptors have lengthy been recognized to force malignant transformation and melanoma development. The epidermal development issue receptor (EGFR, ErbB, HER) procedure is probably going the easiest defined membrane receptor tyrosine kinase kin in malignant tumors. With implementation of the growth-inhibitory anti-HER-2 antibody trastuzumab (Herceptin) for the remedy of HER-2-positive complicated metastatic breast melanoma, a brand new period has dawned within the remedy of this malignant affliction. regrettably, trastuzumab-sensitive cancers at all times enhance resistance to the antibody after it slow. contemporary scientific reports have published that those refractory tumors are nonetheless aware of inhibition of the HER receptor relations utilizing twin HER-1/-2 inhibitors reminiscent of lapatinib (Tykerb/Tyverb). in addition, a multiplicity of novel, stronger irreversibly appearing small molecular HER tyrosine kinase inhibitors are within the pipeline of many drug constructing businesses and are being evaluated within the medical environment.

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Extra resources for Drugs for HER-2-positive Breast Cancer (Milestones in Drug Therapy)

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Liebow C, Reilly C, Serrano M, Schally AV (1989) Somatostatin analogues inhibit growth of pancreatic cancer by stimulating tyrosine phosphatase. Proc Natl Acad Sci USA 86:2003 2007 163. Prasad NK, Tandon M, Badve S, Snyder PW, Nakshatri H (2008) Phosphoinositol phospha tase SHIP2 promotes cancer development and metastasis coupled with alterations in EGF receptor turnover. Carcinogenesis 29:25 34 164. Stambolic V, Suzuki A, de la Pompa JL, Brothers GM, Mirtsos C, Sasaki T, Ruland J, Penninger JM, Siderovski DP, Mak TW (1998) Negative regulation of PKB/Akt dependent cell survival by the tumor suppressor PTEN.

Indeed, the ability to revert this inhibition is critically relevant to the clinical efficacy of therapeutics targeting EGFR or Her2/neu in breast and in other tumours, because hypersensitivity of the PI3K pathway resulting from complete loss of PTEN expression has been associated with resistance to trastuzumab and to EGFR tyrosine kinase inhibitors, but less so with resistance to lapatinib which more efficiently shuts down phosphorylation of all ErbB family members and sequesters them from associating with IGF1R [90, 165, 171 177].

Hudelist G, Kostler WJ, Attems J, Czerwenka K, Muller R, Manavi M, Steger GG, Kubista E, Zielinski CC, Singer CF (2003) Her 2/neu triggered intracellular tyrosine kinase activa tion: in vivo relevance of ligand independent activation mechanisms and impact upon the efficacy of trastuzumab based treatment. Br J Cancer 89:983 991 83. Scaltriti M, Verma C, Guzman M, Jimenez J, Parra JL, Pedersen K, Smith DJ, Landolfi S, Ramon y Cajal S, Arribas J et al (2009) Lapatinib, a HER2 tyrosine kinase inhibitor, induces stabilization and accumulation of HER2 and potentiates trastuzumab dependent cell cyto toxicity.

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