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This book provides a current review of the field of Trastuzumab pharmacology from a variety of chemical, biochemical, physiological, pharmacokinetical, pharmacodynamical, biophysical and medical perspectives. This book covers breast cancer treatment including current Trastuzumab therapy, radiation therapy and excision of tumors within the limits of healthy tissue. The text presents current knowledge and analysis of pertinent literature and knowledge. This book reports results from experimental models of HER2 oncogene overexpression and treatments which have been used in an effort to understand the relationship between HER2 and response to therapeutics. In this book the HER2 oncogene has been extensively discussed as a prognostic factor and as a predictor of response to chemotherapy and endocrine therapy. The book includes data regarding the expression of HER2 oncogene in lung cancer and response to trastuzumab alone or in combination with chemotherapeutic agents. The interaction of HER2 with others drugs such as alkylating agents, platinum analogs and topoisomerase inhibitors, as well as additive interactions with taxanes, anthracyclines and some metabolites and antimetabolites are presented. Special cardiological supervision for patients with an increased risk of cardiotoxicity that have hypertension, ischemic heart disease, hypothyroidism or are heavy smokers during adjuvant trastuzumab therapy will also be reviewed.

Growth factor receptors have long been known to drive malignant transformation and cancer progression. The epidermal growth factor receptor (EGFR, ErbB, HER) system is likely the best described membrane receptor tyrosine kinase family in malignant tumors. With implementation of the growth-inhibitory anti-HER-2 antibody trastuzumab (Herceptin) for the treatment of HER-2-positive advanced metastatic breast cancer, a new era has dawned in the therapy of this malignant disease. Unfortunately, trastuzumab-sensitive cancers invariably develop resistance to the antibody after some time. Recent clinical studies have revealed that these refractory tumors are still responsive to inhibition of the HER receptor family using dual HER-1/-2 inhibitors such as lapatinib (Tykerb/Tyverb). Moreover, a multiplicity of novel, improved irreversibly acting small molecular HER tyrosine kinase inhibitors are in the pipeline of many drug developing companies and are being evaluated in the clinical setting.