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  • 1
    UID:
    gbv_1651287007
    Format: Online-Ressource (IX, 110p, digital)
    ISBN: 9783034600941
    Series Statement: Milestones in Drug Therapy
    Content: Growth factor receptors have long been known to drive malignant transformation and cancer progression. The epidermal growth factor receptor (EGFR, ErbB, HER) system probably represents 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 started for therapy of this malignant disease. Unfortunately, trastuzumab-sensitive cancers invariably develop resistance against the antibody after some time. Recent clinical studies 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.
    Note: Includes bibliographical references and index , Drugs for HER-2-positive Breast Cancer; Preface; Contents; The EGFR/ErbB Family in Breast Cancer: From Signalling to Therapy; Trastuzumab as Adjuvant Treatment for Early Stage HER-2-positive Breast Cancer; Trastuzumab Resistance in Breast Cancer; Treatment with Trastuzumab Beyond Progression; Pertuzumab - a HER-2 Dimerisation Inhibitor - for the Treatment of Breast and Other Cancers; Beyond Trastuzumab: Second-Generation Targeted Therapies for HER-2-positive Breast Cancer; Index
    Additional Edition: ISBN 9783034600934
    Additional Edition: Buchausg. u.d.T. Drugs for HER2-positive breast cancer Basel : Springer, 2011 ISBN 9783034600934
    Language: English
    Subjects: Medicine
    RVK:
    Keywords: Brustkrebs ; Therapie ; Gen BRCA 1 ; Brustkrebs ; Gentherapie ; Gen BRCA 2 ; Brustkrebs ; Gentherapie
    URL: Volltext  (lizenzpflichtig)
    URL: Cover
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