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  • Book
    editors, Robert C. Bast, Jr, Carlo M. Croce, William Hait, Waun Ki Hong, Donald W. Kufe, Martine Piccart-Gebhart, Raphael E. Pollock, Ralph R. Weichselbaum, Hongyang Wang, James F. Holland.
    Summary: "The original reference resource for medical oncologists, radiation oncologists, internists, and allied specialties involved in the treatment of cancer patients, Holland-Frei Cancer Medicine covers the ever-expanding field of current cancer science and clinical oncology practice. In this new ninth edition an outstanding editorial team from world-renowned medical centers continue to hone the leading edge forged in previous editions, with timely information on biology, immunology, etiology, epidemiology, prevention, screening, pathology, imaging, and therapy. Holland-Frei Cancer Medicine, Ninth Edition, brings scientific principles to clinical practice and is a testament to the ethos that innovative, comprehensive, multidisciplinary treatment of cancer patients must be grounded in a fundamental understanding of cancer biology. This ninth edition features hundreds of full color illustrations, photographs, tables, graphs and algorithms that enhance understanding of complex topics and make this text an invaluable clinical tool. Over 15 brand new chapters covering the latest advances, including chapters on Cancer Metabolism, Bioinformatics, Biomarker Based Clinical Trial Design, Health Services Research and Survivorship bring this comprehensive resource up-to-date. Each chapter contains overview boxes, select references and other pedagogic features, designed to make the content easy to access and absorb"--Provided by publisher.
    Digital Access Wiley 2016
  • Book
    Thomas A. Reardon, Taladidia Thiombiano, Christophe L. Delgado.
    Print [1988]
  • Article
    Allen EM, Moore VL, Stevens JO.
    J Immunol. 1977 Jul;119(1):343-7.
    C57BL/6 mice (haplotype H-2b) responded in a dose-dependent fashion to killed BCG by marked enlargement of the spleen and lung. Neither CBA nor C3H mice (haplotype H-2k) responded to such treatment. Pulmonary inflammation in responder B6 animals was characterized by a marked chronic interstitial and alveolar granulomatous process, and was accompanied by occasional granulomata, hyperemia, and loss of architecture in the spleen. Inflammation in non-responder CBA and C3H animals was minimal in both the lung and spleen. The response does not appear to be controlled by genes within the major histocompatibility complex, but is associated with a C57 background. B10.BR mice (responder background, H-2k) were responder animals and C3H.SW mice (nonresponder background, H-2b) were nonresponders. In addition, all animals tested with a C57 background were responders even though two of these strains were not H-2b (C57BL/Ks, H-2d and C57Br/cd, H-2k). The resolution of the mechanism of genetic control of this response in mice may provide information relevant to possible genetic control of chronic pulmonary inflammation in man.
    Digital Access Access Options