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  • Book
    Jonathan Strauss, William Small, Gayle E. Woloschak, editors.
    Summary: Breast Cancer Biology for the Radiation Oncologist is the first textbook of its kind devoted to describing the biological complexities of breast cancer in a way that is relevant to the radiation oncologist. Radiation Oncology has long treated breast cancer as a single biological entity, with all treatment decisions being based on clinical and pathologic risk factors. We are now beginning to understand that biological subtypes of breast cancer may have different risks of recurrence as well as different intrinsic sensitivity to radiotherapy. Multi-gene arrays that have for years been used to predict the risk of distant recurrence and the value of systemic chemotherapy may also have utility in predicting the risk of local recurrence. Additionally, the targeted agents used to treat breast cancer may interact with radiotherapy in ways that can be beneficial or undesirable. All of these emerging issues of central importance to radiation oncologists are extensively discussed in this book, and practical treatment recommendations based on available clinical evidence are presented whenever possible.

    Contents:
    Biological subtypes of breast cancer
    Oncogene amplification and Herceptin
    Current clinical use of genetic profiling
    Biology of DCIS and progression to invasive disease
    Cancer Stem Cells and Radiotherapy
    Genetic basis of normal tissue radiosensitivity and late toxicity
    Genetic syndromes and radiotherapy in breast cancer
    Experimental therapies in breast cancer.
    Digital Access Springer 2015
  • Article
    Shirodaria PV, Fraser KB, Armstrong M, Roberts SD.
    Infect Immun. 1979 Jul;25(1):408-16.
    When rheumatoid factor in rheumatoid arthritis and multiple sclerosis sera was titrated by the fluorescent antibody method on measles virus-infected cells, there was a marked and variable drop in titer on acetone-fixed cells as compared with unfixed cells. This was accounted for by the failure of measles virus hemolysin-inhibiting (HLI) antibody of the immunoglobulin G class to bind to acetone-fixed infected cells. It was shown by staining unfixed and acetone-fixed measles virus-infected cells that rheumatoid factor in most rheumatoid arthritis sera combined with measles virus-specific hemagglutinin-inhibiting and HLI antibodies, whereas rheumatoid factor in multiple sclerosis sera combined only with HLI antibody. Rheumatoid factor of similar specificity was also observed in normal sera and occasionally in rheumatoid arthritis sera. Both rheumatoid arthritis and multiple sclerosis sera showed almost identical increases in average titer above normal of measles virus-specific fluorescent staining immunoglobulin G and HLI antibodies.
    Digital Access Access Options