Biology and Management of Multiple Myeloma (Current Clinical by James R. Berenson

By James R. Berenson

Professional physicians and scientific researchers summarize and clarify all of the contemporary advances within the biology and therapy of bone marrow-based malignancy. at the organic facet, the authors convey the features of the malignant phone and describe the numerous roles performed via oncogenic alterations, chromosomal anomalies, Kaposi's sarcoma herpes virus, and cytokines. New epidemiological findings and prognostic components also are analyzed. at the medical part, the authors supply a finished evaluation of traditional therapy regimens, in addition to a dialogue of more moderen experimental ways regarding immunologic concentrating on, inhibitors of drug resistance, and antitumor brokers.

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Example text

Many of the exposures discussed above are clearly carcinogenic. Appropriate precautions are only judicious at this point, not just for myeloma, but in general, because many individuals at risk for myeloma have already been exposed. What can be done for them? A recent report illustrating that Olestra can dramatically accentuate the excretion of dioxins highlights the possibility that high-risk individuals can be screened and receive short-term treatment to remove toxins that are present at elevated levels (97).

Low levels of hepatitis C virus RNA in serum, plasma, and peripheral blood mononuclear cells of injecting drug users during long antibody-undetectable periods before seroconversion. Blood 1999; 94:1183–1191. 90. Goedert J, Coete T, Virgo P, et al, for the AIDS-Cancer Match Study Group. Spectrum of AIDS-associated malignant disorders. Lancet 1998; 351:1833–1839. 91. Retting MB, Ha HJ, Vescio RA, et al. Kaposi’s sarcoma-associated herpes virus infection of bone marrow dendritic cells from multiple myeloma patients.

The remaining B lymphocytes undergo apoptosis. As the surviving B cells divide within the germinal center, a second and important process 40 Vescio and Berenson Fig. 2. Pre B cells that have undergone immunoglobulin gene rearrangement migrate to the lymph node, where they are exposed to antigens. If the B cell surface antibody binds antigen, it undergoes replication whereby mutations within the immunoglobulin gene variable region occur by chance. If the resultant antibody is dysfunctional, the B cell can no longer bind antigen and the cell undergoes apoptosis.

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