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A Role for Progesterone in Multidrug Resistance

  • Shyamali Mallick
  • Susan Band Horwitz
Part of the Hormones in Health and Disease book series (HHD)

Abstract

Each year in the United States, over 1 million people are diagnosed with cancer and 500,000 will die from the disease (Pratt et al, 1994). One of the mainstays of treatment is chemotherapy. However, a major problem in the treatment of most malignancies is the development of resistance to chemotherapeutic agents. Initially, many believed that the mechanisms of resistance to cancer chemotherapeutic agents were similar to those described for antibiotic resistance, in that there was an overproduction or alteration in the target protein for the drug. Therefore by using combinations of drugs with different mechanisms of action, it should be possible to reduce the frequency with which resistance developed. Resistance to agents like methotrexate follow this paradigm. The target enzyme for methotrexate, dihydrofolate reductase (DHFR), is overexpressed or mutated in many methotrexate-resistant cell lines (Bertino, 1984). The multidrug resistance (MDR) phenotype, however, is distinct because cells treated with a single agent develop cross-resistance to a broad spectrum of structurally and functionally unrelated compounds to which they have never been exposed. (See Table 1.) (Ling, 1992; Roninson, 1992; Gottesman and Pastan, 1993; Chin et al, 1993; Licht et al, 1994).

Keywords

Multidrug Resistance Sodium Butyrate Cystic Fibrosis Transmembrane Regulator Chloramphenicol Acetyl Transferase MDR1 Expression 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1997

Authors and Affiliations

  • Shyamali Mallick
  • Susan Band Horwitz

There are no affiliations available

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