Molecular Genetics of Antigen Receptors and Associated Chromosomal Abnormalities in Human Leukemias

  1. T.H. Rabbitts*,
  2. R. Baer*,
  3. L. Buluwela*,
  4. L. Mengle-Gaw*,
  5. A.M. Taylor, and
  6. P.H. Rabbitts
  1. *Laboratory of Molecular Biology, Hills Road, Cambridge, CB2 2QH, England
  2. University of Birmingham, Cancer Research Laboratories, Department of Cancer Studies, The Medical School, Birmingham, B15 2TJ, England
  3. Ludwig Institute, Hills Road, Cambridge, CB2 2QH, England

This extract was created in the absence of an abstract.

Excerpt

The etiology of human cancer is known to involve several independent events incorporating genetic changes that do not necessarily cooperate with each other. One clear indication of genetic change in the tumor cell is the observation of chromosomal abnormalities, which may be translocation, inversion, or interstitial deletion. These changes may occur in an idiopathic fashion that may be specific to one tumor or in a tumor-specific, consistent fashion. The latter type of change has been particularly well documented in the leukemias, where abundant quantities of individual cells can be obtained for cytogenetic analysis. The most obvious examples of consistent chromosomal abnormalities are the Philadelphia chromosome in acute myeloid leukemia, which involves t9;22 (q32;q11), and the translocations in Burkitt's lymphoma (t8;14, t8;22 and t2;8), which will be discussed below.

There are a significant number of chromosomal abnormalities whose breakpoints occur at human chromosome 14 band q32 or band q11. These two...

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