Regulation of clinical chemoresistance by bcl-2 and bax oncoproteins in B-cell chronic lymphocytic leukaemia.
The bcl-2 gene was first shown to be dysregulated in the majority of follicular lymphomas in which a t(14;18) chromosomal translocation is present, but is also over-expressed in the absence of gene rearrangements in most cases of B-cell chronic lymphocytic leukaemia (B-CLL). The bcl-2 oncoprotein is a regulator of apoptosis and the activity of this protein is opposed by bax, a homologous protein that accelerates the rate of cell death. B-lymphocyte bcl-2 and bax protein levels were found to be significantly altered in B-CLL patients when compared to those of a normal control group. Increased bcl-2/bax ratios were observed in both the treated and untreated patients when compared to those of normal controls. These alterations were particularly pronounced in those treated patients found to be clinically unresponsive to chemotherapy.
Pepper
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Department of Haematology, Llandough Hospital, South Glamorgan.
Bentley
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Hoy
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T
D019008:Drug Resistance, Neoplasm / Q000235:genetics; D005455:Fluorescent Antibody Technique; D015870:Gene Expression; D019254:Genes, bcl-2; D006801:Humans; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000188:drug therapy* / Q000235:genetics; D011379:Prognosis; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein
C494826:BAX protein, human; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein