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Institut de Pathologie Moléculaire, INSERM U.129 et LA 85 CNRS, 24, rue du Faubourg Saint-Jacques 75014 Paris [A. H., F. S.]; Unité de Recherches de Physiopathologie Hépatique, INSERM U.24, Hópital Beaujon, 92118 Clichy-Cedex [G. F., J. G.]; and Institut de Recherches Scientifiques sur le Cancer, Bolte Postale 8, 94800 Villejuif, France[C. F.]
The resurgence of aldolase isozymes in cancerous tissues is a well-known but poorly understood phenomenon. This resurgence poses the problem of whether or not adult and fetal aldolase isozymes are produced by the same cells.
For clarification of this question, the immunoperoxidase technique was used to locate aldolases A, B, and C in one type of fast-growing hepatoma, the LF hepatoma and, by comparison, in normal adult liver. Under optical microscopy, aldolases A and C were located in the cytoplasm of almost all of the cancerous cells. An isozyme antigenically identical with aldolase B was also demonstrated to be present in almost all of the cells, but the reaction indicating the presence of this isozyme was weaker. In normal adult liver, only aldolases A and B were demonstrated to be present in almost all the hepatocytes. Under electron microscopy in LF hepatoma, the three isozymes were found to be present mainly in the cytoplasm.
These facts suggest that the three types of aldolase are very probably present in the same cells at the same time, and they provide indirect arguments leading us to think that the resurgence of fetal aldolase isozymes in cancer is not the consequence of cellular selection but is due to a disturbance at the gene control level.
1 Preliminary results have been presented at the Twenty-fourth Annual Colloquium "Protides of the Biological Fluids," Brugge, Belgium, 1976 (17), and at the Conference on Onco-Developmental Gene Expression, San Diego, Calif., 1976 (16). This work was supported in part by Grant INSERM 7650817.
2 To whom requests for reprints should be addressed.
Received 7/20/76. Accepted 10/ 5/77.
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