An unusually high level of expression of the c-myc protooncogene was observed in peripheral blood lymphocytes of a patient with prolymphocytic leukemia (atypical chronic lymphocytic leukemia). The overexpression of c-myc could not be attributed to a high level of proliferating activity of the leukemic cells in the blood. Treatment with cytosine-arabinoside at high doses abolished this altered expression of c-myc and resulted in a twofold increase in the expression of a gene sequence encoding the invariant gamma-chain of class II histocompatibility antigens, preferentially expressed in resting B lymphocytes. These observations suggest that the leukemic cells may have been arrested in the cell cycle outside the G0 phase. Our findings demonstrate that growth-regulated genes can be useful molecular markers of diseases with altered mechanisms of cellular proliferation.
The effect of cytosine-arabinoside treatment on the overexpression of c-myc protooncogene in a case of prolymphocytic leukemia / Kaczmarek, L; Elfenbein, Ib; Narni, Franco; Vonderheid, Ec; Barry, We; Calabretta, Bruno. - In: CANCER GENETICS AND CYTOGENETICS. - ISSN 0165-4608. - STAMPA. - 27:(1987), pp. 89-99.
The effect of cytosine-arabinoside treatment on the overexpression of c-myc protooncogene in a case of prolymphocytic leukemia.
NARNI, Franco;CALABRETTA, Bruno
1987
Abstract
An unusually high level of expression of the c-myc protooncogene was observed in peripheral blood lymphocytes of a patient with prolymphocytic leukemia (atypical chronic lymphocytic leukemia). The overexpression of c-myc could not be attributed to a high level of proliferating activity of the leukemic cells in the blood. Treatment with cytosine-arabinoside at high doses abolished this altered expression of c-myc and resulted in a twofold increase in the expression of a gene sequence encoding the invariant gamma-chain of class II histocompatibility antigens, preferentially expressed in resting B lymphocytes. These observations suggest that the leukemic cells may have been arrested in the cell cycle outside the G0 phase. Our findings demonstrate that growth-regulated genes can be useful molecular markers of diseases with altered mechanisms of cellular proliferation.
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