myelomonocytic leukemia absence of the initially activated N-ras oncogene in a patient with acute Relapse cell population differs from acute onset clone as shown by (original) (raw)

2010

Abstract

family (H-, K-, and N-ras) acquire their transforming potential mainly through distinct point mutations leading to alterations in structure and function of the 21 kd ras gene product.'2 These activating mutations are found in a wide variety of tumors. In hematobogic disorders, ras activation is predominantly found in N-ras.39 Our results (unpublished observations)9 show, in agreement with others,7 an N-ras

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