C‐myc amplification, double minutes and homogenous staining regions in a case of AML

Abstract

c-myc amplification is usually associated with lymphoid malignancies and Burkitt's lymphoma in particular. We present a case of AML with c-myc amplification which was associated with homogenous staining regions (hsr) and double minutes (dmin). The administration of GCSF following induction chemotherapy resulted in a marked increase in blast numbers. The GCSF was stopped and further courses of chemotherapy given, which resulted in complete remission. The patient relapsed 7 months after diagnosis and failed to go into a second remission with reinduction therapy. We conclude that c-myc amplification is a rare event in AML, but may be associated with chemotherapy resistance and a poor prognosis, are as dmins and hsr. Growth factors should be used with caution in these patients.

Involvement of STAT3 in the Granulocyte Colony-stimulating Factor-induced Differentiation of Myeloid Cells

“…For example, the expression of MPO and neutrophilic elastase is up-regulated, while the expression of the c-myc oncogene is repressed (8,36). To examine whether the expression of these genes is regulated by STAT3, GM-I62M, GM-S3F, and GM-S3D cells were cultured in the presence of G-CSF, and the expression levels of MPO and c-myc were followed by Northern hybridization.…”

Co-existence of pseudo-Chediak–Higashi anomaly and double minutes containing C-MYC oncogene in three patients with AML M2

“…The patients in the present study required more than one induction course to achieve remission, lending some support to the opinion that dmins and possibly pseudo-Chediak-Higashi anomaly may be associated with chemotherapy resistance, disease progression and outcome. 3 In conclusion, our observations of simultaneous appearance of pseudo-Chediak-Higashi anomaly and double minutes (C-MYC) should draw attention of hematologists to this coincidence, which then might be regarded as causal.…”

“…2 The role of C-MYC oncogene and relationship between dmins and other cytogenetic abnormalities in AML is poorly understood. 3 Dmins have been suggested to represent a sign of disease progression rather than a primary malignant event due to observations of concomitant occurrence of dmins and trisomy of chromosomes 4 or 6 although AML cases with dmins as a sole cytogenetic abnormality have been reported. 1,2 Pseudo-Chediak-Higashi anomaly can be found in different forms of AML although they are most frequent in acute promyelocytic leukemia.…”

“…2 C-MYC oncogene has been shown to be amplified in several but not all cases of AML with dmins and reported to be associated with chemotherapy resistance and disease aggressiveness. 3 It has also been suggested that AML patients with normal karyotype and numerous dmins might respond better to treatment and have a better prognosis than patients with complex karyotype and few dmins. 2 The role of C-MYC oncogene and relationship between dmins and other cytogenetic abnormalities in AML is poorly understood.…”

“…For hematologic malignancies, alterations of the p53 gene are found in blast cells of patients with chronic myelogenous leukemia in blast crisis, in acute myelogenous leukemia and in MDS. 3 MDS provide an excellent model to reveal the mechanism of leukemogenesis.…”