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Showing papers on "Promyelocytic leukemia protein published in 1983"



Journal ArticleDOI
01 Aug 1983-Blood
TL;DR: Tumor cells obtained from leukemia and lymphoma patients were investigated for specific insulin receptors and data suggest that the insulin receptor may be a new marker of acute leukemia and chronic myelocytic leukemia.

22 citations


Book ChapterDOI
TL;DR: The evidence for a possible third mechanism for onc gene activation in neoplastic cells, that of gene amplification, is reviewed, which may be involved in the leukemic transformation in this case.
Abstract: Substantial evidence indicates that retroviral transforming (v-onc) genes originated by means of recombination between a present nontransforming virus and normal cellular sequences (Duesberg et al., this volume). These sequences, called cellular onc gene, are highly conserved during evolution, suggesting that they may code for protein products which are essential for cell growth or tissue differentiation. As these normal cellular genes are homologous to viral- transforming genes, their potential role in tumorigenesis is of great interest. As an alternative to direct transformation by a viral onc gene, abnormal activation of a cellular onc gene may cause transformation. Two models have been proposed for such a mechanism. First, high levels of expression of a cellular onc gene may be caused by the insertion nearby of a viral promoter [12, 15, 16, 17] or by alteration of the physiological promoter by a mutagenic agent such as a chemical carcinogen. Secondly, a cellular onc gene may be relocated in a transcriptionally active region of the genome as a consequence of chromosomal rearrangements [2, 5, 6, 13]. In this chapter we review the evidence for a possible third mechanism for onc gene activation in neoplastic cells, that of gene amplification. The human homologue, c-myc, of the transforming gene of avian myelocytomatosis virus (MC29), which is expressed at relatively high levels in the human promyelocytic leukemia cell line HL-60, is stably amplified in the genome of these cells [7]. Amplification was also detected in primary, uncultured leukemic cells from the same individual, suggesting that the c-myc amplification may have been involved in the leukemic transformation in this case.

19 citations


Journal ArticleDOI
TL;DR: Two new human myeloid cell lines, PL-21 and KCL-22, were established from acute promyelocytic leukemia and chronic myelocytes leukemia, respectively.
Abstract: Two new human myeloid cell lines, PL-21 and KCL-22, were established from acute promyelocytic leukemia and chronic myelocytic leukemia, respectively. PL-21 was positive to peroxidase staining and differentiated into mature myeloid cells in vitro. KCL-22 had Ph1 chromosomes and differentiated into granulocytes in vivo.

14 citations