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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phorbol ester-induced differentiation of human B-chronic lymphocytic leukaemic cells was found to be preceded by a rapid transient induction in expression of the c-jun proto-oncogene, which paralleled that of c-fos. Induced expression of c-myc but not of c-fos/c-jun proto-oncogenes was markedly higher in a proliferating variant leukaemic cell population compared with that seen in typical lymphocytic leukaemia cells. These data suggest that the c-fos/c-jun nuclear oncogenes play a role in induced differentiation, whilst c-myc is more important in the proliferative response of B lymphocytes.
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PMID:Patterns of nuclear proto-oncogene expression during induced differentiation and proliferation of human B chronic lymphocytic leukaemia cells. 231 71

We and others have previously demonstrated expression of the co-fms proto-oncogene during human monocytic differentiation. The c-fms gene has since been shown to encode for the macrophage specific colony stimulating factor (CSF-1) receptor. The present results demonstrate that both CSF-1 and c-fms transcripts are induced during monocytic differentiation of human HL-60 leukemia cells. The results further demonstrate that normal human monocytes express CSF-1 RNA and that the level of these transcripts increases upon treatment with phorbol ester. Finally, the detection of CSF-1 RNA in HL-60 cells and in monocytes is associated with production of the CSF-1 gene product. These findings would suggest that monocytes are capable of regulating their own survival, growth and differentiation through CSF-1 production.
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PMID:Expression of the macrophage specific colony-stimulating factor (CSF-1) during human monocytic differentiation. 243 85

Recent studies have demonstrated by Northern blot analysis that both the c-fms proto-oncogene and the CSF-1 gene are expressed during human monocytic differentiation. In order to examine c-fms and CSF-1 expression at the cellular level, we have applied alkaline phosphatase detection of biotinylated v-fms and CSF-1 cDNA probes in situ. Using this approach, we demonstrate that c-fms and CSF-1 transcripts are detectable in HL 60 cells induced along the monocytic lineage but not in uninduced cells. The specific detection of these transcripts is further supported by the absence of histochemical staining in RNase-treated cells and when using pBR322 plasmid without insert as the biotinylated probe. Finally, the results indicate that most of the induced HL-60 cells have detectable levels of both c-fms and CSF-1 RNA. This approach should be useful for studying expression of these genes in populations of leukemic blasts and normal hematopoietic cells.
Leukemia 1987 Jun
PMID:Detection of c-fms and CSF-1 RNA by in situ hybridization. 244 33

We examined the ability of the trans-acting factor p40tax of human T-cell leukemia virus type I (HTLV-I), which is thought to be a crucial molecule in T-cell transformation by HTLV-I, to activate expression of a set of endogenous cellular genes related to T-cell proliferation. For this purpose we established a subclone (JPX-9) of Jurkat cells that was stably transfected with an expression plasmid containing the p40tax gene, whose expression is definitely dependent on heavy-metal ions. Expression of the interleukin-2 receptor alpha chain in JPX-9 cells was induced in response to the induction of p40tax expression, as has been demonstrated by others in transient transfection experiments with Jurkat cells. In addition, we found that significant enhancement of expression of the nuclear proto-oncogene c-fos was closely associated with expression of p40tax. Continous enhancement in the level of c-fos mRNA was observed in the presence of p40tax. In contrast, mRNA levels of other nuclear proto-oncogenes (c-myc, c-myb, and c-jun) were not appreciably effected by the expression of p40tax. These results suggest that (i) in addition to the interleukin-2-interleukin-2 receptor system, cellular genes such as c-fos, which regulate normal T-cell growth, are also activated directly or indirectly by p40tax and (ii) p40tax-induced modulation of gene expression plays a crucial role in T-cell transformation by HTLV-I.
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PMID:Activation of endogenous c-fos proto-oncogene expression by human T-cell leukemia virus type I-encoded p40tax protein in the human T-cell line, Jurkat. 250 14

Aberrations in nuclear proto-oncogene organisation and/or gene expression have been implicated in cell transformation mediated by the v-abl gene. For example, it has been suggested that amplification of the c-myc proto-oncogene is a co-operative event in v-abl induced fibroblast transformation. We have investigated amplification of the c-myc, p53 and c-fos nuclear proto-oncogenes in several Abelson murine leukaemia virus (A-MuLV) transformed fibroblast lines. None of these proto-oncogenes were detectably rearranged or amplified in v-abl transformed Swiss 3T3 lines. In contrast, NIH3T3 fibroblasts transformed by the v-abl gene consistently showed a 4 to 16-fold amplification of the c-myc gene. These data show that c-myc gene amplification is not an obligatory event associated with A-MuLV transformation, but may be restricted to cell lines derived from NIH3T3. c-myc gene amplification also did not correlate with a reduced latency period for tumour induction in nude mice. In addition, c-myc amplification was not selected during tumourigenesis, indicating that this event is not required for A-MuLV transformed Swiss 3T3 cells to display a full tumourigenic phenotype.
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PMID:Analysis of A-MuLV transformed fibroblast lines for amplification of the c-myc, p53 and c-fos nuclear proto-oncogenes. 254 44

Several lines of evidence point to the involvement of the proto-oncogene c-raf-1 in the development of lymphoma and leukemia and in a previous study we found variants of this gene in 3 lymphoma patients. To see whether variation at this locus plays a role in predisposition to these cancers, we have examined the frequency of an unusual EcoRI allele of c-raf-1 in 99 non-Hodgkin's lymphoma and 28 acute lymphoblastic leukemia patients, and in 182 controls. To optimize the chance of detecting a difference, we selected 113 of the controls from geriatric patients with no family history of cancer. No difference in the frequency of the allele was found between patients and controls, thereby refuting our hypothesis that this polymorphism of the c-raf-1 locus contributes to genetic susceptibility to these two related cancers. We estimate that the frequency of the rarer b EcoRI allele of this locus is 0.091 +/- 0.012 in the Australian Caucasian population.
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PMID:Allelic variation of the c-raf-1 proto-oncogene in human lymphoma and leukemia. 256 45

We have used Southern blot analysis to type individuals for the presence or absence of a rare EcoRI RFLP at the c-mos proto-oncogene locus. This polymorphism has previously been reported to be associated with cancer. Ninety-eight patients with non-Hodgkin's lymphoma (NHL) or acute lymphoblastic leukemia (ALL) and 154 cancer-free individuals, including 108 geriatric patients with no family history of cancer, were studied. Because 4 geriatric patients (aged 67-94) were found to have the rate c-mos allele (A2), and the frequency of this A2 allele was no higher among the lymphoma/leukemia patients than among cancer-free individuals, it is unlikely that it constitutes a marker for NHL or ALL.
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PMID:The EcoRI RFLP of c-mos in patients with non-Hodgkin's lymphoma and acute lymphoblastic leukemia, compared to geriatric and non-geriatric controls. 256 85

A new linkage testing stock of the laboratory mouse has been constructed. The stock, designated MEV (multiple ecotropic provirus), was developed by inbreeding and selection beginning with the cross of strains C58/J and AKXD-14. Eleven different murine leukemia virus (MuLV) proviruses have been fixed in the MEV/1Ty strain. Nine of these can be uniquely identified by Southern blotting of PvuII-digested DNA and probing with a cloned fragment of the ecotropic viral genome. Two proviruses had been mapped previously to chromosome 7, while single proviruses had been mapped to chromosomes 2, 9, and 11. The mapping of six additional proviruses, derived from C58/J, to chromosomes 1, 3, 5, 10, 18, and 19 is described. Another C58/J provirus was mapped to chromosome 8 and proved to be identical to the previously mapped C58v-1 virus inducibility gene of strain C58/Lw. Three dominant visible markers, hammer-toe (Hm), steel (Sl), and caracul-J (CaJ), located on chromosomes 5, 10, and 15, respectively, have been introduced onto the MEV genetic background by repeated backcrosses to provide additional linkage markers. It is estimated that approximately 50% of the genome can be screened by scoring 50 fully informative gametes from a linkage cross of the MEV-Hm, -Sl, -CaJ stock for the combination of viral and visible markers. A strategy for efficiently mapping new recessive visible mutations by pooling tissues for DNA extraction from mutant homozygotes among F2 progeny is described. Ways of further improving the MEV stock are discussed. The location of the Myb proto-oncogene is defined relative to Sl and one of the C58/J proviruses on chromosome 10.
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PMID:A mouse linkage testing stock possessing multiple copies of the endogenous ecotropic murine leukemia virus genome. 257 72

Tiazofurin (2-beta-D-ribofuranosylthiazole-4-carboxamide, NSC 286193) is a synthetic nucleoside inhibitor of inosine monophosphate dehydrogenase. This agent has recently been shown to induce differentiation of human leukemia cell lines. In the present study, we have monitored the effects of tiazofurin on differentiation and proto-oncogene expression in K562 erythroleukemia cells. Tiazofurin induced K562 cell hemoglobin production in a concentration-dependent manner. This induction of a differentiated phenotype was also associated with a loss of proliferative capacity. In contrast to the reversible effects of hemin on induction of K562 cell hemoglobin synthesis, the effects of tiazofurin were irreversible. Northern blot analysis of K562 cells treated with 10 microM tiazofurin demonstrated the accumulation of alpha- and gamma-globin mRNA. The results also demonstrate that there was little if any effect of tiazofurin on levels of c-myc, c-myb, or c-abl mRNA. Furthermore, there were no detectable changes in Ki-ras, Ha-ras or N-ras expression at the mRNA and protein levels in tiazofurin-treated K562 cells. These findings suggest that tiazofurin induces changes in levels of globin transcripts but has little if any effect on c-myc, c-myb, c-abl, or c-ras gene expression in K562 cells.
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PMID:Effects of tiazofurin on globin and proto-oncogene expression in K562 erythroleukemia cells. 263 29

Point mutations within codon 12 of the Harvey (H-) ras proto-oncogene have recently been implicated in the progression of hemopoietic malignancy, particularly chronic myeloid leukemia. We have analyzed DNA from 170 cases of acute and chronic leukemia by using a restriction fragment length polymorphism. No evidence for clonal allelic H-ras codon 12 activation was found among these cases, which included 23 cases of chronic myeloid leukemia, 12 of which were in accelerated phase or blastic transformation. These data suggest that H-ras codon 12 mutations occur infrequently in hemopoietic neoplasms generally and may be less important in disease progression than has been previously suggested.
Leukemia 1989 Jan
PMID:Activation of Harvey ras oncogene by mutation at codon 12 is very rare in hemopoietic malignancies. 264 80


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