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

In the work it has been decided to evaluate the occurrence of locus bcl-1 rearrangement in type B chronic lymphatic leukemia and that of gene bcl-2 in non-Hodgkin's lymphoma with diffuse morphology, as well as in reactive lymph nodes. The study material comprised DNA isolated from fragments of lymph nodes sent for routine diagnostic examinations at the Institute of Pathology--Pomeranian Medical Academy. Southern's method was used to examine DNA having been cut with restrictive enzymes, estimating the distribution of gene bcl-2 and locus bcl-1. Resorting to Polymerase Chain Reaction (PCR) translocation t (14;18) was assessed by means of short nucleotides hybridizing with 14 and 18 chromosome sequences restricting this translocation. The amplification product was subsequently studied by Southern's method with probe bcl-2. In 1 out of 18 examined cases of type B chronic lymphocyte leukemia it was disclosed that locus bcl-1 had been rearranged. In 45 cases of non-Hodgkin's lymphoma with diffuse morphology the gen bcl-2 was found to display germline arrangement. Germline position of gen bcl-2 was also revealed in 60 cases of reactive lymph nodes.
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PMID:[Molecular-genetic evaluation of translocation of bcl-2 gene and locus bcl-1 in selected lymphoproliferative changes]. 129 Mar 53

Early studies examining the effects of purified or recombinant granulocyte colony-stimulating factor (G-CSF) on human leukemia cell lines demonstrated that some cell lines, such as HL-60, could be induced to differentiate in response to G-CSF. In two recent studies reporting the cloning of the human G-CSF receptor (hGCSFR), four classes of receptor cDNA were identified and, surprisingly, the message for this receptor was reportedly expressed by HL-60 at either very low levels or not at all. Using a mouse G-CSF receptor probe, we cloned and sequenced a cDNA for hGCSFR from an HL-60 cDNA library in plasmid and used it to identify 31 additional clones from an HL-60 cDNA library in phage. Polymerase chain reaction analysis of the 31 phage clones established that 29 were derived from class I hGCSFR mRNA, one was derived from class III mRNA, and one was derived from class IV mRNA. In addition, the hGCSFR gene was chromosomally localized by Southern blot analysis of its segregation pattern in a panel of rodent-human hybrid DNAs using the radiolabeled cDNA probe. The hGCSFR locus was present in hybrids retaining the distal short arm of human chromosome 1 and absent in hybrids that did not retain this region. Chromosomal in situ hybridization refined the localization of the hGCSFR gene to region 1p32-p34. The combination of hybrid DNA analysis and in situ hybridization places the hGCSFR gene telomeric to the CSF1, JUN, and TCL-5 loci.
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PMID:Molecular cloning of cDNAs for the human granulocyte colony-stimulating factor receptor from HL-60 and mapping of the gene to chromosome region 1p32-34. 137 13

Polymerase chain reaction (PCR) is a highly sensitive technique to detect minimal residual disease (MRD) of hematological malignancy by amplifying tumor specific nucleotide sequences. When breakpoint is located over large lesions of genomic DNA, like t(9;22) leukemia, PCR amplifying cDNA of chimeric mRNA, called reverse transcriptase PCR (RT-PCR), can be utilized. We applied this method for the detection of MRD in patients with t(1; 19) acute lymphoblastic leukemia. RT-PCR detection of MRD in patients with leukemia might be useful for estimating of the depth of remission, for disclosing preclinical relapse, and for evaluating the efficacy of in vitro purging in autologous bone marrow transplantation.
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PMID:[Detection of minimal residual disease using reverse transcriptase polymerase chain reaction technique]. 138 48

The ability to conveniently detect single-base mutations in the DNA of clinical material without prior knowledge of the mutant sequence remains a diagnostic challenge. Most techniques suffer from a lack of general applicability to all DNA sequences, poor sensitivity, requirement for RNA samples rather than DNA, or necessity for performing DNA sequencing to uncover unknown point mutations. Recently, Montandon, et al. (8) described a novel method whereby segments of DNA amplified by the Polymerase Chain Reaction (PCR) can be rapidly screened for mutations through their formation of heteroduplexes with an end-labeled reference DNA followed by site-specific chemical cleavage at mispaired bases. Here we have applied this PCR-mismatch technique to a portion of the BCL-2 gene, using DNA samples derived from the biopsy specimens of patients with lymphomas or lymphocytic leukemias. The BCL-2 gene becomes activated through a t(14;18) chromosomal translocation in the majority of non-Hodgkin's lymphomas. Somatic point mutations were detected in the BCL-2 genes of 3 of 5 patient samples that contained a t(14;18). No mutations were observed for lymphomas lacking a t(14;18), nor in the DNA of over 20 normal persons. Further analysis excluded the possibility that the detected mutations represented hereditary polymorphisms or PCR-artifacts. Based on comparisons with direct DNA sequencing, the PCR-mismatch technique appeared to be both highly specific and sensitive. The possible mechanisms responsible for these somatic mutations in translocated BCL-2 genes and their functional significance are discussed.
Leukemia 1992
PMID:Application of a PCR-mismatch technique to the BCL-2 gene: detection of point mutations in BCL-2 genes of malignancies with A t(14,18). 160 14

DNA sequence analysis was performed on a 235-bp region of the p21 e transmembrane protein gene of the human T-cell lymphoma/leukemia virus type I (HTLV-I) which encompassess the putative immunosuppressive peptide. Polymerase chain reaction-based amplification was used to generate multiple molecular clones from isolates derived from fresh or cultured cells from 19 individuals. A dendrogram was constructed using the p21e DNA sequence information to compare the sequences among isolates in the current study and other previously published HTLV-I isolates including strains from Africa and Papua New Guinea. Examination of multiple clones from individual isolates revealed the presence of multiple genotypes in patients with tropical spastic paraparesis/HTLV-I-associated myelopathy and adult T-cell leukemia/lymphoma. These findings suggest that HTLV-I, like HIV, may be present as a quasispecies in vivo. Our studies, however, failed to identify specific sequence motifs that segregated exclusively with the lymphoproliferative or neurological forms of the disease.
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PMID:DNA sequence analysis of the gene encoding the HTLV-I p21e transmembrane protein reveals inter- and intraisolate genetic heterogeneity. 173 4

A leukemia line KOPN30bi was established from a patient of acute lymphoblastic leukemia with Philadelphia chromosome. The clonal rearrangement of the immunoglobulin heavy chain gene was identical between KOPN30bi and the predominant clone in the fresh sample (S1) from which KOPN30bi was established, indicating that they are of the same clonal origin. The study of the T cell receptor (TCR) genes including TCR beta, gamma, delta loci showed none of these loci was identical between KOPN30bi and S1. The result of the TCR delta region analysis which was rearranged on one of the alleles in KOPN30bi and was deleted on both alleles in S1, however, indicated KOPN30bi was not a derivative of S1. Polymerase chain reaction, using oligonucleotide probe corresponding to the N region sequence of V gamma-J gamma juncture of KOPN30bi, indicated that only one % of the blast cells in S1 corresponded to KOPN30bi. These studies indicated that the predominant clone in the fresh sample, although it occupied more than 99% of the blasts, did not represent the characteristics of the target cell for leukemogenesis, and furthermore that the leukemogenic molecular mechanisms such as P190 type BCR/ABL translocation are not enough to freeze the differentiation of the target cell.
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PMID:[Antigen receptor gene analysis in lymphoid malignancies--a study using the polymerase chain reaction]. 189 Jul 40

Human T-cell leukemia virus type I (HTLV-I) is the etiologic agent of adult T-cell leukemia, and the clonally derived leukemic cells all contain proviral genomes. Polymerase chain reaction with a variety of primers which span the HTLV-I genome was used to determine that a significant fraction of patients (at least 32%) carry deleted viral genomes in their leukemic cells. The pX region of the HTLV-I genome encoding the regulatory genes tax and rex was preferentially retained. The fact that the tax coding region was retained provides supporting evidence that the tax protein contributes to leukemogenesis in vivo. The reasonably high fraction of patients with adult T-cell leukemia carrying deleted genomes in their tumor cells suggests that the deletions have a role in leukemogenesis.
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PMID:Polymerase chain reaction analysis of defective human T-cell leukemia virus type I proviral genomes in leukemic cells of patients with adult T-cell leukemia. 189 96

Polymerase chain reaction (PCR) was used to amplify the DNA fragments of the complementarity determining region 3 of the immunoglobulin (Ig) gene heavy chain from the leukemic cell specimens of patients with acute and chronic lymphoid leukemias of B-cell lineage. Two different pairs of primers were tested. Fourteen of the 17 (82%) cases of acute lymphoblastic leukemia (ALL), and all 15 cases (100%) of B-cell chronic lymphocytic leukemia, who had rearrangement of the Ig gene heavy chain by Southern analysis, were positive by PCR with either one or both pairs of primers. This technique was able to detect leukemic cells at the level of 0.1%. Applying it to study the remission marrow specimens following induction chemotherapy was more useful than morphology alone in predicting early relapse of the leukemia.
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PMID:Detection of immunoglobulin gene rearrangement in acute and chronic lymphoid leukemias of B-cell lineage by polymerase chain reaction gene amplification. 195 17

The catalytic activity of the nuclear enzyme poly(ADP-ribose) polymerase (NAD+ ADP-ribosyl transferase, EC 2,4,2,30) is totally dependent upon the presence of DNA strand breaks. Having isolated a full-length cDNA for the polymerase, we have now evaluated the effect of endogenously and exogenously induced DNA strand breaks on the transcriptional control of this enzyme. During retinoic acid or dimethyl-sulfoxide-induced differentiation of HL-60 human leukemia cells, which may involve DNA breaks as well as other changes in chromatin, mRNA levels for the polymerase increased very early and remained high for up to 48 h after which it decreased to pre-induced levels. Polymerase transcript levels did not change, however, during the induction of DNA strand breaks by dimethylsulfate, a variety of other alkylating agents, X-irradiation, or UV-irradiation in several mammalian cell lines. It appears that in sharp contrast to the catalytic requirement of the polymerase, the induction of transcription of the polymerase gene may not be a strand-break-dependent process. The noninducibility of the polymerase gene following DNA damage suggested that there may be adequate levels of the polymerase in the cells to cope with DNA damage. To test this hypothesis we examined the efficacy of DNA repair in Cos cells engineered to overexpress the polymerase. Although there was a slight augmentation of the repair rate, this increase was apparent only after very high levels of DNA damage and only at early repair times. After a longer repair period, the extent of repair in control cell was similar to that in the cell overexpressing the polymerase. We thus conclude that the basal levels of the polymerase are adequate for significant amounts of DNA damage.
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PMID:Expression of the poly(ADP-ribose) polymerase gene following natural and induced DNA strand breakage and effect of hyperexpression on DNA repair. 210 80

The ets-1 gene belongs to the ets gene family (ets-1, ets-2, erg, and elk) and is homologous to the v-ets oncogene found in the avian leukemia virus E26. The ets-1 gene products were characterized using a specific monoclonal antibody developed against a bacterially expressed v-ets protein. The ets-1 gene product in the human T-cell line CEM was found to consist of at least six species: four major species with apparent molecular weights of 51 kDa (p51), 48 kDa (p48), 42 kDa (p42), and 39 kDa (p39); and two minor species of 52 kDa (pp52) and 49 kDa (pp49), which are demonstrated to be the phosphorylated forms of p51 and p48, respectively. All of the ets-1 proteins are related to each other and are considered products of the ets-1 gene. Subcellular localization showed that the pp52 and p51 are found mainly in the cytoplasm, while p48 and p39 are found mainly in the nucleus. Specific antibodies against various exons of ets-1 showed that both p42 and p39 lack a region corresponding to exon VII. Polymerase chain reaction analyses revealed the presence of an additional RNA product that corresponds to mRNA lacking exon VII. These results suggest that the human ets-1 gene encodes multiple proteins that are generated by at least two distinct mechanisms: alternative splicing of mRNA and protein phosphorylation.
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PMID:Isoforms of the human ets-1 protein: generation by alternative splicing and differential phosphorylation. 218 4


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