Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

WT1 (Wilms tumor gene) expression is a new tumor marker of leukemic blast cells of AML, ALL, and CML. Minimal residual disease (MRD) of leukemia can be detected at frequencies as low as 1 in 10(3) to 10(4) normal bone marrow (BM) cells and 1 in 10(5) normal peripheral blood (PB) cells by means of the quantitation of expression levels of the WT1 gene using reverse transcriptase-polymerase chain reaction (RT-PCR). This is regardless of the types of leukemia or the presence or absence of tumor-specific DNA markers. Thus, the WT1 assay makes it possible to rapidly assess the effectiveness of treatment and to evaluate the degree of eradication of leukemic cells in individual leukemia patients. Moreover, molecular relapse using PCR can be diagnosed by the monitoring of WT1 expression levels in BM or PB 1-24 months (means, 7 months for BM and 8 months for PB) before the clinical relapse became apparent. In case of rapid or gradual increase in WT1 expression levels to or over 10(-2) after return to normal BM levels during CR; or retention of the WTI expression at levels near or over 10(-2) in BM without return to normal BM levels even in CR (WT1 expression level in K562 cells was defined as 1.0), it seems that clinical relapse is impending. Since WT1 antisense oligomers inhibit the growth of leukemic cells, it is apparent that the WT1 gene plays an important role in leukemogenesis.
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PMID:Wilms tumor gene (WT1) as a new marker for the detection of minimal residual disease in leukemia. 966 76

It is well-known that low dose cytosine arabinoside (LDAC) has activity in elderly patients with acute myeloid leukemia (AML). Several studies have shown that AML patients with t(8;21) in long term complete remission (CR) following intensive chemotherapy or allogeneic bone marrow transplantation (BMT) still have persistence of AML1-MTG8 transcripts by reverse transcriptase polymerase chain reaction (RT-PCR) method. We report here a patient who has no evidence of residual disease detectable by RT-PCR after LDAC. A 69-year-old patient did not obtain CR after two courses of intensive chemotherapy with behenoyl-ara-C, daunorubicin, 6-mercaptopurine and prednisolone. He received subcutaneous LDAC 10 mg every 12 h and granulocyte colony-stimulating factor (G-CSF) for 29 days and achieved CR. He continued on a 21 to 28-day course of LDAC without G-CSF every 2 or 3 months and has remained well and in CR for 5 years without chimeric AMLI-MTG8 transcript by RT-PCR. LDAC therapy seems to be effective in eradicating the leukemic clone as post-induction or maintenance therapy in this patient. This is the first case report of the disappearance of AML1-MTG8 transcript by RT-PCR in a patient with t(8;21) in long-term remission after LDAC.
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PMID:Disappearance of AML1-MTG8 transcript by reverse transcriptase polymerase chain reaction in a patient in remission of acute myeloid leukemia (M2) after low-dose cytosine arabinoside. 971 19

A 48-year-old patient was admitted to our hospital for leukocytosis. The blast cells were positive for peroxidase and he was tentatively diagnosed as acute myeloid leukemia according to the French-American-British criteria. By flow cytometry, the bone marrow cells were positive for CD10, CD13, CD33 and HLA-DR, but two-color analysis revealed that most of the CD13- and CD33-positive cells did not express CD10. The marrow cells had Philadelphia chromosome with no additional abnormalities. Major bcr-abl fusion gene was observed by the reverse transcriptase-polymerase chain reaction method. Southern blot analysis disclosed rearrangement of both immunoglobulin heavy chain and T-cell receptor beta chain genes. He received combined chemotherapy for myeloid lineage and lymphoid lineage, but the response was quite poor. He died 64 days after admission due to pulmonary bleeding. Although the association of Ph1 with multilineage differentiation is unclear, our case has significant implication for further investigation of the relationship between Ph1-positive cells and lineage selection.
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PMID:Dual rearrangement of immunoglobulin and T-cell receptor genes in a case of Philadelphia chromosome-positive acute leukemia. 973 Jan 56

The t(8;21)(q22;q22) is the second-most frequently observed nonrandom karyotypic abnormality associated with acute myelogenous leukemia (AML), especially in FAB M2. Trisomy 4 is also a specific chromosomal abnormality for AML FAB M2 or M4. We experienced a 37-year-old woman with a morphologically AML FAB M2 carrying a rare complex translocation (6;21;8)(p21;q22;q22) resulting in AML1 gene rearrangement. A subclone with an additional chromosomal abnormality, trisomy 4, was also revealed. Similarly to the typical t(8;21), a conventional chemotherapy successfully induced into complete remission associated with a recovery of normal karyotype, 46,XX, although AML1/MTG8 (ETO) chimera mRNA was detected by reverse transcriptase polymerase chain reaction.
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PMID:Complex translocation (6;21;8), a variant of t(8;21), with trisomy 4 in a patient with acute myelogenous leukemia (M2). 997 64

B lineage-derived malignant proliferation is a well recognized complication of HIV infection. Acute myeloid leukemias have been reported but no complete review of these cases has been performed. The Medline database was reviewed for the years 1980-1997. Eighteen cases of AML have been reported. When previously known, HIV infection was present for 40 months. In 7 patients HIV infection and AML were diagnosed simultaneously. According to the FAB classification, 5 cases were M2, 8 M4, 5 M5. Extramedullary localizations (skin, testis, spleen) were noticed in 10 patients. Non-treated patients had a survival of 2.7 weeks versus 9.8 months in patients treated with chemotherapy. Pathophysiologic studies were performed in 3 cases: reverse transcriptase activity and p24 antigen were noted in tumoral cultured cells in 1 case; absence of viral particules in culture in another one; absence of cloned DNA provirus integration in blasts cells in a third patient. Based on the observed high rate of M4/M5 (72%) versus 19-36% expected in a non HIV-infected population, we postulate that the association of AML and HIV is not coincidental. The monocytotropism of HIV, the chronic cytokines-mediated activation of monocyte/macrophages, the immunodeficiency may explain this association.
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PMID:[Acute myelocytic leukemia in immunodeficiency virus infection]. 1002 98

The differentiation inhibitory factor nm23 inhibits the differentiation of murine and human myeloid leukemia cells. The inhibition of differentiation may be associated with the aggressive behavior of leukemia. To clarify the role of nm23 in human myeloid leukemia, we investigated the relative levels of nm23-H1, nm23-H2 and c-myc transcripts in bone marrow and blood samples from 110 patients with acute myeloid leukemia (AML) using the reverse transcriptase polymerase chain reaction. The expression levels of nm23-H1 and nm23-H2 in these AML samples were significantly higher than in normal blood cells, and a higher level of nm23-H1 expression was correlated with poor prognosis for AML patients. Analysis of the correlation between nm23 expression and clinical parameters demonstrated that increased nm23-H1 mRNA levels were associated with resistance to initial chemotherapy and reduced overall survival. Multivariate analysis of putative prognostic factors revealed that elevated nm23-H1 mRNA levels significantly influenced the prognosis of patients with AML, particularly in AML-M5.
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PMID:Differentiation inhibitory factor Nm23 as a prognostic factor for acute myeloid leukemia. 1003 98

The AML1 gene encoding the DNA-binding alpha-subunit in the Runt domain family of heterodimeric transcription factors has been noted for its frequent involvement in chromosomal translocations associated with leukemia. Using reverse transcriptase-polymerase chain reaction (RT-PCR) combined with nonisotopic RNase cleavage assay (NIRCA), we found point mutations of the AML1 gene in 8 of 160 leukemia patients: silent mutations, heterozygous missense mutations, and biallelic nonsense or frameshift mutations in 2, 4, and 2 cases, respectively. The mutations were all clustered within the Runt domain. Missense mutations identified in 3 patients showed neither DNA binding nor transactivation, although being active in heterodimerization. These defective missense mutants may be relevant to the predisposition or progression of leukemia. On the other hand, the biallelic nonsense mutants encoding truncated AML1 proteins lost almost all functions examined and may play a role in leukemogenesis leading to acute myeloblastic leukemia.
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PMID:Biallelic and heterozygous point mutations in the runt domain of the AML1/PEBP2alphaB gene associated with myeloblastic leukemias. 1006 52

We examined mRNA expression and internal tandem duplication of the Fms-like tyrosine kinase 3 (FLT3) gene in haematological malignancies by reverse transcriptase-polymerase chain reaction (RT-PCR) and genomic PCR followed by sequencing. By RT-PCR, expression of FLT3 was detected in 45/74 (61%) leukaemia cell lines and the frequency of expression of FLT3 was significantly higher in undifferentiated type (B-precursor acute lymphoblastic leukaemia; ALL) than in differentiated type cell lines (B-ALL) (P = 0.0076). Using the genomic PCR method, 194 fresh samples including 87 acute myeloid leukaemias, 60 ALLs, 32 myelodysplastic syndromes (MDSs) and 15 juvenile chronic myelogenous leukaemias (JCMLs) were examined. Tandem duplication was found in 12 (13.8%) AMLs and two (3.3%) ALLs. Sequence analyses of the 14 samples with the duplication revealed that eight showed a simple tandem duplication and six a tandem duplication with insertion. Most of these tandem duplications occurred within exon 11, and two duplications occurred from exon 11 to intron 11 and exon 12. No tandem duplications of FLT3 gene were detected in MDS or JCML. The frequency of tandem duplication of FLT3 gene in childhood AML was lower than that in adult AML so far reported. All of the 12 AML patients with the duplication died within 47 months after diagnosis, whereas two ALL patients with the duplication have survived 44 and 72 months, respectively. These two ALL patients expressed both lymphoid and myeloid antigens and were considered to have biphenotypic leukaemia. These results suggest that tandem duplication is involved in ALL in addition to AML, but not in childhood MDS or JCML, and that childhood AML patients with the tandem duplication have a poor prognosis.
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PMID:Tandem duplication of the FLT3 gene is found in acute lymphoblastic leukaemia as well as acute myeloid leukaemia but not in myelodysplastic syndrome or juvenile chronic myelogenous leukaemia in children. 1023 79

MLL (ALL1, Htrx, HRX), which is located on chromosome band 11q23, frequently is rearranged in patients with therapy-related acute myeloid leukemia who previously were treated with DNA topoisomerase II inhibitors. In this study, we have identified a fusion partner of MLL in a 10-year-old female who developed therapy-related acute myeloid leukemia 17 months after treatment for Hodgkin's disease. Leukemia cells of this patient had a t(11;17)(q23;q25), which involved MLL as demonstrated by Southern blot analysis. The partner gene was cloned from cDNA of the leukemia cells by use of a combination of adapter reverse transcriptase-PCR, rapid amplification of 5' cDNA ends, and BLAST database analysis to identify expressed sequence tags. The full-length cDNA of 2.8 kb was found to be an additional member of the septin family, therefore it was named MSF (MLL septin-like fusion). Members of the septin family conserve the GTP binding domain, localize in the cytoplasm, and interact with cytoskeletal filaments. A major 4-kb transcript of MSF was expressed ubiquitously; a 1.7-kb transcript was found in most tissues. An additional 3-kb transcript was found only in hematopoietic tissues. By amplification with MLL exon 5 forward primer and reverse primers in MSF, the appropriately sized products were obtained. MSF is highly homologous to hCDCrel-1, which is a partner gene of MLL in leukemias with a t(11;22)(q23;q11.2). Further analysis of MSF may help to delineate the function of MLL partner genes in leukemia, particularly in therapy-related leukemia.
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PMID:MSF (MLL septin-like fusion), a fusion partner gene of MLL, in a therapy-related acute myeloid leukemia with a t(11;17)(q23;q25). 1033 4

The v-myb oncogene of the avian myeloblastosis virus (AMV) is unique among known oncogenes in that it causes only acute leukemia in animals and transforms only hematopoietic cells in culture. AMV was discovered in the 1930s as a virus that caused a disease in chickens that is similar to acute myelogenous leukemia in humans (Hall et al., 1941). This avian retrovirus played an important role in the history of cancer research for two reasons. First, AMV was used to demonstrate that all oncogenic viruses did not contain a single cancer-causing principle. In particular, although both Rous sarcoma virus (RSV) and AMV could replicate in cultures of either embryonic fibroblasts or hematopoietic cells, RSV could transform only fibroblasts whereas AMV could transform only hematopoietic cells (Baluda, 1963; Durban and Boettiger, 1981a). Second, chickens infected with AMV develop remarkably high white counts and therefore their peripheral blood contains remarkably large quantities of viral particles (Beard, 1963). For this reason AMV was often used as a prototypic retrovirus in order to study viral assembly and later to produce large amounts of reverse transcriptase for both research and commercial purposes. Following the discovery of the v-src oncogene of RSV and the demonstration that it arose from the normal c-src proto-oncogene, a number of acute leukemia viruses were analysed by similar techniques and found to also contain viral oncogenes of cellular origin (Roussel et al., 1979). In the case of AMV, it was shown that almost the entire retroviral env gene had been replaced by a sequence of cellular origin (initially called mab or amv, but later renamed v-myb) (Duesberg et al., 1980; Souza et al., 1980). Remarkably, sequences contained in this myb oncogene were shared between AMV and the avian E26 leukemia virus, but were not contained in any other acutely transforming retroviruses. In addition, the E26 virus contained a second sequence of cellular origin (ets) that was unique. The E26 leukemia virus was first described in the 1960s and causes an acute erythroblastosis in chickens, more reminiscent of the disease caused by avian erythroblastosis virus (AEV) than by AMV (Ivanov et al., 1962).
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PMID:Transformation by v-Myb. 1037


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