Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe previously published work as well as new data on the molecular biology of human T-cell leukemia virus (HTLV) and its associated disease, adult T-cell leukemia-lymphoma (ATLL). This specific kind of disease is endemic to certain areas of Japan and the Caribbean, and several isolated cases have been described also in the United States, Israel, South America, and Africa. The disease is probably also endemic to Africa and South America, but sufficient studies of these areas have not been performed. We have molecularly cloned the HTLV genome and used the viral DNA as a probe in a large molecular study of the DNAs of human hematopoietic malignancies. The results showed that HTLV sequences could be detected in the fresh leukemic cells of all cases of ATLL tested. The neoplastic cells are of clonal origin and contain one or few copies of integrated HTLV. Detailed comparative analyses by restriction enzyme mapping of the proviral DNA in U.S., Japanese, Caribbean, and Israeli cases revealed that the viruses are almost indistinguishable. The DNA from neoplastic cells of other cases of hematopoietic neoplasias analyzed were negative for HTLV sequences with the exception of two. DNA from cells of a patient (MO) with a T-cell variant of hairy cell leukemia did contain a provirus only distantly related to HTLV (less than 10% of DNA sequence homology). The virus isolated from the MO cells has been designated HTLV-II. The second case was a patient with chronic myeloid leukemia whose cells contained exogenous DNA sequences distantly related to HTLV. Different fragments of the clones HTLV genome have been used to hybridize to DNA from uninfected normal tissues of several vertebrate species, including humans, in a search for cell-derived sequences related to the HTLV genome. No homologous sequences were found except sequences distantly related to the pol and env genes, indicating that HTLV does not carry a cellularly derived onc gene. Surprisingly, however, infection of normal human fresh T cells by HTLV transforms them into cells with permanent growth and with several other properties similar to neoplastic T cells. We have also studied the expression of viral and cellular genes in fresh and cultured neoplastic cells from patients with ATLL. Several species of viral mRNAs are always detected in the cultured neoplastic cells, whereas in some fresh samples expression of normal mRNA was not detected.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Molecular studies of human T-cell leukemia virus and adult T-cell leukemia. 633 Feb 24

We have previously demonstrated the presence of a reverse transcriptase-like enzyme in retroviral particles from patients with essential thrombocythemia, polycythemia vera, and chronic myelogenous leukemia. It was subsequently shown that the human genome contains 50 copies of HERV-K. HERV-K is a human endogenous class I retroviral element that contains gag, pol, and env open reading frames. Using both reverse transcriptase-polymerase chain reaction and ribonuclease protection assays, it is demonstrated that the HERV-K pol is expressed in human blood leukocytes. The data indicates that this expression is restricted in CML white cells and is the result of gene regulation.
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PMID:Expression of human endogenous retrovirus (HERV-K) in chronic myeloid leukemia. 750 41

The human genome contains at least 50 copies of the human endogenous retrovirus K (HERV-K) family which is related to the mouse mammary tumor virus (MMTV). Some members have been shown to be transcriptionally active and to have large open reading frames. Using the RT-PCR method we have investigated the HERV-K env transcription pattern in several malignant tissues and in peripheral blood mononuclear cells PBMCs). Samples were derived from chronic myelogenous leukemia (CML), breast cancer, colon cancer, high and low grade non-Hodgkin's lymphomas, Hodgkin's disease, myelodysplastic syndrome, thyroid adenoma (TA) and from PBMCs of patients with breast cancer, gastric cancer, and of healthy individuals. We found abundant HERV-K env transcripts in all tissues under investigation. Using HERV-K 10 specific primers for amplification we detected in addition to transcripts with high homology to HERV-K 10 (ca. 96% homology on the amino acid level) also transcripts of low homology to HERV-K10 (ca. 71%). Interestingly, all solid tissues containing high percentages of malignant cells such as breast cancer, colon carcinoma, low and high grade non-Hodgkin's lymphomas showed exclusively HERV-K env related transcripts with low homology to HERV-K 10. In contrast, in samples containing only a low proportion of malignant cells or no malignant cells at all we observed both types of transcripts. Thus, our data suggest that the expression pattern of HERV-K elements in human cells is very heterogenous and subjected to a complex transcriptional regulation.
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PMID:Two groups of endogenous MMTV related retroviral env transcripts expressed in human tissues. 942 77

Infection of a human T-cell leukaemia cell line (HSB-2) with HHV-6 led to the induction of exosome-like-particles attached to newly formed HHV-6 enveloped particles and to amplification of a 1642 bp molecule consisting of a partial human endogenous retrovirus (HERV)-E polymerase gene and repetitive sequences. We initiated an analysis of transcriptional patterns of predicted genes from HERV-E sequences in normal and malignant haematopoietic cells. Transcription patterns of regions corresponding to gag, pol and env genes at different chromosomal loci varied among cell types tested. Several specific transcripts were only observed in malignant haematopoietic cells and transcriptional activity varied among different malignant cell types. A transcript of 7.1 kb spanning the complete gag, pol and env gene region, originating from chromosome 8p23, was identified in normal peripheral blood cells and cells of the chronic myeloid leukaemia cell line K562. Our study describes new active HERV-E sequences and new loci throughout the human genome.
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PMID:Transcription of HERV-E and HERV-E-related sequences in malignant and non-malignant human haematopoietic cells. 1892 81