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

Genetic marker systems have been employed to investigate the origin and development of many human tumors. The type of information already gained with such systems includes the probable single cell origin of chronic myelocytic leukemia in a marrow stem cell. The G-6-PD system has also confirmed the hypothesis that at least some hereditary and viral tumors have multiple cell origin. However, Burkitt lymphoma, the malignancy in man for which there is a great amount of circumstantial evidence for a viral cancer, has a clonal origin. Of particular interest is the demonstration that early relapses after remissions of Burkitt lymphoma represent reemergence of the original malignant cell lines, whereas some late recurrences may be the result of newly induced malignant clones. Similarly, some recurrences of acute lymphoblastic leukemia in patients treated with marrow transplantation may be new occurrences of disease. These observations have important implications for the etiology and pathogenesis of Burkitt lymphoma and acute lymphoblastic leukemia.
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PMID:Human tumors studied with genetic markers. 82 56

Two established North American Burkitt lymphoma cell lines were studied by chromosomal banding techniques. The SU-AmB-1 line previously shown to be negative for the Epstein-Barr virus (EBV) was found to have, among other changes, a translocation from the long arm (q) of chromosome 8 onto 14q. The SU-AmB-2 line, which contains the EBV genome, also displayed the same 8/14 translocation. These results were compared with data from three EBV-positive tumor cell lines derived from patients with African Burkitt's lymphoma. Our findings indicate that a translocation from 8q onto 14q occurs in both African and North American Burkitt lymphomas, and that this abnormality apparently is not related directly to EBV. This chromosome translocation therefore may be an important event in the development of human lymphocytic malignancy, analogous to the occurrence of the Philadelphia chromosome rearrangement in chronic myelogenous leukemia.
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PMID:Chromosome 14 translocation in African and North American Burkitt's lymphoma;. 84 16

An antigen with a molecular weight of 150 kilodaltons expressed on certain leukemia and lymphoma cells was recognized by a human monoclonal antibody (3H12), which had been established by the fusion of lymphocytes from a small cell lung cancer patient with a mouse myeloma cell line (P3U1). Peripheral blood mononuclear cells from 3 out of 4 cases with lymphoid crisis of chronic myelogenous leukemia (CML) were positively stained by 3H12, while cells from 5 cases with myeloid crisis of CML did not react to this antibody. The antibody did not show any reactivity to cells from the chronic phase of CML, other types of leukemias or normal hematopoietic cells. We further examined 29 cell lines of hematopoietic origin and found that 2 undifferentiated cells (BV-173 and K-562) reacted to the 3H12 antibody. In addition, we found that 3 out of 6 Burkitt lymphoma cells (DAUDI, RAJI and HR1K) reacted to 3H12. Taken together, these results suggest that the antigen recognized by 3H12 is a differentiation-associated antigen expressed on immature lymphoid cells, and could potentially be a reliable cell lineage marker.
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PMID:Human monoclonal antibody detects a cell surface antigen expressed on hematopoietic malignant cells of lymphoid lineage. 190 Aug 25

Usefulness of DNA analysis in diagnosis of hematopoietic malignancy was discussed. Examination on the presence of rearrangement in immunoglobulin (Ig) and T cell receptor (TCR) was the first DNA analysis used for clinical diagnosis of lymphoid malignancy to determine the cell-lineage and clonality of proliferating lymphoid cells. One point mutation in ras oncogene has also been used to detect residual leukemic cells as well as diagnosis of the early relapse of leukemia, although not all leukemic cells have this mutation. Presence of BCR-abl fused gene is a genetic marker for Ph1 chromosome. Analysis of BCR-abl gene has made it possible to diagnose the Ph1 ALL and masked Ph1 CML. Development of PCR technique markedly increased the possibility for the use of DNA analysis in clinical medicine. In addition to Ph1 chromosome, various chromosomal abnormalities resulted in a reciprocal translocation between Ig or TCR gene and other genes in various lymphoid malignancies, such as Burkitt lymphoma and follicular lymphoma. These translocations can be analyzed by Southern hybridization and used for clinical diagnosis.
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PMID:[DNA diagnosis of human cancers: lymphoid malignancies and leukemia]. 198

Rearrangements of immunoglobulin and T cell receptor (TCR) genes have been demonstrated in malignant lymphoid tumors of B and T cell origin. In Philadelphia chromosome-positive chronic myeloid leukemia and acute lymphocytic leukemia cells the bcr and c-abl genes are reorganized and transcripts composed of both genes are expressed. We analyzed the organization of bcr, immunoglobulin and TCR genes in malignant lymphomas. Our data show that in all B cell lymphomas analyzed the JH genes and in some cases also the J kappa genes were rearranged. In a Burkitt lymphoma and in a Kil lymphoma distinct rearranged TCR gamma fragments were detected, in a second Burkitt lymphoma two rearranged TCR beta gene fragments occurred together with a rearranged JH gene fragment. In two T cell lymphomas rearranged TCR beta genes were observed; one of these lymphomas also carried rearranged TCR gamma and JH genes. In Hodgkin's disease in 3 out of 7 cases rearranged immunoglobulin genes were detected. In 1 case, which was diagnosed as a follicular hyperplasia, rearranged JH and TCR gamma fragments appeared. In none of the analyzed lymphomas could bcr rearrangements be observed.
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PMID:Analysis of immunoglobulin, T cell receptor and bcr rearrangements in human malignant lymphoma and Hodgkin's disease. 216 Jun 31

Although determination of chromosomal abnormalities may be of limited usefulness for the diagnosis of leukemia, the recent advances in the molecular mechanism associated with chromosome aberration has been rapid. Chromosome translocation in Burkitt lymphoma and chronic myeloid leukemia was the most striking evidence for the oncogene activation. Other specific chromosome abnormalities for FAB-classified leukemias are also known. Translocated type of chromosome abnormalities between immunoglobulin or T-cell receptor genes and oncogenes may also affect the T and B-cell leukemogenesis. However, the role of trisomies found in human and experimental leukemias and the gene dosages had been thought to be most important until 1982, has not been unclear. Many types of phenotypically heterogeneous leukemias have been reported. t(4 ; 11) acute leukemia is one such leukemia which shows early B-cell and myelomonocytic nature. Heterogeneous leukemias have been called biphenotypic, hybrid and acute mixed leukemias. The terminology must be used the unified. Recent trials to use paraffin-fixed tissues and bone marrow smear for molecular analysis has been successfully reported. Basic analysis on the DNA degradation mechanism revealed the enzymatic activity might play an important role before the complete fixation.
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PMID:[Chromosome aberrations and genes in human and experimental leukemias]. 219 1

Chromosome 1 is known to often be involved in various malignant diseases. Its numerical and structural aberrations have been observed in chronic and acute leukemias and solid tumors as well. Recently five protooncogenes have been assigned to the long and short arms of chromosome 1. The frequent and nonspecific occurrence of chromosome 1 rearrangements in human tumors suggests that they play an important role in the pathogenesis and progression of these diseases. The frequency, types, and time of the occurrence of chromosome 1 aberrations and their relation to the stage of the disease were studied in 317 patients with various malignant diseases. In ten patients nonrandom aberrations of chromosome 1 were observed. Two patients had CML, two PRV followed by ANLL, and the remaining six patients suffered from ANLL, ALL, Burkitt lymphoma, MF, SMMoL, and IRSA, respectively. In six patients, total or partial trisomy of the long arm or of the whole chromosome 1 was present, and in three cases balanced translocations involving chromosome 1 could be found. In the cells of one patient a duplication of the centromeric heterochromatin was seen. We analyzed the breakpoints involved. Finally, the aberrations of chromosome 1 were almost always be observed at the terminal stage of the diseases.
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PMID:Abnormalities of chromosome 1 in relation to human malignant diseases. 259 63

Somatic cell hybrids, obtained after fusion of translocation (11;22)-positive Ewing sarcoma cells and Chinese hamster fibroblasts, were assayed for the presence of immunoglobulin C lambda, Philadelphia chromosome breakpoint cluster region, and c-sis oncogene sequences. It was found that c-sis was translocated from chromosome 22 to chromosome 11 in the Ewing sarcoma cells used, indicating that the breakpoint must be proximal to this locus. Moreover, we found that the chromosome 22-linked C lambda and breakpoint cluster region sequences are not translocated. This result confirms an earlier cytogenetic observation that the Ewing sarcoma-associated breakpoint in chromosome 22 is distal to those observed in translocation (8;22)-positive Burkitt lymphoma and in Philadelphia chromosome-positive chronic myeloid leukemia.
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PMID:Translocation of oncogene c-sis from chromosome 22 to chromosome 11 in a Ewing sarcoma-derived cell line. 298 95

Within a very short time the application of molecular biology to cancer research has resulted in an essential change and extension of our knowledge of transformation processes and tumor development. For the first time these mechanisms can be understood in a causal manner and causal cancer therapy seems to be possible in the near future. In this manuscript an attempt is made to give a brief survey of the influence of oncogenes on carcinogenesis. An account is given of the origin of viral oncogenes, viral mechanisms of cell transformation and activation of cellular oncogenes. Additionally, kinetics and targets of tumor proteins are discussed. The complexity and diversity of genetic regulation of growth and differentiation is discussed in some well known diseases such as chronic myeloid leukemia, Burkitt lymphoma, retinoblastoma and acute myeloid leukemia.
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PMID:[Oncogenes]. 303 83

We have performed in situ hybridization of a probe for the lambda IGLC constant region to metaphase spreads from two DiGeorge syndrome (DGS)-related chromosomal rearrangements with breakpoints in 22q11. In this study we have demonstrated that the breakpoints are proximal to the lambda IGLC constant region cluster. Thus, at the molecular level, DGS-related breakpoints can be distinguished from the 22q11 breakpoint of CML, but not from the 8;22 translocation of Burkitt lymphoma or from the 21;22 translocations that we have previously studied.
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PMID:In situ hybridization and translocation breakpoint mapping. III. DiGeorge syndrome with partial monosomy of chromosome 22. 393 Jan 57


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