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)

The P210bcr/abl protein is produced in cells from patients with Philadelphia chromosome-positive chronic myelogenous leukemia (CML). Retroviral transfer of the gene encoding P210bcr/abl into murine bone marrow induces a granulocytic leukemia that models the chronic phase of human CML. We have transferred the leukemic clone to syngeneic animals, albeit with surprising inefficiency, and have observed CML and clonally related acute leukemias of lymphoid or myeloid phenotype in some transplant recipients. These data show that murine CML can result from retroviral transfer of the bcr/abl gene into pluripotent hematopoietic stem cells, that infected clones repopulate poorly after adoptive transfer, and that these clones can give rise to acute leukemia, reflecting evolution to a phase resembling blast crisis in the human disease.
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PMID:Blast crisis in a murine model of chronic myelogenous leukemia. 176 47

A case of typical Ph-positive chronic myelogenous leukemia developed in a 58-year old female with a 7-year history of chronic lymphoproliferative disease is described. With the second disease progression, the features of lymphoid proliferation disappeared almost completely. Possible causes of this rare combination of two diseases are discussed.
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PMID:[Reversibility of the development of malignant lymphoma with 7-years of leukemization, associated with the development of chronic myeloleukemia]. 177 92

Activity of 8 glycosidases (6 acid lysosomal and 2 neutral cytosolic enzymes) was estimated in lymphoid cells of 28 patients with different forms of lymphoproliferative disorders: B- and T-chronic lymphocytic leukemia (CLL), non-Hodgkins lymphoma (NHL), Sezary syndrome, hairy cell leukemia (HCL) and B- and T-acute lymphoblastic leukemia (ALL). Activity of these glycosidases was also studied in mononuclear cells and granulocytes of healthy volunteers and in immature myeloid cells of 16 patients with chronic myeloid leukemia (CML). In lymphoid cells of all the patients studied (except of ALL) the glycosidases activity was decreased as compared with that of normal mononuclear cells and immature myeloid cells. Activity of the majority enzymes studied was higher in T-lymphoid cells of patients with lymphoproliferative disorders as compared with B-cells. The highest glycosidases activity was found in ALL cells and the lowest--in CLL cells of the patients with B-lymphoid cells forms of the disease. Activities of N-acetyl-beta-D-hexosaminidase, alpha-D-mannosidase and beta-D-glucuronidase were distinctly dissimilar in cells of the patients with B-CLL, B-NHL and HCL. Estimation of these glycosidases activity in lymphoid cells may be of importance in differential diagnosis of lymphoproliferative disorders.
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PMID:[Lymphoid cell glycosidases in various forms of lymphoproliferative disorders]. 181 21

Enzyme negative blast cells from 27 patients with chronic myeloproliferative disorders (CMPDs) in blastic transformation were analysed with a panel of monoclonal antibodies (MoAbs). According to morphologic features of the bone marrow and laboratory data, the 27 cases were divided into 8 cases of myelofibrosis (MF), 3 cases of chronic megakaryocytic granulocytic myelosis (CMGM) and 16 cases of chronic myeloid leukaemia (CML). Of the 27 cases, 23 showed a positive reaction with myeloid MoAbs, but in 12 cases expressing myeloid markers, megakaryocytic, monocytic or lymphoid cell features were also detected. In 7 cases of MF, 1 case of CMGM and 1 case of CML a bilineage, myelo-megakaryocytoid immunophenotype of peripheral blast cells was seen. Of the 4 patients with CML expressing lymphoid markers, 2 showed early B-cell, 1 T-cell surface antigens, and 1 both myeloid and early B-cell features. In this group of cytochemically immature blastic transformation of CMPD, only 1 case was termed "undifferentiated" blastic transformation.
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PMID:Enzyme negative blastic transformation of chronic myeloproliferative disorders: immunophenotyping of the blastic cell population. 181 60

The configuration of the T-cell receptor (TCR) beta, gamma and delta chain genes was analyzed in 16 cases of B-lymphoid blastic crisis of chronic myeloid leukemia (BC-CML) for a better definition of the biological aspects of this cellular population, in comparison with the molecular features of B-precursor acute lymphoblastic leukemia (ALL). All cases displayed B-phenotypic features, were Ph'-positive and had a rearranged configuration of the breakpoint cluster region (bcr) and of the immunoglobulin heavy chain gene region (JH). The TCR beta chain gene was rearranged in four cases (25%), all of which displayed a monoallelic rearrangement involving the J beta 2 region. The TCR gamma chain gene was rearranged in 13 cases (81%); 13 rearranged alleles utilized the J1/2 regions, while the remaining five utilized JP1. The V regions of the group I were mostly involved. The TCR delta chain gene was rearranged or deleted in 15 cases (94%); the 10 rearranged chromosomes displayed exclusively two patterns referable to partial recombinations, a V2-(D)-D3 and a (D)-D3 type. These two configurations are predominant in B-precursor ALL (75% of rearranged chromosomes) and almost absent in T-ALL. Taken together, these results document the close similarities between the genotypic features of B-lymphoid BC-CML and B-precursor ALL, not only in terms of the incidence of rearrangement but more relevantly with regard to the choice of regions involved in the recombinations. This aspect is particularly evident at the TCR delta locus level.
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PMID:Identical utilization of T-cell receptor gene regions in B-lymphoid blast crisis of chronic myeloid leukemia and B-precursor acute lymphoblastic leukemia. 182 53

Leukemic transformation was shown to be associated with alteration in the level, profile, amino acid composition and metabolic activity of nuclear nonhistone proteins (NHP) of human leukocytes. The level of HMG-protein in patients with blast crisis of chronic myeloid leukemia of the lymphoid type was 5 times that in patients with the myeloid type of blast crisis. The NHP of both transformed and non-transformed leukocytes were shown to undergo glycosylation. A correlation was established between carbohydrate precursor uptake level, on the one hand, and cell specificity, degree of cell differentiation, and cell proliferation rate, on the other. Successful treatment was followed by a rise in NHP level and metabolic activity, improvement in their profile (it became similar to that in donors) and an increase in the share of high-molecular components.
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PMID:[Nuclear nonhistone proteins in normal and leukemic leukocytes]. 184 33

The pattern of immunoglobulin (Ig) and T cell receptor (TCR) gene rearrangements was determined in 87 patients with acute and chronic leukaemias and myelodysplastic syndromes by Southern blot hybridisation. All 31 cases of common, B cell and null cell acute lymphoblastic leukaemia, and B cell chronic lymphocytic leukaemia showed Ig heavy chain (JH) rearrangement, and TCR (beta-chain) rearrangement was seen in all 5 cases of T cell acute lymphoblastic leukaemia. Inappropriate JH and TCR (beta) rearrangements were present in some cases of T-ALL (60%) and common acute lymphoblastic leukaemia (18%), respectively. For the 19 patients with acute leukaemias following chronic myeloid leukaemia, blastic transformation, all 4 with lymphoid transformation and 3 of the 15 with myeloid transformation had JH rearrangement, and 3 CD10-positive lymphoid transformation and 2 myeloid transformation had their TCR (beta) genes rearranged. In conclusion, the pattern of Ig and TCR gene rearrangements correlated well with the cell lineage. However, cross-lineage rearrangements were more commonly seen in patients with acute leukaemias following chronic myeloid leukaemia blastic transformation, as compared to the de novo cases.
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PMID:Rearrangement of immunoglobulin and T cell receptor genes in acute and chronic leukaemias. 185 Sep 43

v-abl, the oncogene transduced by Abelson murine leukemia virus, was first characterized by its ability to transform lymphoid cells. bcr-abl, the oncogene formed by a t(9;22) translocation thought to occur in human hematopoietic stem cells, is detectable in almost all cases of chronic myelogenous leukemia (CML), a malignancy of granulocytic cells. bcr-abl also causes a CML-like syndrome in mice whose bone-marrow cells are infected with a retrovirus transducing the gene. More recent reports have suggested that v-abl can, however, cause a disease similar to CML. We demonstrate here that v-abl, when transduced in a helper virus-containing system, causes disease similar to, but distinct from, the CML-like syndrome induced by bcr-abl. Animals whose bone marrow has been infected by v-abl virus develop modest splenomegaly, marked granulocytosis, and malignant disease of several hematopoietic cell types. Unlike animals with CML-like disease resulting from bcr-abl, the polymorphonuclear leukocytes from animals infected with a v-abl construct do not contain the v-abl provirus at a significant frequency. Histopathologic analysis also shows significant differences between the diseases caused by v-abl and bcr-abl.
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PMID:v-abl causes hematopoietic disease distinct from that caused by bcr-abl. 186 78

The Bcl-2 proto-oncogene was discovered at the t(14;18) breakpoint found in most follicular B-cell lymphomas and some diffuse large-cell lymphomas. Bcl-2 is unique among proto-oncogenes, being localized to mitochondria and extending cell survival by blocking programmed cell death. We examined Bcl-2 protein expression in 82 hematologic malignancies and reactive lymphoid processes. All lymphomas with Bcl-2 rearrangement demonstrated high levels of Bcl-2 protein. However, most follicular and diffuse lymphomas without Bcl-2 rearrangement also displayed intense Bcl-2 staining. In these cases, mechanisms other than classic translocation may be deregulation Bcl-2. The pattern of Bcl-2 staining in follicular lymphoma is the inverse of the pattern in reactive hyperplasia, confirming a role for Bcl-2 immunolocalization in routine diagnosis. Small lymphocytic malignancies, including small lymphocytic lymphoma, mantle zone lymphoma, and chronic lymphocytic leukemia, expressed intermediate levels of Bcl-2. Bcl-2 protein varied in plasma cell dyscrasias. Bcl-2 protein levels in T-cell lymphomas reflected their corresponding stage of development. No substantial Bcl-2 was present in the Reed-Sternberg cells of nodular sclerosing Hodgkin's disease. Chronic myelogenous leukemia was strongly positive for Bcl-2, consistent with the presence of Bcl-2 in normal myeloid progenitors. Immunohistochemistry identified an expanded spectrum of hematopoietic neoplasms in which Bcl-2 may provide a cell survival advantage.
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PMID:Immunolocalization of the Bcl-2 protein within hematopoietic neoplasms. 186 40

Various lymphohaematopoietic compartments represented by cells from T-cell colonies, myeloid progenitor cells (CFU-GM), erythroid progenitor cells (BFU-E), and bone marrow after short-term culture (BM) have simultaneously been analysed in 15 patients receiving 17 bone marrow transplants for Philadelphia chromosome (Ph) positive chronic myeloid leukaemia (CML) or acute lymphoblastic leukaemia (ALL). The marrow grafts were not T-cell depleted. Ten patients without relapse did not show any myeloid cells of host origin until their last follow-up or until death. However, in four of these patients single lymphoid host cells not carrying the Ph chromosome were found after BMT without clinical consequences. In patients with cytogenetic or haematological relapse Ph positive metaphases were first detected in any of the progenitor cell compartments along with residual donor cells in two of three patients. BM became Ph positive after various time intervals. Another patient with CML became Ph positive in all compartments investigated at the same time. The only patient with Ph positive ALL remained completely Ph negative also when haematological and clinical relapse was evident. All patients with relapse exhibited complex clonal and non-clonal chromosomal aberrations at the time of recurrence of the Ph chromosome. Such abnormalities not identical to those usually found with evolution of the disease and preferentially occurring in progenitor cells preceded the reappearance of Ph positive metaphases in one of our patients.
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PMID:Lymphohaematopoietic chimaerism after bone marrow transplantation for chronic myeloid leukaemia: results of simultaneous cytogenetic analyses on T-cell colonies, myeloid, and erythroid progenitor cells. 187 19


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