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)

Leukemic cells from all human chronic granulocytic leukemia (CGL) and some acute myelomonocytic leukemia (AMML) donors are lysed by rabbit antisera to a purified glycoprotein of Friend murine leukemia virus (FLV gp71) in a microcytotoxicity assay. These antisera are not cytotoxic to cells from patients with acute myelocytic leukemia (AML), acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), or to peripheral blood lymphocytes from normal donors. A goat antiserum to gradient purified FLV in addition to reacting with cells from CGL and AMML donors also reacted with cells from AML patients and some ALL donors. However, this antiserum failed to react with cells from CLL patients. Peripheral blood and bone marrow leukocytes prepared from leukemic patients in clinical remission failed to react with antisera to FLV and FLV gp71. Absorption experiments demonstrated that the antigen on CGL cells which is reacting with the antiserum to FLV gp71 is also present on normal human platelets and neutrophils. Similar absorption studies showed that the antigen on AML cells detected by the FLV antiserum is not present on normal leukocytes and platelets and appears to be related to the major internal p30 antigens of mammalian RNA tumor viruses. Another antigenic relationship between oncornaviruses and membrane antigens of human leukemia cells was shown by the ability of FLV antigens to absorb the cytotoxic reactivity of nonhuman primate antisera detecting human leukemia-associated antigens. FLV and FLV gp71 antigens were able to absorb all cytotoxic activity of monkey and chimpanzee antisera to human myeloid leukemia antigens when these antisera were tested with CGL cells. These two approaches to an analysis of cross-reactivity indicate that the antigenic determinant(s) detected by the cytotoxic reactions of the FLV gp71 antiserum with human CGL cells is different from the determinant on FLV gp71 which is responsible for the inhibition of the reactivity of simian antisera with CGL cells. Since the goat and rabbit antisera to FLV and FLV gp71 are able to distinguish AML from CGL cells by direct cytotoxicity testing and absorption, they may be valuable reagents for the serological diagnosis of myeloid leukemia. In addition, since peripheral blood cells from AML and CGL patients in clinical remission were seronegative, the antisera may be valuable as management aids. The data in this report indicates that whatever the mechanism of leukemogenesis is in man, cells from CGL and AML patients possess certain membrane antigens which cross-react with FLV structural components such as p30 and gp71.
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PMID:Relationships between membrane antigens of human leukemic cells and oncogenic RNA virus structural components. 5 69

Cytogenetic studies indicate that most tumors are clonal (i.e. unicellular in origin) and have karyotypic alterations. These are not consistent, but non-random abnormalities are being increasingly identified by banding techniques, pointing to the sites on human chromosomes where genes important in neoplastic development are located. It is postulated that tumor progression occurs as a result of genetic lability within the neoplastic clone, leading to emergence of increasingly mutant subpopulations (often recognizable cytogenetically) with more malignant properties. In the context of this hypothesis, acute leukemia, chronic leukemia, and preleukemia can be viewed as differing only in the rate at which an abnormal hemic clone is expanding, with progression to a more aggressive phase (e.g. the "blast crisis" of chronic granulocytic leukemia) reflecting emergence of a new predominant subpopulation as the result of an additional genetic change. These concepts, and the cytogenetic data from which they have been derived, may help our understanding of basic tumor biology, and have some practical applications in the diagnosis of human neoplasms.
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PMID:Tumors as clonal proliferation. 10 6

It was observed that when normal mouse spleen cells were cultured alone in vitro (precultured) for 3 to 7 days, these cells lost the ability to generate cell-mediated cytotoxicity (CML) during subsequent in vitro sensitization with allogeneic spleen cells, trinitrophenyl (TNP)-modified syngeneic spleen cells, or syngeneic tumor cells. These precultured cells, which were themselves unable to generate CML, were also shown in mixing experiments to suppress, actively, the generation of CML by freshly explanted spleen cells. Suppression occurred at the sensitization phase of CML, and not at the effector level; supernatants from suppressive precultured cells were not suppressive. Suppression was totally abrogated by the treatment of spleen cells with a T cell-specific rabbit anti-mouse brain serum and complement (RalphaMB+C) either before or after preculturing, suggesting that a T cell eas essential both to the generation of suppressor activity and to its expression. Suppressor activity was entirely absent in precultured nylon wool column-nonadherent spleen cells, a T cell-enriched population containing most of the RalphaMB+C-sensitive cells in the spleen. Precultured nylon column-adherent cells (T cell-depleted) did have suppressive activity, and a mixture of nylon-adherent and nylon-non-adherent cells was a suppressive after preculture as the precultured unseparated spleen. Moreover, the ability of nylon-adherent spleen cells to generate suppressive activity during preculturing was abrogated by treatment with RalphaMB+C. Thus, the "spontaneous" generation of CML-suppressive activity was dependent upon a limited subpopulation of splenic T cells isolated in the nylon column-adherent fraction. The relationship of these data to a previously described synergy between subpopulations of normal spleen in the generation of CML is discussed, and the findings related to other suppressor systems described in the literature.
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PMID:In vitro generation of suppressor cell activity: suppression of in vitro induction if cell-mediated cytotoxicity. 12 70

Cancer chemotherapy was purely palliative until the early sixties. Tumor cures have been since obtained, first in malignant trophoblastoma and Burkitt's lymphoma, and more recently in Hodgkin's disease, diffuse histiocytic lymphoma, acute lymphocytic leukemia in children, Wilms's tumor and osteosarcoma. Preliminary data are suggestive of tumor cures in testicular teratomas and, possibly, in small cell carcinoma of the lung. Five patients with trophoblastoma, Hodgkin's disease, melanoma, chronic myelocytic leukemia and anaplastic carcinoma of the lung are briefly presented, all without evidence of tumor relapse 3 years or more after chemotherapy. Theoretical bases for improvement of the curative effect of cancer chemotherapy are discussed, including the development of new agents, and new pharmacological problems concerning drug interactions, complexes of drugs with macromolecules or immunoglobulins and liposomes are considered.
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PMID:[Curability of malignant neoplasms: value and limitations of chemotherapy]. 21 68

Permanent in vitro growing leukemic cell lines have been established from all types of immunologically classified childhood leukemias. Essential characteristics of primary blasts and cultured cells are identical. In contrast to lymphoblastoid, non-leukemic cell lines, the Epstein-Barr-virus specific nuclear angiten (EBNA) is not detected. Up to now 8 Non-B-non-T cell lines (6 of them were derived from children with acute lymphoblastic leukemia, 2 from patients with chronic myeloid leukemia), 8 T-lines and one B-line have been established. Three Non-B-non-T lines from children with acute lymphoblastic leukemia (KM-3, RU-3, MH-3) and one T-cell line (JM) were cultivated by ourselves. Cultured blasts represent a pure tumor material which can be propagated in large quantities. Leukemic cell lines reveal a new approach for the search after leukemia-associated proteins and represent another possibility for the experimental investigation of the etiology of leukemia.
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PMID:[Establishment of leukaemia cell lines and their significance for clinical and experimental oncology (author's transl)]. 22 24

A primate (Macaca speciosa) antiserum prepared against the human chronic myelogenous leukemia cell line K-562 suppressed the growth of the human myelosarcomas in nude mice. The ip administration of 0.5 ml of immune serum plus 0.5 ml of guinea pig complement, starting 7 days after sc tumor transplantation, resulted in a fourfold to fivefold decrease in tumor weight at 15 days when compared to nude mice given pre-immune serum plus complement or complement alone. Whereas the other two groups experienced an exponential increase in tumor volume at 7-9 days after tumor transplantation, the immune serum-treated mice remained in a "lag" phase of tumor growth during which the tumor volume neither increased nor decreased substantially. Histopathologic studies revealed various degrees of tumor alterations ranging form focal hydropic cellular degeneration to massive coagulation necrosis. The incorporation of tritiated thymidine into the tumors was also markedly diminished in the mice given immune serum.
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PMID:Suppression of human myelosarcoma growth in athymic mice by a primate antiserum. 27 18

An experimental model system is presented for the investigation in humans of the role of hematopoietic stromal elements in the regulation of hematopoiesis as well as in the pathogenesis of myelofibrosis in myeloproliferative disorders. The model is based on the simultaneous application of three experimental techniques: (1) growth of bone-marrow derived fibroblastic colonies in vitro, (2) cytogenetic demonstration of marker chromosomes associated with hematopoietic malignancies, and (3) the transplantation of isolated stromal elements into athymic (nude) mice. Using this model, we describe the induction of mesenchymal tumors in nude mice by Ph1 negative fibroblasts obtained from the bone marrow of a patient with a Ph1 positive chronic myelogenous leukemia. Mesenchymal tumors also were induced in nude mice with bone marrow-derived fibroblasts from a patient with aplastic anemia, who was successfully treated with bone marrow transplantation, and from a normal human volunteer. Morphologic, cytogenetic and electron microscopic studies of bone marrow mesenchymal elements in culture and of tumors induced in nude mice from the CML patient indicate the cells composing the tumor are of human origin and are negative for the Ph1 chromosome. The results provide the first in vivo morphological and cytogenetic support using human materials, of the hypothesized relationship of progenitors of in vitro fibroblastic colonies to marrow stromal elements.
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PMID:Production of mesenchymal tumors in nude mice by Ph1 negative fibroblasts obtained from a Ph 1 positive CML patient: a preliminary report. 27 72

Spontaneous sister chromatid exchanges and banded karyotypes were studied in blood lymphocytes from 96 individuals: seven patients with chronic myelogenous leukemia, 15 normal controls, and five "cancer families" comprising 12 cancer patients, 40 tumor-free blood relatives and 22 spouses. The families had: malignant melanoma; Epstein-Barr virus-associated malignancies and a birth defect syndrome; non-Hodgkin lymphoma and diverse carcinomas; Hodgkin's lymphoma and adenocarcinomas; and acute myelogenous leukemia. In addition to the Philadelphia chromosome in chronic myelogenous leukemia patients, karyotypic abnormalities, especially breaks and fragments, were found in 29% of cancer family members, but were inconsistent and usually attributable to radiotherapy. Mean sister chromatid exchange values were normal in chronic myelogenous leukemia, but low (by t-test) in tumor patients and their blood relatives in cancer-prone families. In tumor patients, mean sister chromatid exchange levels fell as age increased. After adjusting for this age effect, no significant differences remained among groups. In patients at high risk of cancer (because they have chronic myelogenous leukemia or a strong family history of cancer), spontaneous sister chromatid exchange rates were not a marker of cancer risk.
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PMID:Sister chromatid exchanges and chromosomes in chronic myelogenous leukemia and cancer families. 28 71

A 10-year-old boy, who had been in an uninterrupted remission of acute lymphocytic leukemia (ALL) for six years, developed polycythemia vera (PV). One and a half months after detection of PV, he was found to have active leukemia. Both the polycythemia and leukemia receded with anti-leukemia therapy. Three possible explanations for the development of PV in a child with ALL are discussed: 1) PV was a part of his original ALL and recurred whtn patient relapsed. The PV phase was detected only during relapse because the patient was under close observation. 2) PV was a second neoplasm independent of ALL. 3) PV was part of a second leukemia which was different from the original leukemia; this new ALL was derived from a pluripotential cell line involving both erythroid and lymphoid elements. A precedent for this explanation has been observed in chronic myelogenous leukemia.
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PMID:Polycythemia vera in a child with acute lymphocytic leukemia. 28 32

Leucocytes of normal persons and patients with acute and chronic granulocytic leukemia, chronic lymphocytic leukemia, and non-Hodgkin lymphoma were separated into subfractions by centrifugation in discontinuous Ficoll density gradient. Osmotic resistance was examined in hypotonic NaCl solutions with decreasing concentration and by determining LDH activity in the supernatant. Suspensions of myelocytes, polymorphnuclear granulocytes, and lymphocytes of normal persons and patients with chronic lymphocytic leukemia demonstrated the same osmotic resistance. Only myeloblasts were osmotically less fragile, and tumor cells of non-Hodgkin lymphoma more fragile.
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PMID:[Osmotic fragility in subfractions of leucocytes in hematological diseases (author's transl)]. 29 98


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