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)

Myeloproliferative disease of childhood is frequently associated with chromosomal anomalies, usually of the C group. Clinical features are similar to those of the juvenile type of chronic myeloid leukemia. A child with this disease is described. Marked myeloid proliferation, anemia, thrombocytopenia and hepatosplenomegaly were present; leukocyte alkaline phosphatase and fetal hemoglobin were moderately elevated. Chromosome analysis of bone marrow cells revealed a mosaicism 47,XX,+21/46,XX. Down's syndrome was ruled out by the child's normal phenotype and dermatoglyphic analysis. The cytogenetic finding is probably evidence for the clonal origin of the trisomy 21 cell line.
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PMID:Myeloproliferative disease of childhood associated with a trisomy 21 clone. 11 7

Terminal deoxynucleotidyl transferase (TdT) determinations were carried out on peripheral blood leukocytes or bone marrow cells from 61 adult patients with various types of leukemia. TdT activity was undetectable in the cells of patients with acute myelocytic or acute myelomonocytic leukemia but was present in 12 of 13 patients with acute nonmyelocytic leukemia. None of 3 patients with acute myelocytic transformation of chronic myelocytic leukemia (CML) manifested TdT activity while 4 of 6 patients with lymphoid transformation had such activity. More patients with TdT in their leukemic cells responded to treatment than those without TdT activity. However, our findings suggest that TdT activity may be less useful in management of leukemia than has sometimes been supposed.
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PMID:Terminal transferase in leukemia of adults. 11 12

This is the first report of a case of chronic myeloid leukaemia (CML) complicated by myasthenic syndrome. The patient suffered two prolonged periods of idiosyncratic busulphan-induced marrow aplasia, the first occurring 5 months after busulphan was stopped. Between these two episodes, and at a time when no therapy was required for the leukaemia, myasthenic syndrome developed. After the patient recovered from the second episode, the myasthenic syndrome disappeared, and, despite subsequent recrudescence of CML, there were no further myasthenic symptoms, and treatment with neostigmine was discontinued.
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PMID:Chronic myeloid leukaemia and a myasthenic syndrome. 11 14

The histocompatibility loci of the MHC can be separated into two functionally distinct types. One, loci first defined by lymphocyte reactivity in MLC, LD loci, the phenotypic expression of which leads to proliferation of allogeneic T cells, and two, serologically defined, SD loci, products of which act as targets for cytotoxic lymphocytes. Although the SD loci may be definable by both serological techniques and by lymphocyte reactions in CML, and it may well be that the LD loci products will be defined serologically, the functional difference between them is documented by the apparently converse roles in MLC and CML. The LD loci are most effective in leading to MLC stimulation and do not function as targets in CML for reasons discussed elsewhere; the SD loci function poorly it at all in stimulating proliferation in MLC but are excellent targets in CML. A cellular dichotomy may exist in reaction to these different genetic components of the MHC.
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PMID:Genetic control of major complex histocompatibility antigens. 12 15

The H-2da haplotype was derived from the H-2d haplotype by a mutation localized to the D end of the H-2 complex. Coculture of H-2d and H-2da spleen cells gives rise to bidirectional MLR. However, the H-2d anti-H-2da response is much stronger than that of H-2da anti-H-2d. Both haplotypes give rise to reciprocal CML. B10.D2(R103) strain spleen cells, which differ only at the D end of the H-2 complex from the H-2d haplotype, kill H-2da target cells in CML when sensitized to H-2d stimulators and vice versa. Therefore, both the mutant and strain of origin share a D end CML specificity. H-2d and H-2da reject skin grafts in both directions, although some H-2d grafts show prolonged acceptance on H-2da recipients. These data are consistent with a mutation in the D end of the H-2d haplotype resulting in gain-loss of an antigen(s) that gives rise to reciprocal MLR, CML, and skin graft rejection. Further, the mutant can be distinguished from the strain of origin on the basis of the strength of immune response in MLR.
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PMID:Immunogeneic analysis of H-2 mutations. II. Cellular immunity to the H-2DA mutation. 12

In a female patient with chronic myelocytic leukemia (CML) the translocation 9q +; 22q was constantly found to involve only the variant chromosome 9 with an unusually long secondary constriction. The finding indicates a unicellular origin of CML.
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PMID:Additional chromosomal indication for the unicellular origin of chronic myelocytic leukemia. 12 57

The technique of bone marrow cultures in vitro on semi solid agar medium has been applied to the study of 24 cases of chronic myeloid leukemia in chronic phase and/or in acute blastic crisis. At the chronic phase of the disease the colony forming capacity is normal or above the normal range. In blastic crisis the number of colonies is very low. In the same time clusters are prominent.
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PMID:[Study of chronic myeloid leukemia by marrow culture in vitro (author's transl)]. 12 28

A study has been made of the urinary excretion of glycosaminoglycans (GAG) in 50 patients with malignancies, including 6 patients with acute myeloid leukaemia (AML), 11 with chronic myeloid leukaemia (CML), 10 with chronic lymphatic leukaemia (CLL), 10 with multiple myeloma (MM), 7 with Hodgkin's disease and 6 with mycosis fungoides (MF). The total urinary GAG were isolated by precipitation with cetyltrimethyl-ammoniumbromide (CTAB), and assayed in terms of their hexuronic acid content. A statistically highly significant increase in the excretion of total GAG was observed in all the disorders studied, except Hodgkin's disease, the highest value being seen in myeloid leukaemia (ML). Constant amounts of non-dialysable urinary GAG were electrophoresed in 0.5 M lithium acetate on cellulose acetate strips, and stained with alcian blue. The densitometric tracing derived from the electrophoresis strips were analysed with a Du Pont Curve Resolver. The electrophoretic data suggested the existence of a qualitative deviation in GAG excretion in CLL and in MF, in that patients with these diseases excreted on an average larger than normal amounts of slowly migrating GAG fractions. Pooled crude urinary GAG material from patients with CLL, MF, AML and CML and from control subjects was further purified and subjected to analytical studies. These indicated that a similar qualitative urinary GAG distribution exists in ML and in controls, whereas the urinary GAG in CLL and MF patients contained relatively more dermatan sulphate (DS, in terms of iduronate) than those of the controls.
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PMID:Urinary excretion of glycosaminoglycans in malignant diseases of the haemopoietic and lymphatic tissues. 12 35

Two patients with extramedullary manifestation of the blastic phase of chronic myelocytic leukemia (CML) are reported. 100% of the metaphases derived from extranedullary sites were aneuploid. Despite the absence of blastic changes in the bone marrow and the peripheral blood, a significant proportion of the metaphases derived from these tissues also showed aneuploidy. It is suggested that maturation and differentiation of aneuploid myeloblasts are influenced by their environment.
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PMID:Extramedullary manifestation of the blastic phase of chronic myelocytic leukemia: A chromosome study. 12 37

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


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