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)

Bone marrow (BM) karyotypes from 16 consecutive children presenting with nonlymphocytic leukemia were established with the use of banding techniques, before therapy. The two patients with chronic myeloid leukemia (CML) showed the Philadelphia (Ph1) translocation (9q+;22q-). Five of the 14 patients with an acute nonlymphocytic leukemia (ANLL) presented no acquired cytogenetic abnormalities, but one of these five showed a high level of hypodiploidy. One patient with AML evidenced a variant of the Ph1 chromosome originated as a translocation (12p+;22q-). Nonrandom abnormalities (-7; 7q-; +8; t(8;21); -21) were found in six patients, isolated or in association with otheraberrations. Among the random abnormalities, apparently balanced translocations and chromosomal deletions were observed. In ANLL, no correlation could be found between morphologic diagnosis and cytogenetic findings. On the other hand, the presence of BM cells with a normal karyotype at diagnosis was associated with an improved remission rate and survival time. Followup studies were performed in four ANLL patients with an abnormal cell clone at diagnosis. Three of them achieved hematologic remission; their BM karyotype was found to be normal at that stage. In the 4th patient, generalization of the abnormal karyotype in BM cells was seen in the terminal phase of the disease.
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PMID:Bone marrow karyotypes of children with nonlymphocytic leukemia. 29 69

Despite the incomparability in the reporting of leukemia and lymphoma incidence among populations and the relative rarity of these diseases, real differences in rates are discernible from available data. In general, the incidence of each of the leukemias and lymphomas is lower in Japan than in other Pacific rim populations whose rates are known. Particularly striking is the low incidence of CLL in Japan. Among Japanese in Hawaii, rates of some of these cancers (lymphosarcoma, CML) approach those of whites, whereas rates of other cancers (Hodgkin's disease, multiple myeloma, ALL, CLL, and AML) more closely resemble those of native Japanese. The number of Chinese living in countries served by population-based cancer reporting systems is too small for any firm conclusions to be made about leukemia and lymphoma incidence in this group. The incidence of these diseases in certain other nonwhite Pacific rim residents (i.e., Mexican Americans, blacks, and Maoris) is, by and large, similar to that of whites.
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PMID:Geographical variation in the incidence of the leukemias and lymphomas. 29 90

Among 300 patients with chronic myelocytic leukemia (CML) followed at our institute during the last ten years, 36 (12%) were thought to have Ph1-negative CML. In eight of these patients, chromosomal abnormalities were found in the leukemic cells; in four, the karyotypic abnormalities were established with banding techniques. The data of the present study and a review of the literature regarding chromosomal changes in Ph1-negative CML indicate that: 1) no characteristic or consistent karyotypic change is present in Ph1-negative CML and that diploidy is more common in this than any other leukemia; 2) the most common changes involve group C chromosomes (particularly +8); and 3) a missing Y is less common in Ph1-negative CML than in its Ph1-positive counterpart. The karyotypic changes in Ph1-negative CML resemble more those encountered in Ph1-positive CML than in acute myeloblastic leukemia (AML). The much shorter survival of the Ph1-negative CML patients vs that of the Ph1-positive group was again substantiated, and some of the previously reported clinical and laboratory findings unique to Ph1-negative CML were confirmed. On the basis of the cytogenetic findings it is concluded that Ph1-negative CML appears to be an entity unto itself.
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PMID:The chromosomes and causation of human cancer and leukemia: XXXVIII. Cytogenetic experience in Ph1-negative chronic myelocytic leukemia (CML). 29 77

As prognosis has improved over the last several years, an increasing incidence of meningeal involvement has been recognized in adult patients with acute leukemias and malignant lymphomas. In 210 patients evaluated retrospectively, the incidence of meningeal disease was 33% for patients with acute lymphocytic leukemia (ALL), 20% for patients with acute myelogenous leukemia (AML), 22% for patients with non-Hodgkin's lymphomas with an unfavorable histology (NHL), 3% for patients with chronic myelogenous leukemia (CML), and 1% for patients with chronic lymphocytic leukemia (CLL). In most patients, meningeal involvement appeared several months after diagnosis of acute leukemia, often preceding systemic relapse if bone marrow remission had been achieved before. Prophylactic treatment of the CNS was begun in eight patients with ALL or AML after bone marrow remission was achieved. Of these patients, three with ALL and one with AML were free of disease up to 2 years after diagnosis. Methods, benefits, and risks of prophylactic treatment of the CNS for adult patients are discussed in detail.
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PMID:Meningeal involvement in leukemias and malignant lymphomas of adults: incidence, course of disease, and treatment for prevention. 29 27

The membrane phenotype of leukaemic cells was analysed during different stages of chronic myeloid leukaemia by a panel of markers. These included antisera against ALL antigen, p23,30 (Ia-like structure) and other T cell, B cell and myeloid markers 'Lymphoid' blast crisis shares the phenotype of common ALL (of non-T, non-B variety). Both leukemias react with anti-ALL serum and have pre-myeloid, pre-B lymphoid and pre-thymocyte characteristics. Their phenotype may reflect the characteristics of the pluripotential stem cell from which they derive. Nevertheless both leukaemias retain their undifferentiated characteristics and lack overt myeloid, B cell and thymocyte differentiation markers. Myeloid blast crisis and AML are negative with anti-ALL serum but some of the poorly differentiated myeloblasts react with anti-p23,30 serum (and negative for SmIg). The anti-p23,30 serum (used in a double marker assay combined with anti-immunoglobulin) detects some (4-11%) intermediate sized agranular p23,30+/SmIg-cells in peripheral blood during the chronic phase of CML as well as in normal foetal bone marrow. These could be myeloid stem cells (from which in CML the myeloid blast crisis arises). The results demonstrate that surface membrane analysis can aid exact diagnosis in different stages of CML.
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PMID:Membrane marker analysis of 'lymphoid' and myeloid blast crisis in PH1 positive (chronic myeloid) leukemia. 30 6

Antisera were raised in New Zealand White rabbits against non-B, non-T acute lymphocytic leukemia (ALL) cells coated with antilymphocyte serum. Following minimal absorption with chronic lymphocytic leukemia (CLL) cells, the antiserum reacted mainly with non-B, non-T ALL cells. The following numbers of patients had leukemia cells that reacted with the ALL antisera: 13 of 18 with ALL, 3 of 27 with acute myelocytic leukemia, 1 of 8 with chronic myelocytic leukemia (CML), and 0 of 12 with CLL. The positive CML was a patient in CML blast crisis. Normal peripheral blood B- and T-lymphocytes and normal bone marrow were negative. Reactions of the anti-ALL serum (136K) were compared with the reactions of a rabbit anti-B-cell antiserum (63K) that reacted with approximately 70% of leukemia cells. Cultured lymphoblastoid cell lines from normal donors were negative by both cytotoxicity and immunofluorescence tests. However, by immunofluorescence testing, 8 of 17 known malignant lines from a variety of lymphoproliferative disorders were positive; 4 of these lines were of T-cell origin. By immunoprecipitation and polyacrylamide gel electrophoresis, the ALL antigen appeared to consist of a single polypeptide chain of approximately 98,000 daltons. The anti-ALL antiserum was not cytotoxic for normal myeloid stem cells (colony-forming units).
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PMID:Acute lymphocytic leukemia-associated cell membrane antigen. 30 2

Antisera have been raised in rabbits to the lymphoblastoid cell line NALM 1 precoated with anti-lymphocyte serum (ALS). Following absorption with chronic lymphocytic leukemia cells (CLL) the antisera reacted mainly with acute lymphocytic leukemia (ALL) cells, and were very similar in specificity to antisera raised to ALL cells precoated with ALS. Leukemia cells from the following numbers of patients were positive for the anti-NALM 1 sera in a complement-dependent cytotoxicity test; 11/14 ALL, 3/15 acute myelocytic leukemia (AML), 1/5 chronic myelocytic leukemia (CML) and 0/8 CLL. Normal B and T peripheral blood lymphocytes were negative. The titer of the anti-NALM 1 sera against positive cells was 1:64 to 1:256 whereas the undiluted sera did not react with negative cells. Ten out of 11 of the positive ALL cells were of the non-B non-T type. However, cells from 1/4 T ALL patients and a cultured T ALL line 8402 were also positive. Six of 12 cultured lymphoblastoid cell lines were positive, all of which were of malignant origin. The molecular weight of the ALL antigen detected by anti-NALM-1 serum was determined by immunoprecipitation and sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis (PAGE) to be approximately 98,000 daltons.
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PMID:Heteroantiserum against acute lymphocytic leukemia raised to the lymphoblastoid cell line NALM-1. 30 68

Fifty-six untreated patients with acute leukemia (38 acute myelogenous leukemia, 16 acute lymphoblastic leukemia, and 2 blast crisis of chronic granulocytic leukemia) were randomized on admission to one of three groups--one to receive oral anticandidal prophylaxis through the period of remission induction chemotherapy with nystatin, another to receive natamycin, and the third to receive no anticandidal prophylaxis. Neither of the first two groups show any advantage over the last and it is concluded that provided gut sterilization regimes are not employed, prophylactic oral anticandidal treatment is of no value in these patients and should be reserved until there is clinical evidence of infection.
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PMID:Oral anticandidal prophylaxis in patients undergoing chemotherapy for acut- leukemia. 31 10

The natural killer activity of isolated mononuclear cell populations of acute myelocytic leukemia (AML) patients in remission and relapse was compared with that of mononuclear cells obtained from normal subjects. The target cells consisted of 51Cr-labeled blast cells of the K-562 cell line, which was originally obtained from a patient with chronic myelocytic leukemia in blast crisis. The natural killer activity of lymphocytes from AML patients in remission was similar to or higher than that of normal subjects. A marked depression in this function was associated with relapse, as well as with heavy combined chemotherapy. It is concluded that natural killer activity assessed in vitro is an accurate indicator of the clinical stage of AML patients.
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PMID:Natural killer activity in patients with acute myelocytic leukemia. 31 67

Samples from 49 cases of myeloproliferative diseases were tested by an immunocytochemical technique for leucocyte lysozyme and lactoferrin. The presence of these constituents in myeloid precursors from cases of acute and chronic myeloid leukaemia reflected the degree of cellular maturation, lysozyme appearing (as it does in normal myeloid cells) at the stage of primary granule production (in promyelocytes), while lactoferrin wad detectable only in more mature, secondary granule-containing myeloid cells. Auer rods stained positively for lysozyme, in keeping with their relationship to primary granules. Monocytes from five cases of leukaemia showing predominantly monocytic differentiation were indistinguishable from normal monocytes in their staining reactions for lysozyme despite the presence of raised serum and urinary lysozyme levels. In four cases of acute myeloid leukaemia circulating polymorphs deficient in lactoferrin were detected: in one of these cases a similar percentage of polymorphs was lysozyme negative.
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PMID:Intracellular lysozyme and lactoferrin in myeloproliferative disorders. 32 18


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