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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The sister chromatid exchange (SCE) frequency was studied in the leukemic cells of 12 patients, 10 with Philadelphia chromosome (Ph1)-positive chronic myelocytic leukemia (CML), 1 with Ph1-negative CML, and 1 with acute myeloblastic leukemia. Except for two patients in the blastic phase of CML, the SCE values were within the normal range [3.8 +/- 6.4 (S.D.) SCE/cell; normal is 3.3 +/- 2.2 SCE/cell]. In the two cases with the blastic phase of CML, the values were 7.6 +/- 3.2 and 8.9 +/- 4.7 SCE/cell, a statistically significant difference from the control values. However, in the patient with acute myeoblastic leukemia, the SCE incidence increased from 3.6 to 24.4 SCE per cell when therapy was changed to daunorubicin and vincristine and the disease became progressive. Further studies on SCE and leukemia may prove the usefulness of this determination for therapeutic and clinical purposes.
Cancer Res 1978 Sep
PMID:Sister chromatid exchange in Philadelphia chromosome (Ph1)-positive leukemia. 27 86

Survival rates improved significantly for 28,036 lymphoma and leukemia patients studied between 1950 and 1973. Nine cancers reviewed demonstrated increased one, three and five year survival rates. Greatest improvement was acute lymphocytic leukemia survival. Least improvement was for chronic granulocytic leukemia. Analyses of age-specific trends in U.S. cancer mortality since 1960 indicates death rates decreased 20% for all ages up to 45 years. This included 70% of the population, but less than 10% of all cancer deaths. Age groups over 55 experienced an 8% increase in cancer mortality. Accurate determination of national cancer incidence trends is not presently possible. Available data, representing approximately 15 million population, indicate that cancer incidence rates increased between 1960 and 1973. Age-specific trend analyses indicate unusual divergences. For the group 15 to 29-years-old, incidence increased 28% in 13 years and there was a concomitant decrease of 20% in mortality.
Cancer 1978 Aug
PMID:Impact of cancer therapy on survival. 27 34

Chronic myelogenous leukemia (CML) is a relatively rare disease, with a number of features that make it especially suitable for observations on leukemogenesis in man. These include known etiologic agents, often a prolonged preclinical and active stage, cells with identifiable morphological and histochemical characteristics and the presence of the unique Ph' chromosome. The transition of CML to blast crisis is a catastrophic event; however, recent clinical and biochemical studies have raised important questions as to the nature and origin of blast cells in this disease. During the past 10 years, we have followed 113 cases olf CML throughout their course and results of observations on the clinical, hematological and other apsects of the disease are presented in this communication.
Cancer 1978 Aug
PMID:Chronic myelogenous leukemia. 27 37

Four patients who demonstrated unusually prolonged survival with Philadelphia chromosome positive Ph' (+) chronic myeloid leukemia (CML) were analyzed for factors associated with survival. Survival duration from initial diagnosis ranged from 120 to 222 months, with a mean of 170 months. At diagnosis, age, symptoms, liver or spleen size, hematocrit, white blood cell count, absolute peripheral myeloblast plus promyelocyte count, and uric acid did not have unique prognostic significance. At diagnosis all four patients had normal or low-normal platelet counts, (range: 170,000 to 248,000/mm3). Thrombocytopenia occurred during treatment in three patients. None of the four patients, however, developed severe marrow hypoplasia or leukopenia during treatment for the chronic phase. Cytogenic studies performed from 103 to 156 months after diagnosis did not reveal a large subpopulation of marrow cells with a normal karyotype or cells with the XO genotype in the male patients. These observations suggest that prolonged survival in CML 1) is not contingent upon intensive treatment resulting in marrow hypoplasia, and 2) does not require the persistence of a clone of karyotypically-normal bone marrow cells or a clone of marrow cells in males which has lost the Y chromosome. A normal or low-normal platelet count at diagnosis may be a favorable prognostic indicator.
Cancer 1978 Oct
PMID:Factors associated with prolonged survival in chronic myeloid leukemia. 28 Apr 16

A patient with Ph1+ chronic myelogenous leukemia is presented who upon entering the accelerated phase of her disease developed aneuoploidy, including duplication of the Philadelphia chromosome. Intensive chemotherapy resulted in a marrow remission and reversion of the marrow karyotype to normal. Rather than entering an anticipated prolonged remission she relapsed four weeks later with return of her aneuploid clone. Postmortem examination revealed several unsuspected areas of extramedullary leukemia, perhaps serving as the source for repopulation of the marrow. If a desired goal of therapy is to eradicate the Ph1+ cell line, then we recommend that it be undertaken early in the disease when there is the least likelihood of extramedullary leukemia.
Cancer 1978 Nov
PMID:Eradication of the intramedullary Ph1 positive cell line without accompanying improved survival in chronic myelogenous leukemia. 28 Dec 58

The second reported patient with simultaneous metastatic epidermoid carcinoma and chronic myelogenous leukemia is described. The difficulty of differentiating the leukemia from a leukemoid reaction is discussed. The incidence of, and importance of looking for, second primary cancers in patients known to have cancer is emphasized.
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PMID:Simultaneous metastatic epidermoid carcinoma and chronic granulocytic leukemia. 28 92

The chromosome study of a patient with chronic myelocytic leukemia in blastic phase revealed a 46,XY,Ph1/47,XY,Ph1,+8 cytogenetic constitution in bone marrow cells and a 46,XY,Ph1/48,XY,2Ph1,+19 cytogenetic constitution in spleen cells. As the cell clones exhibiting chromosome abnormalities in addition to the Ph1 chromosome evolved apparently independently, it is suggested that the acute transformation had a bifocal, myeloid and splenic origin.
Cancer 1978 Dec
PMID:Different cell clones in bone marrow and spleen of a patient with chronic myelocytic leukemia (CML) in blastic phase. 28 4

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.
Int J Cancer 1979 Jan 15
PMID:Sister chromatid exchanges and chromosomes in chronic myelogenous leukemia and cancer families. 28 71

Ten of 55 patients with chronic myelogenous leukemia (CML) diagnosed between 1972 and 1977 were found to lack the Philadelphia (Ph1) chromosome. Serial clinical, morphologic, and cytogenetic studies of patients with Ph1-negative CML showed that 30% of them had chromosomal abnormalities. Two had an extra chromosome No. 8 at the time of blast crisis, with a morphological picture of myeloblasts in the bone marrow. A third patient had a 6:14 translocation initially Abnormalities of chromosome No. 14 are frequently seen in lymphoproliferative disorders, and the bone marrow and peripheral blood contained a significant population of lymphoblasts as well as myeloblasts. The median survival for the 10 patients was 19 months. The exact nature of Ph1-negative CML is not yet clear; disease appears to be a distinct entity among the myeloproliferative disorders.
Cancer 1979 Feb
PMID:Evolution of karyotypes in Philadelphia (Ph1) chromosome-negative chronic myelogenous leukemia. 28 74


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