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 human leukemias are a group of hematologic neoplasms characterized by uncontrolled proliferation of cells concerned with blood cell production. The cause(s) of human leukemia remains unknown. Bone marrow (BM) is believed to be the site of origin of human leukemias, although the specific locus(i) and/or cell(s) from which it arises have not been definitively identified. Generally, human leukemias and related proliferative diseases are thought to be clonal in nature; affecting a single hematopoietic stem cell, which then proliferates and replaces the marrow of normal hematopoietic stem cell systems. The condition is believed to be malignant in nature. Results of our current morphologic studies on well-fixed, ideally-stained thin sections of plastic-embedded bone marrow biopsies (BMB) from a large number of acute (AML, ALL) and chronic (CGL, CLL) leukemia patients suggest that human leukemias may not be clonal diseases. Instead, a large population of other resident cells--'endosteal cells'--appears to become involved in the process and it is possible that all members of this group enter the activity simultaneously. This change (transformation) in the endosteal cell population might be due to an abnormality (qualitative or quantitative) of diffusable, humoral factors (yet to be identified) that are responsible for the growth and proliferation of these hematopoietic precursor cells. In this context, the human leukemias may be considered not as malignant, but rather the result of an aberration of factor(s) that control hematopoiesis. In this respect, the human leukemias, particularly AML, ALL and CML, might be analogous to pernicious anemia (megaloblastic anemia) as it was understood 40-50 years ago.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The origin and spread of human leukemia. 143 86

Cell cycle phases of bone marrow cells from 8 patients with iron deficiency anemia (IDA), 8 aplastic anemia (AA), 30 myelodysplastic syndrome (MDS), 41 acute leukemia (AL) before treatment, 8 acute leukemia in relapse, 17 acute leukemia in complete remission (CR), 12 chronic myelogenous leukemia (CML) and 4 chronic lymphocytic leukemia (CLL) were analysed with flow cytometry. The proportions of phases of S. G2 M in patients with IDA, refractory anemia, and refractory anemia with ring sideroblast were similar to these in normal controls (P > 0.05). However, they were significantly lower in patients with AA, refractory anemia with excess of blast (RAEB) and transformed RAEB than those in normal controls (P < 0.01, respectively), and CML patients than in normal controls (P < 0.05). The S G2M% was apparently higher in patients with CML than that in CLL (P < 0.01). But, there was no difference between in ALL and ANLL (P > 0.05). It was higher in patients with AL in CR and in relapse than AL before treatment (both P < 0.01). It was still lower in the former than that in normal controls. (P < 0.05). The clinical significance of cell cycle status was also discussed in this paper.
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PMID:[Flow cytometric analysis of bone marrow cell cycles in patients with hematologic diseases]. 147 30

Chronic myelocytic or Ph1-positive acute lymphoblastic leukemias have been analyzed for alterations in a variety of proto-oncogenes and anti-oncogenes implicated in the progression of chronic myeloid leukemia (CML) from its chronic phase to blast crisis. The most frequent genetic change found in disease evolution is an alteration of the p53 gene involving a point mutation, a rearrangement or a deletion. These gene changes are common in myeloid and undifferentiated variants of blast crisis but are usually undetectable in lymphoid leukemic transformants. Other molecular changes also occur in the clonal evolution of CML. The retinoblastoma-susceptibility (Rb) gene is an anti-oncogene. Structural abnormalities of Rb are frequent in all types of human acute leukemia, but are particularly common in Ph1-positive leukemia of lymphoid phenotype including both Ph1-positive ALL and lymphoid blast crisis of CML. Changes in Rb occur early in the transition to blast crisis with loss of Rb protein being the common factor. Mutations in the N-RAS gene also occur, but are rare in typical blast crisis. They are sometimes seen in Ph1-negative myeloid blast crisis. Since changes in the p53 gene are generally associated with progression of disease of a myeloid phenotype and changes in the Rb gene occur more often with a lymphoid phenotype, a particular molecular alteration may influence the character of disease evolution in CML.
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PMID:Molecular mechanisms in the evolution of chronic myelocytic leukemia. 149 27

Genetic polymorphism of transferrin (Tf) was investigated in Han nationality population in Guangzhou area using isoelectric focusing technique. In addition, three diseases (Leukaemia, Heptocarcinoma, Systemic-lupus-erythematosis, SLE) were also typed for Tf and compared with that in normal population. The increased TfC1 gene frequency in acute myelocytic leukaemia (AML) patients was found (chi 2 = 4.16, P less than 0.05). The increased frequency of TfC1C1 was also observed (P less than 0.05). Relative Incident(RI) was 1.9 But TfC1 gene and TfC1C1 phenotype frequencies did not increase in ALL, CML and primary heptocarcinoma patients. It suggests that TfC1 may relative to AML in this area. Besides, the increased TfC1 gene frequency was observed in SLE patients (chi 2 x 6.15, P less than 0.025). RI of TfC1C2 was 2.3. It suggests that Tfc2 may relate to SLE in this area.
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PMID:[Studies of the relationship between transferrin genetic polymorphism and diseases]. 152 51

A nationwide cooperative incidence survey of leukemia was carried out by the Institute of Hematology, CAMS, from 1986 to 1988. The cooperative survey network covered 46 investigating areas, involving 22 provinces, municipalities and autonomous regions. More than 60 million person-years were supervised and 1670 new cases identified. The annual incidence rate of leukemia was 2.76/10(5) and the 95% confidence interval of population rate ranged from 2.63/10(5) to 2.89/10(5). The incidence rates in oil fields and polluted areas were significantly higher than those in other areas. The incidence rate of ANLL was 1.62/10(5); ALL, 0.69/10(5); CML, 0.36/10(5); CLL, 0.05/10(5); and special types, 0.03/10(5). The incidence rate and constituent ratio of CLL were significantly lower than those in Europe and America. A peak of ALL incidence rate before age 10 was seen; this rate then declined with increasing age until 30. However, the incidence rates of other leukemia rose with age reaching peaks at old age (50-70). The leukemia rate in males was significantly higher than that in females, both in youth (10-29), caused by ALL, and at old age (greater than or equal to 60), mainly caused by ANLL. The incidence rates of ANLL subtypes (including M2b) are also reported.
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PMID:[Incidence survey of leukemia in China. Chinese Epidemiologic Study Group of Leukemia and Aplastic Anemia]. 153 78

Eight cases with Ph1 positive acute leukemia (7 of acute lymphocytic leukemia: ALL, and one of acute myelocytic leukemia: AML) were studied molecular biologically to identify location of breakpoints on BCR gene in each patient. Six of the 8 patients (5 of ALL and 1 of AML) had rearrangements at bcr (M-BCR) region. Their locations of the breakpoint in M-BCR were similar to those of 59 chronic myelocytic leukemia patients. One of the remaining two patients had gene rearrangements at m-BCR-1 region in BCR intron 1, and the last patient did not have gene rearrangements at any site of m-BCR-1 and IgL C lambda region. Two cases had gene deletion at either 3' or 5' side of the bcr. A patient with bcr rearrangement was also analyzed by PCR method with reverse transcriptase (RT-PCR) and had simultaneous expressions of bcr3-abl and bcr2-abl chimeric mRNAs. These results indicate that Ph1 positive acute leukemia have heterogeneous characteristics in terms of the molecular biology. The molecular analysis will help for classifying the leukemic types and for elucidating the pathogenesis in Ph1 positive acute leukemia.
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PMID:[Analysis of breakpoints on BCR gene in acute leukemia patients with Ph1 chromosome]. 154 9

The expression of c-myb mRNA and protein was analyzed in fresh leukemic cells by Northern-blot analyses and by immunofluorescent staining using monoclonal c-myb specific antibodies. Staining of the cells was evaluated by flow cytometry. The results demonstrate c-myb mRNA expression predominantly in acute lymphocytic leukemia (ALL, 4/4 cases), acute myeloic leukemia (AML, 17/17) and chronic myeloic leukemia (CML, 12/12) but rarely in chronic lymphocytic leukemia (CLL, 1/17). Immunofluorescent analyses revealed expression of c-myb protein in the nucleus of ALL (5/7) and AML (9/9) with a good correlation of c-myb-positive cells and with the number of proliferating (Ki67-positive) blast cells.
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PMID:Heterogeneous expression of c-myb protein in human leukemia detected by simultaneous two color flow cytometric analysis. 156 Jun 75

A new cell line designated JA-CML was derived from the peripheral blood of a patient with blastic phase CML. Sequential evolution of phenotypic and genetic markers was demonstrated during adaptation from primary to continuous culture in vitro. In the primary sample the majority of blast cells displayed the early T-cell markers, CD7, HLA-DR, and TdT, but were negative for the common ALL antigen (CALLA), CD4 and CD8. Simultaneously, unstimulated metaphase cells showed great karyotypic variation with a range of 43-46 chromosomes per cell. Clonal changes included the Ph chromosome t(9;22), loss of the Y and gain of several altered chromosomes. The cells grew slowly in suspension during the first 10 weeks of culture. During that time, cells still expressed the CD7 and HLA-DR antigens. Karyotypic analysis at ten weeks showed a pattern of 46,X,-Y,t(9;22),+8 in more than 90% of metaphases with disappearance of all other abnormal chromosomes noted in the original sample. A tetraploid subline exhibiting duplication of most chromosomes, including the Ph, comprised the remaining metaphases. Upon further cultivation in vitro, the cells transformed spontaneously over a period of several weeks, from T-lymphoid into myeloid cells. Expression of CD7 was lost, but reactivities with monoclonal antibodies to CD34, CD33 and CD13 were newly acquired. The karyotype was hypertriploid and all cells carried two copies of t(9;22) and lacked normal copies of No. 9 or Y. The cells have since maintained stable cytogenetic and phenotypic profiles. Molecular rearrangement of the breakpoint cluster region was identified in the primary blasts and the established line and T-cell receptor gene rearrangements were not found. These observations suggest that the leukemic blast arose from primitive stem cells, not irreversibly committed T cells, and that these stem cells retained the capacity to differentiate along the myeloid pathway.
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PMID:Emergence of myeloid stem cell line from T-lymphoid blastic phase of chronic myeloid leukemia in culture. 162 78

Eight cases of Philadelphia positive acute leukemia (Ph+AL) were compared with 13 cases of Ph+ chronic myelogenous leukemia in blast crisis (BC) and 10 cases of Ph negative acute lymphoblastic leukemia (Ph-ALL) based on the clinical and molecular biological findings. Distinguishing clinical features were a high leukocyte count (median; 147.9 x 10(3)/microliters) for Ph+AL, and a high incidence of tumor formation and basophilia for BC. A cytogenetic study demonstrated the disappearance or marked reduction of Ph+ metaphases in Ph+AL in remission, while Ph+ cells persisted in BC. The major bcr gene was not rearranged in 4 Ph+AL cases, whereas it was found rearranged in 4 other cases of Ph+ AL and 6 cases of BC. Reverse transcriptase polymerase chain reaction technique demonstrated the presence of minor bcr/abl mRNA in the former three cases, and major bcr/abl mRNA in the latter 4 cases. Remission rates were 63% for Ph+AL, 38% for BC, and 100% for Ph-ALL, and the 50% survival were 12, 5 and 29 months, respectively. It was concluded that Ph+AL can be differentiated from BC by a marked reduction of Ph+ cells at remission, and that the prognosis of Ph+AL is better than BC, but worse than Ph-ALL.
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PMID:[Clinical and molecular biological study of Ph positive acute leukemia: comparison with blast crisis of chronic myelogenous leukemia and Ph negative acute lymphoblastic leukemia]. 163 16

Ten leukemic patients were treated with allogeneic bone marrow transplantation (BMT). The diagnosis were ANLL in 6 cases, CML in 3 and ALL in one. Pretransplant immuno suppressive measures including total body irradiation cyclophosphamide and daunorubicin were given. All the patients were infused with health stem cell preparation, so that the hemopoietic function was restored. Graft versus-host disease of grade I to II was present in 5 of the patients. Leukemia recurred 76 days after BMT in one patient who received the procedure during a relapse of the disease, while in the remaining 9 patients disease-free survival from 1 to 23 months has been observed.
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PMID:[Allogeneic bone marrow transplantation in the treatment of leukemia: analysis of 10 cases]. 168 16


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