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)

Immunophenotypic studies have a limited role in the diagnosis of chronic myelogenous leukemia (CML) but are increasingly being used in CML blast transformation (BT). Determination of the cell lineage of CML blasts is clinically important because patients with lymphoid blast transformation have a better response to chemotherapy and longer survival than those with other lineages. We studied the morphologic, cytochemical, immunophenotypic, cytogenetic, and molecular features of 20 patients with Philadelphia chromosome-positive CML and more than 10% blast cells in peripheral blood or bone marrow. The blasts were morphologically heterogeneous. CD33 was expressed in 19 cases (95%), followed by CD13 (85%), CD11c (80%), CD36 (60%), CD117 (40%), and CD15 (30%). Seven cases (35%) had a precursor-B lymphoid immunophenotype, and 13 (65%) had a predominantly myeloid immunophenotype. Of the former group, of which only one had a pure lymphoid phenotype, terminal deoxynucleotidyl transferase (TdT) and CD19 were expressed in 100%, CD10 in 85.7%, and CD20 in 14.3%. Of the latter group, all 13 expressed from 3 to 6 myeloid antigens, with 46.2% myeloperoxidase positive and 69.2% CD61 positive. No cases were interpreted as T lineage, but the T-cell antigens CD3, CD4, CD5, and CD7 were expressed in 5.0, 40.0, 5.3. and 30.0% of all cases, respectively. In most cases, the immunophenotype of the CML blasts could not be predicted from their morphologic features. Polymerase chain reaction showed that 80.0% of the lymphoid group and 37.5% of the myeloid group had immunoglobulin heavy-chain gene rearrangements. The frequent lineage infidelity of the blast cells in CML BT seems to be related to the stem cell origin of this disorder. Such lineage infidelity, however, makes classification of many cases difficult and the significance of and criteria for biphenotypic blast crisis of CML is yet to be determined.
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PMID:The immunophenotype of blast transformation of chronic myelogenous leukemia: a high frequency of mixed lineage phenotype in "lymphoid" blasts and A comparison of morphologic, immunophenotypic, and molecular findings. 987 54

Single cell gel electrophoresis (SCGE) was used to evaluate the level of DNA damage in peripheral blood (PB), bone marrow (BM), and lymphatic node (LN) cells of patients with acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), chronic myeloid leukemia (CML) and non-Hodgkin's lymphoma (NHL). The level of DNA damage was compared with the level of basal DNA damage in control group, represented by healthy donors. Statistically significant increase of basal DNA damage was found in leukemia/lymphoma cells of patients suffered from AML, CML, ALL of T-cell subtype (T-ALL), and NHL, however, no difference in basal DNA damage was found in patients with ALL of early B-cell subtype (B-ALL) and CLL in comparison to control group. The mean basal DNA damage increased in the order CLL<early B-ALL<T-ALL<AML<CML<NHL (5.6, 7.2, 10.7, 11.9, 16.9, and 23.4% of tail DNA, respectively) what correlated with survival prediction of patients with particular hematological disease. A large heterogeneity was found in the level of basal DNA damage among patients with AML. By sorting this group according to the immunophenotypic markers and cell maturity a good correlation was found between the level of basal DNA damage and French-American-British (FAB) classification for AML (M1-M2 vs. M4-M5). Though T-ALL group manifested larger homogeneity in comparison with AML, the value of basal DNA damage was also dependent on T-cells maturity and coexpression of surface marker CD10. Chemotherapy resulted in a significant but variable increase of DNA damage in leukemia/lymphoma cells. No increase of DNA damage was repeatedly observed in leukemia/lymphoma cells of patient who did not respond to therapy. The level of DNA damage in cells of patients in remission decreased more or less to the basal level in control cells.
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PMID:The single cell gel electrophoresis: a potential tool for DNA analysis of the patients with hematological malignancies. 1021 Jan 7

To investigate the clinical implications of germline C mu transcription, the splice region between the 3' end of the enhancer and the first exon of immunoglobulin germline mu; was analyzed by RT-PCR in 63 samples from 59 patients with leukemia. Immunophenotypes of 33 samples from patients with acute leukemia were analyzed using a panel of these monoclonal antibodies: anti-immature/stem cell (HLA-DR, CD34); anti-mature myeloid (CD33, CD15); anti-T lymphoid (CD2, CD3, CD5, CD7, CD8), and anti-B lymphoid (CD10, CD19, CD20). Of the 63 samples, 33 (52%) contained germline C mu transcripts: 2/2 patients with chronic lymphocytic leukemia; 17/26 (65.4%) patients with acute myeloblastic leukemia; all 4 patients with chronic myelogenous leukemia in blast crisis and 1 in accelerated phase; 9/12 patients with acute lymphocytic leukemia. A clear correlation between germline transcripts and HLA-DR expression was observed among germline-positive cases (p < 0. 01). C mu expression and response to therapy clearly indicated that germline-mu-positive leukemia patients responded poorly to chemotherapy and had a worse clinical prognosis compared with C mu-negative patients (p < 0.01). After two courses of chemotherapy, 7/9 C mu-negative patients achieved complete remission compared to only 7/29 C mu-positive patients (p < 0.01). We conclude that the gene-regulating immunoglobulin germline C mu may be amplified in myeloid and B-lymphoid cells during leukemogenesis. Such genetic changes may be correlated with cellular terminal differentiation injury, resistance to chemotherapy and uncontrolled malignant cell proliferation.
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PMID:Transcripts of immunoglobulin germline mu: an amplified myeloid and B-lymphoid common gene program in various leukemias. 1035 29

The human myeloid cell nuclear differentiation antigen (MNDA) is a nuclear antigen known to be expressed in mature myelomonocytic cell lines. An extensive immunocytochemical evaluation of fixed tissues confirmed MNDA expression in normal maturing granulocytes and monocytes and in acute nonlymphocytic leukemias and chronic myelogenous leukemia. MNDA was not detected in normal tissue histiocytes but was found in activated macrophages and foreign body giant cells associated with inflammation. Flow cytometric cell sorting of normal bone marrow established that MNDA is initially expressed in myeloid blast cells. Examination of lymphoid tissues showed a low level of expression in a population of normal mande B lymphocytes but not in germinal center cells or plasma cells. A subset of B cell neoplasms expressing MNDA included hairy cell leukemia, parafollicular (monocytoid) B cell lymphoma, mantle cell lymphoma, and small lymphocytic lymphoma. Cell sorting of normal bone marrow showed MNDA expression in CD20+/CD10-/CD5- B cells. MNDA was not detected in other normal bone marrow or all other nonhematopoietic cells. The hematopoietic cell-specific pattern of MNDA expression was elucidated through a comprehensive analysis of normal and neoplastic tissues, and the results provide further evidence of the coexpression of B- and myeloid cell markers in neoplastic B cells and identify a normal B cell population that might be related to the cell of origin of a subset of B cell neoplasms.
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PMID:Immunocytochemical analysis of MNDA in tissue sections and sorted normal bone marrow cells documents expression only in maturing normal and neoplastic myelomonocytic cells and a subset of normal and neoplastic B lymphocytes. 1049 38

We encountered a 44-year-old woman with suspected chronic myelocytic leukemia (CML) in the acute phase that was difficult to be differentiate from Philadelphia chromosome (Ph)-positive acute lymphoblastic leukemia (ALL). At disease onset, her bone marrow showed an increase in blasts that were negative for myeloperoxydase (MPO) and Positive for CD10, 19, 34, and HLA.DR. Standard type Ph was detected by chromosome analysis, and both major and minor BCR/ABL m-RNA were detected by reverse-transcriptase polymerase chain reaction (RT-PCR) methods. Neutrophil alkaliphosphatase (NAP) score was normal, and neither eosinophilia nor basophilia was observed in peripheral blood. Under a presumptive diagnosis of Ph-positive ALL (L2), the patient was given AdVP (doxorubicin, vincristine, and prednisolone) therapy followed by a regimen of LMVP (L-asparaginase, mitoxantrone, and VP), and obtained a complete remission 2 months later. At that time, FISH analyses of her bone marrow and blood cells no longer detected bone marrow Ph or BCR/ABL fusion gene. A month later, however, the leukemia relapsed with an increase in MPO-positive blasts in bone marrow, and the patient died soon thereafter. We finally concluded that her leukemia was not Ph-positive ALL, but CML in the acute phase at disease onset.
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PMID:[Blast crisis of chronic myelocytic leukemia that was difficult to differentiate from Ph+ acute lymphoblastic leukemia]. 1062 28

A 54-year-old female, who had been treated for 4 years in the chronic phase of chronic myelogenous leukemia (CML) was admitted for management of a CML blastic crisis. Blast cells showed strong positive expression of CD7 and HLA-DR, and weakly expressed CD2, CD5 and CD10, as well. The cells were peroxidase negative in peripheral blood and bone marrow. An undifferentiated blastic crisis was diagnosed and she was treated with Interferon-alpha and VP(vincristine 2 mg/week; prednisolone 30 mg/day). A 5-7 mm in diameter tumor in the skin of the anterior right chest appeared one week after VP therapy. The tumor consisted of blasts which were CD13, CD33 and peroxidase positive, unlike the peripheral undifferentiated blasts. This is a rare case of mixed blast crisis with an increase in undifferentiated blasts in peripheral blood and bone marrow, and myeloblastic tumor formation in the skin.
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PMID:[Undifferentiated blastic cell crisis of chronic myelogenous leukemia with myeloblastic tumor in the skin]. 1084 65

We report an unusual case of T-cell blast crisis of chronic myelogenous leukemia (CML) with a clinical presentation more typical of de novo T-cell lymphoblastic lymphoma. The patient was a 32-year-old man who presented with acute superior vena cava syndrome 19 months after an initial diagnosis of CML and 5 months after allogeneic bone marrow transplantation. The tumor was composed of primitive lymphoid cells expressing CD2, CD3, CD4, CD5, CD7, CD8, and CD10. Although the clinical features were more typical of acute lymphoblastic leukemia/lymphoma, fluorescence in situ hybridization analysis showed the bcr-abl fusion gene within blastic tumor cells. This finding confirmed that the mass represented a blastic transformation of CML. We use the unusual features of the current case and the previous reports to suggest that the development of T-cell blast crisis of CML is dependent on the presence of both marrow and extramedullary disease and a mechanism to evade apoptosis.
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PMID:T-cell blast crisis of chronic myelogenous leukemia manifesting as a large mediastinal tumor. 1219 31

We describe here the first case of acute lymphoblastic leukemia (ALL) with an isodicentric Philadelphia [idic(Ph)] chromosome. A 35-year-old man was diagnosed as ALL because of the infiltration of CD10(+)CD19(+)CD33(+)CD34(+) lymphoblasts in the bone marrow and the expression of p190-type BCR/ABL fusion transcript. Chromosome analysis showed 45,XY,der(7;12)(q10;q10),der(9)t(9;22)(q34;q11),idic der(22)t(9;22)(q34;q11). The idic(Ph) chromosome was spindle-shaped and supposed to be formed by two Ph chromosomes joined at their q terminals, whereas idic(Ph) chromosomes in chronic myelogenous leukemia (CML) have been shown to be fused at the satellite regions of p arms. The results indicate that the structure of idic(Ph) chromosomes appears to be different between ALL and CML. The patient did not respond to any chemotherapy and could not achieve remission. This chromosome aberration in ALL may suggest poor prognosis as observed in some cases of CML. Furthermore, considering other three reported cases, der(7;12)(q10;q10) may be one of the recurrent translocations in ALL.
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PMID:Isodicentric Philadelphia chromosome in acute lymphoblastic leukemia with der(7;12)(q10;q10). 1697 35

We examined the pattern of blastic transformation in 90 of 248 patients (36%) with chronic myeloid leukemia who were seen at the King Faisal Specialist Hospital and Research Centre between 1975 and 1988. The mean and median ages of all patients were 38.2 and 36.0 years, respectively. Four of the 90 transformants (4.4%) presented in blastic transformation, and 86 cases (95.5%) evolved from a well-defined chronic phase. Twenty-nine (32.2%) of the patients underwent lymphoid blastic transformation, while 28 (31.1%) were myeloid, seven (7.8%) were myelomonocytic, four (4.4%) were monocytic or erythroblastic, six (6.7%) were megakaryoblastic, ten (11.1%) were of mixed lineage, and two (2.2%) were unclassifiable. The lymphoid blast cells were uniformly common acute lymphocytic leukemia (i.e., Ia and CD10 positive), whereas the myeloid transformations were predominantly Ia negative. Mixed phenotype blasts were also predominantly Ia positive (i.e., 8 of 10), with varying positively for CD10 and myeloid/monocyctic markers. We conclude that blast crisis in chronic myeloid leukemia occurs in Saudi patients in a pattern similar to that seen in patients elsewhere, and that surface Ia antigen positivity in lymphoblast cells is a reliable marker for differentiating lymphoid from nonlymphoid crisis, in which the Ia antigen is not usually demonstrable.
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PMID:Morphological and immunological pattern of blastic transformation in chronic myeloid leukemia in Saudi Arabia: Study of 90 transformations among 248 patients. 1758 2

Flow cytometric analysis of cluster of differentiation (CD) markers of myeloid cells has been used in conjunction with cell morphology to diagnose chronic myelogenous leukemia (CML). In the present study, 16 cases of CML were studied for levels of expression of myeloid markers CD15, CD13, CD33, and CALLA, i.e., CD10 which is also expressed on mature granulocytes. In 11 (68.8%) of 16 cases, a differentiated granulocyte population was detected that showed decreased expression of both CD10 and CD13. CD10 was found to be negative in 1 (6.3%) case and showed decreased expression in 10 (62.5%) of the cases. CD13 showed decreased expression in 11 (68.8%) of the 16 cases. Of the 15 cases analyzed for CD15, 2 (13.3%) were negative and 6 (40%) showed decreased expression. Of the 11 cases which showed simultaneous diminished expression of CD10 and CD13, 8 (72.7%) also showed decreased expression of CD15. Of the antigens studied, CD33 was the only one to be consistently expressed at normal levels, i.e., 13 (81.3%) cases demonstrated normal expression. Therefore, these results point to frequently decreased expression levels of CD10, CD13, and CD15 and rarely decreased expression levels of CD33 in association with CML.
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PMID:Diminished CD10, CD13, and CD15 expression in a differentiated granulocyte population in CML. 1766 71


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