Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the past two decades immunophenotyping has yielded significant new information regarding the biological heterogeneity of ALL and has provided a solid basis for a biologically oriented and reliable classification of this disease. At present, lineage commitment of acute leukaemias can be achieved in more than 98% of cases by applying a standardized panel of mAbs to pan-B-cell (CD19, cyCD22), pan-T-cell (cyCD3, CD7) and pan-myeloid antigens (CD13, CD33, MPO) that are expressed either on the surface or in the cytoplasm of the earliest progenitors of the respective cell lineage. Further subclassification of ALL based on the analysis of antigens more closely associated with different maturational stages of B- and T-cell lineage has proven useful for the identification of biologically and clinically distinct entities in both B-cell precursor and T-lineage ALL. Immunophenotyping in about 2800 patients recruited for the German multicentre trials has shown that children and adults differ markedly in frequency distribution of immunological subgroups, with a higher adult incidence of immature B-cell precursor (i.e., pre-pre-B ALL) and T-lineage ALL immunophenotypes (i.e., pre-T ALL). Detailed immunological analyses using a broad panel of mAbs have recently documented typical ALL cases inappropriately expressing myeloid antigens (My+ ALL) as well as morphologically/cytochemically defined acute myeloid leukaemia (AML) with lymphoid-associated markers (Ly+ AML). Based on our own results and a critical review of published data, leukaemic blasts in 5-20% of ALL patients disclose My+ ALL, whereas a coexpression, mostly of T-cell-associated antigens, can be identified in 10-25% of AML cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunophenotyping of acute lymphatic leukemia: diagnostic aspects and clinical relevance]. 802 15

We report here an uncommon case of neonatal acute leukaemia that presented concomitant with serological evidence of rubella infection. The clinical course was aggressive and the patient died 5 days after diagnosis from septicaemia. Leukaemic blasts had a mixed lineage immunophenotype co-expressing a constellation of B-lymphoid (CD19, cytCD22, TdT) and myeloid (CD13, CD33, CD14, anti-MPO) markers, as well as multiple adhesion molecules and markers associated with early lympho-myeloid progenitor cells (CD34, CD7, HLA-DR). A previously unrecorded discordant expression of different CD10 and CD34 epitopes was identified using different monoclonal antibodies. The karyotype was 46,XX t(4;11)(q21;q23) and molecular analysis confirmed rearrangement of the trithorax-related oncogene HRX at 11q23. There was a clonal biallelic rearrangement of the immunoglobulin heavy-chain gene. The features of this rare case have implications for possible aetiological events leading to leukaemia.
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PMID:Neonatal mixed lineage acute leukaemia. 803 18

Reports of treatment of patients with minimally differentiated acute myeloid leukemia (AML-M0) are limited, heterogeneous, and controversial. We verified the prognosis of this subtype by analyzing the results of 189 consecutive patients with de novo AML. Fifteen cases fitting the criteria of AML-M0 were identified. No clinical features distinguished them from other patients with AML. The median age was 61 years (range 27 to 70), with a leukocyte count ranging from 0.6 to 185 x 10(9)/L. In all cases the leukemic cells expressed CD34 and reacted with at least one of the antibodies to early myeloid antigens, ie, CD13, CD33, or myeloperoxidase. Immunophenotypic analysis also showed positivity for CD7 in seven samples and the multidrug-resistance P-glycoprotein (P-170) in six. Cytogenetic analysis was abnormal in 12 of the 13 patients in whom an adequate number of mitoses could be evaluated. No single abnormality prevailed, the most common findings being trisomy 8 (three cases) and aberrations of chromosome 7 (two cases). Antileukemic treatment differed according to age, but for remission induction, all patients received a combination of cytosine arabinoside and an anthracycline or mitoxantrone. The prognosis of patients with AML-M0 was remarkably poor as compared with the other French-American-British subtypes. Whereas the overall rate of complete remission (CR) was 58% with a median survival of 63 weeks, only 6 of the 15 patients with AML-M0 achieved a CR, and the median survival of this group was 16 weeks (range 3 to 39). The major determinant of treatment failure was unresponsiveness to chemotherapy, as only one patient died of infection during the hypoplastic phase. The CR duration of responders was short, ranging from 3 to 22 weeks, and no second remissions were observed. We conclude that conventional combination chemotherapy yields disappointing results in AML-M0. The reason for this may be the convergence of various unfavorable prognostic factors, such as (1) the high incidence of cytogenetic abnormalities; (2) the lack of differentiation features and the expression of immaturity markers such as CD34 and CD7; and (3) the frequent expression of P-170. Nonconventional therapeutic approaches should be developed to alter the prognosis of this form of leukemia.
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PMID:Analysis of treatment failure in patients with minimally differentiated acute myeloid leukemia (AML-M0). 812 53

A 77-year-old man, in whom chronic myeloid leukemia (CML) had been diagnosed in October 1990, was admitted to hospital with right chest pain in November 1992. Bone marrow examination revealed the chronic phase of CML. Chest X-ray showed right pleural effusion. The cells from pleural effusion were positive for CD7, CD13, CD33, CD41a, including CD33, CD41a-double positive cells in 57.5%. Southern blot analysis revealed 3'bcr rearrangement. Electron microscopic examination showed the presence of platelet peroxidase. An abnormal karyotype with various additional chromosomes was observed. This is a rare case of extramedullary pleural myelo-megakaryoblastic biphenotypic crisis during the chronic phase of CML.
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PMID:[Extramedullary pleural myelo-megakaryoblastic crisis during hematological chronic phase in chronic myeloid leukemia]. 813 19

To characterize AML-MO (MO) and acute undifferentiated leukemia (AUL) clinically, questionnaires were sent to nationwide hematology departments in May and August 1993. From 65 institutions, 71 MO cases (2.2% of acute leukemias, 3% of AML) and 19 AUL cases (0.4% of acute leukemias) were registered. Median age was 55 (15-81) years for MO and 38.5 (15-71) years for AUL, and the M/F sex ratio was 44:27 for MO and 19:2 for AUL. Of 48 cases examined for chromosome analysis, 24 (50%) were abnormal karyotypes. Of 15 cases examined for electron microscopic myeloperoxidase (MPO), 10 (67%) were positive, and of 9 cases examined for cytoplasmic antigen by anti-MPO antibody, 7 (78%), were positive. Examination of TdT, surface antigen of CD7 and CD34 were performed in 22, 61 and 43 cases and each positivity was 59, 51 and 86%, respectively. 3 of 18 cases showed rearrangement of immunoglobulin heavy chain gene and 2 of 13 cases showed rearrangement of T cell receptor beta gene. With the first-line induction chemotherapy, complete remission (CR) was obtained in 34 of 67 MO cases and in 7 of 18 AUL cases. Median CR duration and median survival for MO cases were 361 and 387 days and those for AUL were 541 and 578 days, respectively. The remission rates were 61% for 54 cases treated with AML chemotherapy regimens and 38% for 13 cases treated with ALL chemotherapy regimens. 9 cases of MO and AUL who received bone marrow transplantation (BMT) had excellently good prognosis compared with non-BMT group.
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PMID:[Diagnosis and treatment of acute undifferentiated leukemia and AML-MO]. 815 42

The main clinical, morphological, cytochemical, immunological features and therapy results of eleven patients diagnosed as acute myeloblastic leukemia M0 (AML-M0) are reported here. There were no clinical characteristics, abnormalities on physical examination or initial laboratory parameters that distinguished these eleven patients. Bone marrow aspirates were hypocellular in four patients. The leukemic cells were undifferentiated by light microscopy and myeloperoxidase (MPO) and/or Sudan Black B (SBB) stains were negative in all cases. Myeloid differentiation antigens were present on the leukemic cells of all eleven patients, whereas B and T cell markers were clearly negative except for CD4 and CD7 antigens. Whatever the treatment employed survival was very short. Eight of the eleven patients were treated and two achieved complete remission (CR) but only one of them is alive in continuous CR. Our results like those previously reported, suggest that AML-M0 patients have a very poor prognosis with standard induction therapies and should perhaps be considered for experimental therapeutic approaches.
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PMID:Acute myeloblastic leukemia with minimal myeloid differentiation (FAB AML-M0): a study of eleven cases. 816 25

Acute promyelocytic leukemia represents 5-10% of acute myeloid leukemia cases (AML) recorded in the literature, occurring more frequently in young adults. It has a special clinical and biological behaviour when compared to the other forms of AML, being characterized by a particular morphology of blast cells (M3 in FAB classification), translocation of chromosomes 15;17, and disseminated intravascular coagulation at diagnosis or after the onset of chemotherapy. Within this AML subgroup there are 2 morphological subsets called the hypergranular promyelocytic leukemia and the hypogranular or variant form. We have studied clinical and laboratory aspects of 19 cases of AML M3 out of 217 AML cases, and observed a high incidence of failure to recognize the M3 variant form, although its diagnosis has been mainly based on cytomorphology. Only 4 out of 8 cases of the variant form received in our laboratory were correctly diagnosed, being the other 4 cases wrongly identified as the myelomonocytic subset of AML (M4). Immunophenotyping with monoclonal antibodies using CD2 and CD7 as T cell markers, CD10 and CD19 as B cell markers and CD33, CD13, CD14, CD15 and anti MPO as myeloid markers is a complementary diagnostic tool that permits solving difficult cases. It is important to classify AML correctly because of the special therapeutic and prognostic features of AML M3, which differently from other AML forms, has been successfully treated with cellular differentiating agents.
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PMID:[M3 variant leukemia: clinical and diagnostic features]. 816 87

Blast cells from 40 patients with Philadelphia-positive chronic myeloid leukaemia (CML) in blast crisis were analysed by immunophenotypic methods. In 27 cases, BCR gene studies were also performed. By light microscopy morphology and cytochemistry the cases were classified as follows: undifferentiated (n = 7; 17.5%), myeloid (n = 27; 67.5%), and lymphoid (n = 6; 15%). On the basis of the immunological markers, the cases were reclassified as: myeloid (n = 17; 42.5%), megakaryoblastic (n = 17; 42.5%), and lymphoid (n = 6; 15%). The seven cases initially considered as undifferentiated by morphological and conventional cytochemical criteria were classified as myeloid (four cases) and megakaryoblastic (three cases) by marker analysis. The monoclonal antibody anti-myeloperoxidase (anti-MPO) was the most sensitive myeloid associated marker in these cases, being positive in five of them. A significant proportion (27%) of non-lymphoid blast crisis cases were CD7-positive, and myeloid markers were positive in the four lymphoid CML-CB cases studied. Analysis of the clinico-haematological characteristics on the various subgroups of patients showed that patients with lymphoid blast crisis had shorter duration of the chronic phase, more frequent extramedullary blastic involvement, more favourable response to therapy, and longer survival. Finally, a trend for an association between megakaryoblastic involvement of blast crisis and breakpoint localization in the 3' extreme of the M-bcr segment was also noted.
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PMID:Immunophenotypic characteristics of blast crisis of chronic myeloid leukaemia: correlations with clinico-biological features and survival. 837 86

This report describes 4 cases of T-cell-associated CD7-positive acute myeloid leukemia (AML). Myelo-peroxidase staining of blasts was negative in 2 cases but became positive during their courses. In all cases, the myeloid determinants CD13 and/or CD33 were associated with CD7 expression. Other B-lymphoid (CD10, CD19) or T-lymphoid (CD2) markers were negative. In three cases, dual fluorescence analyses showed co-expression of CD7 and CD13 (CD33). Clinically, compared with CD7+AML, these CD7+AML patients presented higher leukocyte and blast counts in peripheral blood. All patients achieved complete remission with chemotherapeutic regimens for AML, but 3 relapsed within a short time. Systemic lymphadenopathy was found in 2 cases, and interestingly, the surface markers of the lymph-node in one case were CD7+CD33-. These cases of CD7+AML may represent a distinct subgroup that arises from particular, less different myeloid precursors, and may have poor prognosis.
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PMID:[Four cases of CD7-positive acute myeloid leukemia]. 845 Jun 9

The clinical and biologic characteristics of acute myeloid leukemia (AML) with coexpression of lymphoid-associated antigens (Lym+ AML) were studied from 39 cases who represented 24% of 161 newly diagnosed de novo AML. Twenty-seven cases (16.8%) were positive for the expression of T-cell markers (T+ AML) and 12 (7.5%) for B-cell markers (B+ AML). Chromosomal abnormalities t(9;22)(q34;q11) and t/del(11)(q23), which were considered to be associated with acute leukemia coexpressing markers of more than one cell lineage, were detected in five and in four patients, respectively. There was no prognostic significance of B-cell or T-cell antigen expression in AML. Of 12 T+ AML cases in which cells were available for gene analysis, all showed germline configuration of immunoglobulin heavy chain and T-cell receptor beta chain genes, while seven of nine B+ AML showed rearrangements of either or both of the genes. Double labeling of the cells with myeloperoxidase and lymphoid markers demonstrated that individual blasts in all the five T+ AML tested were simultaneously expressing myeloperoxidase activity and CD7; however, most blasts in the three B+ AML studied expressed either myeloperoxidase activity or CD10, but not both. In eight of the nine T+ AML tested, the T-cell antigen-positive leukemic blasts were significantly decreased to less than 10%, after in vitro culture with the differentiation-inducing agent phorbol ester. B-cell markers remained positive (> or = 20%) on the cells in the two B+ AML who had the same study. These findings suggested that T+ AML and B+ AML might have different biologic features. Further studies on more patients are needed to clarify this point.
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PMID:Characterization of acute myeloid leukemia (AML) coexpressing lymphoid markers: different biologic features between T-cell antigen positive and B-cell antigen positive AML. 848 20


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