Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The lack of apoptosis or programmed cell death in human tumor cells has been suggested to be one factor allowing uncontrolled growth of neoplasms. We have developed a mouse monoclonal antibody (MAb) that induces programmed cell death in a human acute leukemia cell line (KM-3) of the pre B-cell type. Stable, antibody-producing hybridomas were produced by fusing mouse myeloma cells to spleen cells from mice immunized with viable KM-3 cells. Incubation of KM-3 cells with the MAb (designated anti-BAL) resulted in growth inhibition and subsequent cell death within 2-3 days. Anti-BAL required cross-linking with a rabbit anti-mouse antibody to induce DNA fragmentation typical of apoptosis. Immunoblotting experiments with anti-BAL identified a 37-kDa protein, apparently different from any previously described apoptosis-related surface antigen. Strongest expression of the antigen was generally found on cells of lymphoid or myeloid origin. However, several other cell types such as fibroblasts and endothelial cells were also stained by anti-BAL in flow cytometry but less intensively. Despite the apparent presence of this cell surface-bound 37-kDa antigen on several normal and malignant cell types, anti-BAL induced cell death only in human malignant cell lines expressing a more immature phenotype.
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PMID:A cell surface antigen (BAL) defined by a mouse monoclonal antibody inducing apoptosis in a human lymphocytic leukemia cell line. 818 58

The aim of this study was to investigate the clinical, pathological and biological features of biphenotypic acute leukemia. The morphology of tumor cells was observed by bone marrow examination; the immunophenotype was assayed by flow cytometry and immunohistochemistry; the chromosomal aberrations were detected by conventional chromosomal analysis and RT-multiplex nested PCR. The results showed that extramedullary skin lesions and myelodysplasia occurred before the onset of overt disease. At the time of diagnosis, this case had more than 30% blasts in bone marrow with meningeal involvement. Large-sized tumor cells predominated morphologically over other cells. Flow cytometry revealed the co-expression of myeloid antigens (cMPO, CD33 and CD117) and T-lymphoid antigens (cCD3, CD5, CD7, dual expression of CD4 and CD8). Immunohistochemical staining showed that CD43 and CD99 were strong positive which define the earliest hematopoietic progenitors. Partial tandem duplication of the MLL gene could be detected with normal cytogenetic method. All above-mentioned results led to the diagnosis of biphenotypic acute leukemia. It is concluded that the biphenotypic acute leukemia is an uncommon type of leukemia which may be preceded by myelodysplastic syndrome and has aggressive clinical and biological behavior. Immunophenotype, cytogenetics and molecular analysis can contribute to early diagnosis of BAL and evaluation of prognosis.
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PMID:[Skin lesions and myelodysplastic syndrome as initial manifestations of biphenotypic acute leukemia]. 1795 70