Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Point mutations of the ras genes have been detected in various hematologic malignancies. This genetic event may either occur in all malignant cells or be acquired by different subclones, which however, cannot be demonstrated adequately by analyzing only DNA derived from patient specimens. The availability of the ras p21 monoclonal antibody (MoAb) Y 13259 makes possible the direct study of the distribution of the ras gene product in human malignant cells. In this report the expression of the ras p21 oncoprotein in the bone marrow smears of 35 children with acute leukemia has been analyzed. The smears were treated with the MoAb Y 13259, biotinylated goat anti-rat IgG, streptavidin, peroxidase and stained with diaminobenzidine (DAB). The intensity of the staining was evaluated by two independent observers as negative or equivocal (-/+), moderate (+) or intense (++), by counting one thousand cells. Patients were also classified according to the percentage of the stained cells into four groups (0, I, II, III). It was found that 22/35 (63%) were (+) or (++) positive as follows: 11/21 (52%) with ALL CALLA (+), 2/2 ALL-B, 3/3 ALL-T and 6/9 AML. In Group 0 (none of the blasts was stained) were 13/35 (37%), as well as in Group I (1 to 25% of the blasts stained 1+ or 2+ positive), while in Group II (26 to 50% positive stained) 3/35 and in Group III (more than 51% stained) 6/35, all of which were AML (6/9). It is concluded that the immunohistochemical analysis of the ras p21 in blast cells of children with acute leukemia may demonstrate that ras gene expression in some subclones, the intensity and percentage of which may be of some clinical importance.
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PMID:The expression of the ras p21 oncoprotein in the bone marrow smears of children with acute leukemia. 129 65

Leukemic cell chromosomal findings in 27 infants were analyzed. Among the 18 cases of acute nonlymphoblastic leukemia (ANLL), all but two were classified as monocytic or myelomonocytic. The remaining nine cases were acute lymphoblastic leukemia (ALL), seven lacking the common ALL antigen and two having cytoplasmic immunoglobulin (pre-B phenotype). Twenty-five cases (93%) had an abnormal karyotype, 21 (84%) being pseudodiploid. Chromosomal translocations were detected in 67% of the ANLL cases and in 78% of the ALL cases. Nonrandom chromosomal abnormalities included the t(9;11)(p21-22;q23) in three cases of monocytic leukemia, inversion of chromosome 16 in three cases of myelomonocytic leukemia with bone marrow eosinophilia, and t(4;11)(q21;q23) in one case of ALL. Chromosomal regions preferentially involved in infant leukemia included 11q23-25 (13 cases), 9p21-22 and 10p11-13. All but one of the 24 cases with chromosomal breakage or rearrangement had breakpoints that corresponded to known fragile sites, half of which were at 11q23-25, a finding that may have pathogenetic importance. The CALLA- or pre-B phenotype and the presence of chromosomal translocations in most infants with ALL provide a biological explanation for their poor prognosis.
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PMID:An analysis of leukemic cell chromosomal features in infants. 295 82

An 83-year-old male was admitted with a right pleural effusion and generalized lymphadenopathy. Serum LDH level was elevated to 801 IU/L, and the pathological diagnosis from inguinal lymph node needle biopsy was malignant lymphoma (ML) of diffuse, large cell, non-cleaved type, according to the working formulation. The surface phenotypes of the malignant cells from the pleural effusion were analyzed by a fluorescent-activated cell sorter with a panel of monoclonal antibodies (MAbs). The ML cells coexpressed antigens detected by MAbs CD10 (CALLA), CD19, CD20, CD22, CD24, CD38, Ia, c-neu and surface immunoglobulin G kappa. A high expression of NRAS p21 was also detected by cytoplasmic immunofluorescence technique. The patient died 19 days later despite a combination of chemotherapy and intensive supportive therapy. From these findings it seems that c-neu may be a prognostic indicator not only for breast cancers but also for lymphoproliferative disorders. Further accumulation of such cases is needed.
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PMID:[Aggressive diffuse lymphoma with malignant pleural effusion expressing c-erbB-2 (neu) oncogene products]. 810 89

The t(9;11) (p21-22;q23) translocation is frequently associated with acute monoblastic leukemia but may occasionally be seen in patients with acute lymphoblastic leukemia (ALL). We report a case of childhood ALL associated with t(9;11) (p21-22;q23) as the unique recurring chromosomal abnormality. A 3-month-old girl presented with "lymphomatous" ALL (renal enlargement), a high leukocyte count and central nervous system (CNS) involvement. Leukemic cell typing revealed a sIg+ B-cell immunophenotype without CD10 and CD34 antigenic expression while the blast cell morphology was of the FAB-L1 type. Splitting of a YAC encompassing the MLL gene was shown by fluorescence in situ hybridization (FISH) studies of the patient's metaphase chromosomes. Rearrangement of the MLL gene was confirmed by Southern blot analysis. Despite treatment with an hyperintensive polychemotherapeutic regimen, the patient achieved a complete remission but relapsed 9 months later. These results provide further evidence that the t(9;11) may be observed in ALL, involves the MLL gene and is associated with a poor outcome. Moreover, this observation clearly illustrates that sIg+ B-cell ALL is not necessarily associated with a Burkitt (L3) morphology.
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PMID:Childhood B-cell acute lymphoblastic leukemia with FAB-L1 morphology and a t(9;11) translocation involving the MLL gene. 897 90

We present the case of a child with acute lymphoid leukemia (ALL) who was morphologically classified as FAB L1 (PAS and peroxidase were negative). Remission was achieved with an ALL-type protocol (GBTLI). Five months after the discontinuation of therapy, the patient presented mixed leukemia (CD10, CD19, CD13 and CD33 were positive) with t (9;11) (p21;q23) translocation. Unfortunately, as cytogenetic and immunophenotype studies were not performed at diagnosis, two possibilities could be considered for the relapse; secondary mixed leukemia with clonal chromosome changes, or mixed leukemia from the beginning.
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PMID:A t(9;11) translocation in childhood acute mixed leukemia. 907 22

At present, there is no case report of HHV8- primary effusion lymphoma (PEL) with t(9;14)(p13;q32) involving both PAX-5 and immunoglobulin heavy chain gene rearrangement, which is a rare translocation in B-cell non-Hodgkin's lymphoma, in an HIV- patient. We examined an HIV-seronegative 63-year-old Japanese man with hepatitis C virus-associated liver cirrhosis and hepatocellular carcinoma manifesting peritoneal lymphomatous effusion without tumor mass at any body site. The lymphoma cells were examined twice by light microscopy, immunohistochemistry, three-color flow cytometry, cytogenetics, and molecular analyses. The nuclear morphology of lymphoma cells was similar to that of large noncleaved cells, although the lymphoma cell size was a little smaller that of the usual large-cell lymphoma. Immunophenotyping of lymphoma cells in the ascitic fluid revealed a mature peripheral B-cell phenotype (CD5- CD10- CD19+ CD20+ CD22+ Ig G+ lambda+). Cytogenetics showed a clonal population: 45,X,-Y, der(2) t(2;6)(q31;p21.3), t(4;8)(q21;q11.2), der(6) t(2;6)(q31;p21.3) add(6)(q15), t(9;14)(p13;q32.3) [10]/47, idem, +der(6) t(2;6), +16[10]. Southern blot analysis revealed rearranged fragments with a probe for immunoglobulin heavy chain, some of which were a size similar to those with a PAX-5 gene probe. Polymorphism, not rearrangement, of the c-MYC gene, was also found. HHV8 and the Epstein-Barr virus were not detected by polymerase chain reaction. This case is the first report of an HHV8- PEL with t(9;14) involving a PAX-5 gene rearrangement in an HIV-seronegative patient. This primary effusion lymphoma manifested spontaneous regression without any therapy. These findings suggest that there may be an additional subcategory of primary effusion lymphoma that is not associated with HHV8 nor c-MYC(R) but is pathogenetically associated with the PAX-5 gene or hepatitis C virus.
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PMID:Herpes virus type 8-negative primary effusion lymphoma associated with PAX-5 gene rearrangement and hepatitis C virus: a case report and review of the literature. 1063 3

Expression of neutral endopeptidase (NEP) 24.11 is diminished in metastatic, androgen-independent prostate cancers (PCs; C. N. Papandreou et al., NAT: MED:, 4: 50--57, 1998). To determine the effects on androgen-independent PC cells of overexpressing cell-surface NEP, an inducible tetracycline-regulatory gene expression system was used to stably introduce and express the NEP gene in androgen-independent TSU-Pr1 cells generating WT-5 cells, which expressed high levels of enzymatically active NEP protein when cultured in the absence of tetracycline. TN12 cells, which contain the identical vectors without the NEP gene and do not express NEP, were used as control. Expression of NEP in WT-5 cells after removal of tetracycline from the media resulted in a >80% inhibition in cell proliferation over a 1-week period (P < 0.005) compared with control cells. Tumor formation occurred in the prostate glands of orthotopically injected athymic mice killed at 30 days in 4 of 5 mice that were given injections of 2 x 10(6) WT-5 cells and were fed doxycycline (NEP suppressed), and in all mice that were given injections of TN12 cells and were fed with or without doxycycline. In contrast, only 1 of 5 mouse prostates developed a tumor in mice that were given injections of WT-5 cells and that did not receive doxycycline. Analysis of the mechanisms of NEP-induced growth suppression revealed that NEP expression in WT-5 cells induced a 4-fold increase in the number of PC cells undergoing apoptosis, and increased the expression of p21 tumor suppressor gene protein and the level of unphosphorylated retinoblastoma protein as determined by Western blot. Flow cytometric analysis show that induced NEP expression in WT-5 cells resulted in a G(1) cell cycle arrest. These data show that NEP can inhibit PC cell growth and tumorigenicity and suggest that NEP has potential as therapy for androgen-independent PC.
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PMID:Tumor-suppressive effects of neutral endopeptidase in androgen-independent prostate cancer cells. 1135 Sep 8

We describe the establishment and characterization of a new multiple myeloma (MM) cell line, KYdelta-1, which expressed delta/kappa type immunoglobulin (Ig). The patient was a 65-year-old woman with MM, who presented extramedullary dissemination, lymphadenopathy and short survival. The KYdelta-1 cell line was derived from the pleural fluid obtained in the terminal phase of the disease. The cells expressed delta/kappa Ig in the cytoplasm, and CD10, CD29, CD33, CD38, CD44, CD54, and HLA-DR antigens on the cell surface. Chromosomal analysis revealed two independent translocations, t(3;14)(p21;q32) and t(3;11)(p21;q13), which were confirmed by fluorescence in situ hybridization using chromosome painting probes. Reverse transcriptase-mediated polymerase chain reaction (PCR) and Northern blot analyses demonstrated overexpression of the CCND1 gene, suggesting alteration of the BCL1-CCND1 locus. We thus performed long-distance inverse PCR using nested primers for the Calpha constant region of immunoglobulin heavy chain gene (IGH) and obtained a clone that encompassed the 11q13/IGH fusion. Nucleotide sequencing determined that the fusion occurred at the Salpha2 switch region and at the centromeric side of the major translocation cluster of BCL1. The other IGH allele consisted of a VDJ complex that was adjacent to the Cdelta constant gene, indicating that a class switch-like mechanism from the C(mu) to Cdelta was involved in the production of the Ig delta heavy chain. Point mutations within the P53 and N-RAS genes were presumably related to the rapidly progressive disease in this particular MM patient.
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PMID:Establishment and characterization of a new human myeloma cell line, KYdelta-1, producing the delta/kappa type immunoglobulin. 1167 73

We describe 15 patients (9 children) with precursor B-cell (pB) acute lymphoblastic leukemia (ALL) with surface immunoglobulin (sIg) light chain restriction revealed by flow cytometric immunophenotyping (FCI). The same sIg+ immunophenotype was present at diagnosis and in 3 relapses in 1 patient. In 15 patients, blasts were CD19+ CD10+ (bright coexpression) in 14, CD34+ in 12, surface kappa+ in 12, surface lambda+ in 3; in 8 of 8, terminal deoxyribonucleotidyl transferase (TdT)+; and in 4, surface IgD+ in 2 and surface IgM+ in 1. The 3 CD34- cases included 1 TdT+ case, 1 with t(1;19)(q23;p13), and 1 infant with 70% marrow blasts. One adult had CD10- CD19+ CD20- CD22+ CD34+ TdT+ sIg+ blasts with t(2;11)(p21;q23). Blasts were L1 or L2 in all cases (French-American-British classification). Karyotypic analysis in 12 of 12 analyzable cases was negative for 8q24 (myc) translocation. Karyotypic abnormalities, confirmed by fluorescence in situ hybridization in 6 cases, included hyperdiploidy, t(1;19)(q23;p13), t(12;21)(p13;q22), t(9;22)(q34;q11), t(2;11)(p21;q23), and trisomy 12. The sIg light chain restriction in pB ALL might be present in neoplasms arising from the early, intermediate, and late stages of precursor B-cell maturation; sIg light chain restriction revealed by FCI does not necessarily indicate a mature B-cell phenotype, further emphasizing the importance of a multidisciplinary approach to diagnosing B-lymphoid neoplasms.
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PMID:Precursor B lymphoblastic leukemia with surface light chain immunoglobulin restriction: a report of 15 patients. 1508 Mar 3

A human acute lymphoblastic leukemia (ALL)-derived cell line, BALM-25, was established from the bone marrow specimen of a 59-year-old male patient with B-cell ALL L3 type (ALL-L3) at diagnosis. Immunophenotyping indicated mature B-cell characteristics including expression of cell surface and cytoplasmic immunoglobulin (Ig) chains, CD10, CD19, CD20, CD38, CD39, CD40, CD71, NU-B1 and HLA class II. T-cell and myeloid associated antigens tested were negative except CD5. BALM-25 cells have a morphological appearance typical for L3-type lymphoblasts. Regarding the expression of Ig chains, while the original leukemia cells expressed Ig lambda delta mu and hence a single light (L) chain isotype, the established line revealed double L chain expression both at the cell surface and the cytoplasmic level. Definitive double L chain expression was confirmed by flow cytometry and Western blot analysis. Southern blot analysis demonstrated rearrangement of the IgJH, the Ckappa and the Clambda genes. Cytogenetic analysis of BALM-25 revealed the following numerical and structural abnormalities: 55, X, add(X)(q12), + 2, add(3)(p21), + 5, add(7)(p13), add(11)(p11.2), add(11)(q?23), add(12)(p11.2), add(14)(q22), - 15, + 16, + 16,add(18)(11.2), + 20, + marl, + mar2, + mar3, + mar,inc. The established cell line, BALM-25, provides an unlimited supply of cell material for analyzing the unique (patho)physiology of Ig expression in general and for clarifying the pathogenesis of this type of B-cell malignancy in particular.
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PMID:A novel ALL-L3 cell line, BALM-25, expressing both immunoglobulin light chains. 1516 Sep 21


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