Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P06126 (CD1a)
 2,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hematopoietic neoplasm coexpressing CD4 and CD56 includes a subset of acute myeloid leukemia with myelomonocytic differentiation, plasmacytoid monocyte tumor, and other immature hematopoietic neoplasms of undefined origin. Herein, we report a CD4+CD56+CD68+ hematopoietic tumor that was thought to be a tumor of plasmacytoid monocytes. This case is unique in the absence of accompanying myelomonocytic leukemia and the faint expression of cCD3 on the tumor cells. The patient was a 22-yr old man presented with multiple lymphadenopathy and an involvement of the bone marrow. Tumor cells were large and monomorphic with an angulated eosinophilic cytoplasm of moderate amount. Nuclei of most tumor cells were eccentric and round with one or two prominent nucleoli. Rough endoplasmic reticulum was prominent in electron microscopic examination. Tumor cells expressed CD4, CD7, CD10, CD45RB, CD56, CD68, and HLA-DR and were negative for CD1a, CD2, sCD3, CD5, CD13, CD14, CD20, CD33, CD34, CD43, CD45RA, TIA-1, S-100, and TdT. cCD3 was not detected in the immunostaining using paraffin tissue, but was faintly expressed in flow cytometry and immunostaining using a touch imprint slide. T-cell receptor gene rearrangement analysis and EBV in situ hybridization showed negative results. Cytochemically, myeloperoxidase, Sudan black B, and alpha naphthyl butyrate esterase were all negative.
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PMID:CD4+CD56+CD68+hematopoietic tumor of probable plasmacytoid monocyte derivation with weak expression of cytoplasmic CD3. 1248 12

A 77-year-old woman presented to the outpatient hematology clinic in August 2001 with leukocytosis, recurrent bacterial infections, sweating and weight loss. Bone marrow biopsy showed 80% infiltration with lymphoid cells having a prolymphocytic morphology. Flow-cytometric immunophenotype analysis showed that over 80% of the cells were positive for CD2, CD3, CD4, CD5 and CD7 antigens and negative for terminal deoxynucleotidyl transferase and CD1a antigens. T cell prolymphocytic leukemia (T-PLL) was diagnosed on the basis of these findings. The diagnosis was later confirmed by cytogenetic analysis and fluorescence in situ hibridization. The patient had the following karyotype: 46,X,der(X)t(X;3) (q28;p25) t(X;16)(p14;q12), der(3) t(X;3)(q28;p25), der(6) t (X;6) (p14;q25), (8) (q10), del(11) (q14q23), der(13) t (5;13) (q34;p11), der(13) t(13;14)(q22;q11), inv(14)(q11q32), der (16) t(X;16)(q28;q12), r(17)(p13q21), der(20) t(17;20) (q21; q13),22p+. The cytogenetic rearrangements der(6)t(X;6) (p14;q25), der(13)t(13;14)(q22;q11),t(5;13)(q34;p11), r(17) (p13q21) and t(17;20)(q21;q13) have not been described previously in the literature in patients with T-PLL.
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PMID:T cell prolymphocytic leukemia with new chromosome rearrangements. 1503 40

T-cell prolymphocytic leukemia (T-PLL) is a rare postthymic T-cell disorder. The disease is characterized by lymphadenopathy, splenomegaly, skin lesions, a high white blood cell count, and an aggressive clinical course. The small cell variant of T-PLL occurs in approximately 20% of patients. Most T-PLL patients express membrane T-cell receptors (TCR) of the alphabeta phenotype. The diagnosis of small cell variant T-PLL in a 56-year-old woman was based on the findings of abnormal lymphocytosis, immunophenotype, lymphadenopathy, and aggressive clinical behavior. Immunophenotype analysis showed that lymphocytes were positive for CD2, CD3, CD5, CD7, CD8, and TCR gammadelta antigens and negative for CD1a, CD4, and TCR alphabeta antigens. Southern blot analysis revealed rearrangement of the TCR Jgamma and Jdelta-1 genes. A cytogenetic study of peripheral blood showed a normal karyotype. T-PLL with a TCR gammadelta phenotype is very rare. This case was typical T-PLL except for the morphologically small cell type and the lack of the typical chromosome aberration. If cases accumulate in the future, the specific features of the gamma8 type of T-PLL will become clearer.
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PMID:Small cell variant of T-cell prolymphocytic leukemia with a gammadelta immunophenotype. 1571 92

To evaluate the sensitivity and specificity analysis of the lineage related antibodies in acute leukemia immunophenotyping by flow cytometry (FCM), immunophenotyping in 184 patients with acute leukemia was performed by FCM analysis. The results showed that in the lineage-related antibodies of acute myelocytic leukemia (AML), the sensitivity of CD13 and CD33 was higher (95.5% and 91.2%, respectively), the specificity of them was deficient (72.5% and 62.2%, respectively); the sensitivity of MPO was low (69.1%), but the specificity was high (100%); the sensitivity and specificity of CD117 were high (88.2% and 100%, respectively); the sensitivity of CD14 and CD15 was low (18.4% and 27.2%, respectively); the specificity of CD14 with monocytes was high. As the lineage-related antibodies of B-lineage ALL were concerned, CD19 showed high sensitivity and low specificity (100% vs 83.4%); the sensitivity and specificity of CD79a (96.4% vs 100%) and CD22 (100% vs 100%) were high; the sensitivity and specificity of CD10 (53.6% vs 82.5%) and CD20 (70.4% vs 87.5%) were low. In T-lineage ALL, the specificity of CD3 was high (97.5%), but the sensitivity was below the mark (80.0%); the sensitivity of CD7 was high (100%), but the specificity was low (77.9%); while the sensitivity and specificity of CD5, CD2 and CD1a were all deficient. In conclusion, the sensitivity and specificity analysis of the lineage-related antibodies in acute leukemia immunophenotyping are coincident with St Jude immunophenotyping project. It seems only that CD117 is superior to MPO in defining AML, but the sensitivity and specificity analysis of CD22 and CD79 are similar in defining B-lineage ALL, therefore, anyone of them may be selected as your need.
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PMID:[Sensitivity and specificity analysis of the lineage related antibodies in acute leukemia immunophenotyping by flow cytometry]. 1585 4

Association of T-lymphoblastic lymphoma (LBL) and Langerhans cell histiocytosis (LCH) in the same lymph node is very rare. Herein, we report such two cases with expression of CD56 in Langerhans cells. Immunohistochemically, lymphoblasts were positive for anti-polyclonal CD3 antibody, CD34, CD7, CD99, and terminal deoxynucleotidyl transferase. LCH cells were positive for anti-S100 protein, CD1a, CD4, CD56, and CD68. Although those two populations were separated topographically, many histiocytes intermingled with lymphoblasts in the paracortex and a few lymphoblasts were scattered within the intrasinusoidal sheets of histiocytes. Neither admixed eosinophils nor multinucleated giant cells were observed. The pathogenetic mechanism of CD56 expression in LCH associated with LBL is discussed.
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PMID:Expression of CD56 antigen in Langerhans cell histiocytosis associated with T-lymphoblastic lymphoma in a same lymph node. 1622 26

Adoptive cell transfer (ACT) of tumor-reactive lymphocytes has been shown to be an effective treatment for cancer patients. Studies in murine models of ACT indicated that antitumor efficacy of adoptively transferred T cells is dependent on the differentiation status of the cells, with lymphocyte differentiation inversely correlated with in vivo antitumor effectiveness. T-cell in vitro development technologies provide a new opportunity to generate naive T cells for the purpose of ACT. In this study, we genetically modified human umbilical cord blood-derived hematopoietic stem cells (HSCs) to express tumor antigen-specific T-cell receptor (TCR) genes and generated T lymphocytes by coculture with a murine cell line expressing Notch-1 ligand, Delta-like-1 (OP9-DL1). Input HSCs were differentiated into T cells as evidenced by the expression of T-cell markers, such as CD7, CD1a, CD4, CD8, and CD3, and by detection of TCR excision circles. We found that such in vitro differentiated T cells expressed the TCR and showed HLA-A2-restricted, specific recognition and killing of tumor antigen peptide-pulsed antigen-presenting cells but manifested additional natural killer cell-like killing of tumor cell lines. The genetic manipulation of HSCs has broad implications for ACT of cancer.
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PMID:Extrathymic generation of tumor-specific T cells from genetically engineered human hematopoietic stem cells via Notch signaling. 1736 59

A novel nude mice model of human extranodal nasal type NK/T-cell lymphoma was established by subcutaneously implanting the sample taken from the patient with secondary extranodal nasal type NK/T-cell lymphoma of the stomach into the right axillary region of a BALB/c (nu/nu) nude mouse. This model had been successfully transplanted in vivo for thirty-two generations with a stable growth cycle. The survival rates of both resuscitation and transplantation were 100%. Histologically, the tumor cells were medium to large size and arranged in sheets, with a little mesenchyma, and disseminated almost in all passages of the lymphoma-bearing nude mice. Immunologically, the tumor cells were positive for CD56, cytoplasmic CD3, granzyme B or TIA-1 and LMP1, sometimes for CD8 but negative for surface CD3, CD7, CD20 and CD1a. EBER1/2 was found. No T-cell receptor gamma gene rearrangement was detected in the transplanted tumors. Furthermore, both human sequencing-tagged sites SY14 and Y chromosome were detected by PCR or fluorescent in situ hybridization, respectively, in the transplanted tumor. The transplanted tumor in this novel nude mice model maintained the essential features of human extranodal nasal type NK/T-cell lymphoma, and it would be an ideal tool in vivo for further research of the tumor.
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PMID:A novel nude mice model of human extranodal nasal type NK/T-cell lymphoma. 1785 53

A 57-year-old man became aware of left supraclavicular lymph node swelling, which was subsequently diagnosed as Langerhans cell sarcoma, based on a positive immunophenotype for CD1a, S-100 protein, and langerin, and histologically bizarre pleomorphism. The tumor became leukemic 3 months later. Despite intensive chemotherapy, he died of disease progression 7 months after the initial diagnosis. Tumor cells in the leukemic phase expressed CD5, CD7, CD13, CD33, CD34, CD68, and CD123. These findings suggested leukemic transformation from Langerhans cell sarcoma. Leukemic transformation may be a clinical manifestation of advanced Langerhans cell sarcoma, and should be differentiated from acute myelogenous leukemia.
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PMID:Leukemic transformation of Langerhans cell sarcoma. 1836 Jul 46

We describe a case of human immunodeficiency virus-associated T-lymphoblastic leukemia/lymphoblastic lymphoma in a 43-year-old Italian man with a history of human immunodeficiency virus infection lasting 9 years. Immunoperoxidase stains showed that neoplastic cells were positive for CD3, TdT, CD45, CD10, CD1a, CD2, CD7, CD5, and CD43 (focal). The proliferation rate was approximately 70%, assessed by Ki-67/MIB-1 staining. Flow cytometry of the marrow aspirate revealed an intermediate/cortical T-lymphoblastic phenotype: negative for surface CD3 and positive for cytoplasmic CD3, CD1a, TdT, CD2, CD7, CD5, and CD8, with partial coexpression of dimCD4. Analysis of T-cell receptor gamma polymerase chain reaction products showed clonality. T-lymphoblastic leukemia/lymphoblastic lymphoma is a very rare occurrence in the clinical setting of human immunodeficiency virus infection. It is not listed in the World Health Organization classification of lymphomas associated with human immunodeficiency virus infection. Only 4 cases of human immunodeficiency virus-associated T-lymphoblastic leukemia/lymphoblastic lymphoma are reported in the current medical literature.
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PMID:Human immunodeficiency virus-associated precursor T-lymphoblastic leukemia/lymphoblastic lymphoma: report of a case and review of the literature. 1942 18

T-cell development follows a defined set of stage-specific differentiation steps. However, molecular and cellular events occurring at early stages of human T-cell development remain to be fully elucidated. To address this, human umbilical cord blood (UCB) hematopoietic stem cells (HSCs) were induced to differentiate to the T lineage in OP9-DL1 cocultures. A developmental program involving a sequential and temporally discrete expression of key differentiation markers was revealed. Quantitative clonal analyses demonstrated that CD34(+)CD38(-) and CD34(+)CD38(lo) subsets of UCB contain a similarly high T-lineage progenitor frequency, whereas the frequency in CD34(+)CD38(+/hi) cells was 5-fold lower. Delta-like/Notch-induced signals increased the T-cell progenitor frequency of CD34(+)CD38(-/lo) cells differentiated on OP9-DL1, and 2 distinct progenitor subsets, CD34(+)CD45RA(+)CD7(++)CD5(-)CD1a(-) (proT1) and CD34(+)CD45RA(+)CD7(++)CD5(+)CD1a(-) (proT2), were identified and their thymus engrafting capacity was examined, with proT2 cells showing a 3-fold enhanced reconstituting capacity compared with the proT1 subset. Furthermore, in vitro-generated CD34(+)CD7(++) progenitors effectively engrafted the thymus of immunodeficient mice, which was enhanced by the addition of an IL-7/IL-7 antibody complex. Taken together, the identification of T-progenitor subsets readily generated in vitro may offer important avenues to improve cellular-based immune-reconstitution approaches.
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PMID:Characterization in vitro and engraftment potential in vivo of human progenitor T cells generated from hematopoietic stem cells. 1949 95


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