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

The goal of the present paper was to define the immunophenotype of bone marrow mast cells (BMMC) from healthy controls and patients with hematologic malignancies (HM) based on the use of multiple stainings with monoclonal antibodies analyzed by flow cytometry. Our results show that BMMC from both groups of individuals display a similar but heterogeneous immunophenotype. The overall numbers of BMMC are higher in the HM group of individuals (p = 0.08). Three patterns of antigen expression were detected: (1) markers constantly positive in all cases analyzed (CD9, CD29, CD33, CD43, CD44, CD49d, CD49e, CD51, CD71, CD117, and Fc(epsilon)RI), (2) antigens that were constantly negative (CD1a, CD2, CD3, CD5, CD6, CD11a, CD14, CD15, CD16, CD19, CD20, CD21, CD23, CD25, CD30, CD34, CD38, CD41a, CD42b, CD65, CD66b, HLA-DR, and CD138), and (3) markers that were positive in a variable proportion of cases--CD11b (50%), CD11c (77%), CD13 (40%), CD18 (20%), CD22 (68%), CD35 (27%), CD40 (67%), CD54 (88%) and CD61 (40%). In addition, BMMC from all cases explored were CD45+, and this antigen was expressed at an intensity similar to that of mature granulocytes. In summary, our results show that BMMC from both healthy controls and HM patients display a relatively heterogeneous immunophenotype. Interestingly, we have observed clear differences between the immunophenotype of BMMC and MC from other tissues. This could be due either to the heterogeneity of human MC according to their tissue localization or to the sensitivity of the method used for antigen detection.
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PMID:Immunophenotypic characterization of human bone marrow mast cells. A flow cytometric study of normal and pathological bone marrow samples. 969 44

Cytologic, immunologic, and cytogenetic studies were performed on the blast cells of a newborn with Down syndrome and transient myeloproliferative disease. This hematologic disorder is uncommon, and occurs primarily in infants with Down syndrome. This boy presented with a high white blood cell count and a high percentage of blast cells, without anemia or thrombocytopenia. Chromosome analysis showed a constitutional trisomy 21 without any other clonal abnormality. A three-color flow cytometric analysis was performed and revealed two different CD45 dim, CD34(+), CD117(+), CD56(+) immature subpopulations: the normal immature myeloid precursor and an immature blast cell population that expressed CD41, CD42, CD61, CD36, CD13, CD1a, and CD2. We postulate that this population could be the leukemic precursor involved in the acute megakaryoblastic leukemia frequently observed in children with Down syndrome.
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PMID:Immunophenotype of a transient myeloproliferative disorder in a newborn with trisomy 21. 1079 50

At the ISAC 2000 Congress, the Clinical Cytometry Society organized a meeting of international experts to reach consensus on the minimum number of antibodies required for a full evaluation of hematologic and lymphoid neoplasias. A questionnaire was distributed prior to the meeting to numerous experts from US and European institutions and 13 responses were received. At the meeting, 25 individuals, including most of those who returned responses, participated in the discussions and voted on the issues presented. In chronic lymphoproliferative disorders (CLD), 9 antibodies (anti-CD5, CD19, kappa, lambda, CD3, CD20, CD23, CD10, and CD45) were deemed essential for initial evaluation by 75% of the participants. There was near unanimity that additional markers (selected from CD22, FMC7, CD11c, CD103, CD38, CD25, CD79b and heavy chains for B-cell disorders, and CD4, CD7, CD8, CD2, CD56, CD16, TCRa/b, and TCRg/d for T-cell disorders) would be needed to fully characterize CLD, although not every marker would be useful in all cases. Tissue lymphomas were believed to be similar to CLD, needing a minimum of 12--16 markers. However, for some cases, CD30, bcl-2, TdT, CD71, CD1a, and CD34 were cited as useful by the participants. Markers mentioned for plasma cell disorders included kappa, lambda, CD38, CD45, CD56, CD19, CD20, CD138, and heavy chains. Of 17 voting participants, 16 agreed that between 5 to 8 markers would be essential reagents for plasma cell disorders. For acute leukemia (AL), 10 markers (CD10, CD19, CD13, CD33, CD34, CD45, CD7, CD14, CD3, and HLADR) were considered essential by 75% of participants for initial characterization of the leukemia lineage. Most (>75%) agreed that at least one more B (CD20, CD22, CD79a, IgM), T (CD1a, CD2, CD4, CD5, CD8), myeloid (CD11b, CD15, CD64, CD117, myeloperoxidase), erythroid (CD36, CD71, glycophorin A), and megakaryocytic (CD41, CD61) reagents should be included in the essential panel. However, there was no agreement as to which was optimal. Thus, approximately 13--15 of those reagents would be considered essential in all cases of AL, whereas others (CD16, CD56, CDw65, TdT, and cytoplasmic CD3) were mentioned as useful in some cases. Almost all voting participants believed that the appropriate number of markers for complete characterization of AL would average 20--24. The majority of the responders (11 of 13) indicated that fewer reagents could be used in monitoring or staging patients with previously characterized disease, but not all ventured a specific number of reagents. From the above results, we conclude that the phenotypic analysis of hematologic and lymphoid neoplasia requires a rather extensive panel of reagents. Supplementary reagents might even be necessary if they prove to become relevant for diagnostic purposes. Reducing the number of antibodies could significantly compromise the diagnostic accuracy, appropriate monitoring, or therapy of these disorders.
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PMID:Optimal number of reagents required to evaluate hematolymphoid neoplasias: results of an international consensus meeting. 1124 3

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

We describe here--presumably for the first time--a Cajal-like type of tubal interstitial cells (t-ICC), resembling the archetypal enteric ICC. t-ICC were demonstrated in situ and in vitro on fresh preparations (tissue cryosections and primary cell cultures) using methylene-blue, crystal-violet, Janus-Green B or MitoTracker-Green FM Probe vital stainings. Also, t-ICC were identified in fixed specimens by light microscopy (methylene-blue, Giemsa, trichrome stainings, Gomori silver-impregnation) or transmission electron microscopy (TEM). The positive diagnosis of t-ICC was strengthened by immunohistochemistry (IHC; CD117/c-kit+ and other 14 antigens) and immunofluorescence (IF; CD117/c-kit+ and other 7 antigens). The spatial density of t-ICC (ampullar-segment cryosections) was 100-150 cells/mm2. Non-conventional light microscopy (NCLM) of Epon semithin-sections revealed a network-like distribution of t-ICC in lamina propria and smooth muscle meshwork. t-ICC appeared located beneath of epithelium, in a 10-15 microm thick 'belt', where 18+/-2% of cells were t-ICC. In the whole lamina propria, t-ICC were about 9%, and in muscularis approximately 7%. In toto, t-ICC represent ~8% of subepithelial cells, as counted by NCLM. In vitro, t-ICC were 9.9+/-0.9% of total cell population. TEM showed that the diagnostic 'gold standard' (Huizinga et al., 1997) is fulfilled by 'our' t-ICC. However, we suggest a 'platinum standard', adding a new defining criterion- characteristic cytoplasmic processes (number: 1-5; length: tens of microm; thickness: < or =0.5 microm; aspect: moniliform; branching: dichotomous; organization: network, labyrinthic-system). Quantitatively, the ultrastructural architecture of t-ICC is: nucleus, 23.6+/-3.2% of cell volume, with heterochromatin 49.1+/-3.8%; mitochondria, 4.8+/-1.7%; rough and smooth endoplasmic-reticulum (1.1+/-0.6%, 1.0+/-0.2%, respectively); caveolae, 3.4+/-0.5%. We found more caveolae on the surface of cell processes versus cell body, as confirmed by IF for caveolins. Occasionally, the so-called 'Ca2+-release units' (subplasmalemmal close associations of caveolae+endoplasmic reticulum+mitochondria) were detected in the dilations of cell processes. Electrophysiological single unit recordings of t-ICC in primary cultures indicated sustained spontaneous electrical activity (amplitude of membrane potentials: 57.26+/-6.56 mV). Besides the CD117/c-kit marker, t-ICC expressed variously CD34, caveolins 1&2, alpha-SMA, S-100, vimentin, nestin, desmin, NK-1. t-ICC were negative for: CD68, CD1a, CD62P, NSE, GFAP, chromogranin-A, PGP9.5, but IHC showed the possible existence of (neuro)endocrine cells in tubal interstitium. We call them 'JF cells'. In conclusion, the identification of t-ICC might open the door for understanding some tubal functions, e.g. pace-making/peristaltism, secretion (auto-, juxta- and/or paracrine), regulation of neurotransmission (nitrergic/purinergic) and intercellular signaling, via the very long processes. Furthermore, t-ICC might even be uncommitted bipotential progenitor cells.
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PMID:Novel type of interstitial cell (Cajal-like) in human fallopian tube. 1596 70

We describe here an interstitial Cajal-like cell type (ICLC) in human gallbladder, resembling the archetypal enteric interstitial cells of Cajal. Gallbladder ICLC were demonstrated in fresh preparations (tissue cryosections) using methylene-blue, and fixed specimens in Epon semi-thin sections stained with toluidine blue or transmission electron microscopy (TEM). The positive diagnosis of gallbladder ICLC was further verified by immunohistochemistry: CD117/c-kit, CD34, and another 16 antigens: vimentin, desmin, nestin, alpha-smooth muscle actin, NK-1, S-100, PGP-9.5, tau protein, chromogranin A, NSE, GFAP, CD1a, CD62-P, CD68, estrogen and progesterone receptors. Double immunostaining was performed for CD117, CD34 and CD117 and nestin, respectively. In fresh specimens, the spatial density of gallbladder ICLC was 100-110 cells/mm(2). ICLC mainly appeared beneath the epithelium and in muscularis (about 7%, and approximately 5%, respectively). In toto, ICLC represent in gallbladder approximately 5.5% of subepithelial cells. TEM showed that diagnostic criteria were fulfilled by ICLC. Moreover, TEM indicated that the main ultrastructural distinctive feature for ICLC, the cell processes, develop into the characteristic shape at a relatively early stage of development. It remains to be established if, in humans, ICLC are involved in gallbladder (dis)functions (e.g. pace-making, secretion (auto-, juxta- and/or paracrine), intercellular signaling, or stone formation).
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PMID:Interstitial Cajal-like cells in human gallbladder. 1754 11

Lymphoepithelioma-like carcinoma (LELC) of the urinary bladder is often mixed with conventional transitional cell carcinoma and/or other histotypes. The pathologist's determination of the morphologic purity of a given LELC at the biopsy stage is a clinically relevant endeavour, because there is some anecdotal evidence suggesting that pure or predominant LELC may be comparatively chemosensitive and have a favorable prognostic profile, which may potentially offer the possibility of effective therapy without bladder resection. The precise degree of cellular pleomorphism that is allowed in a pure LELC is unclear. We describe herein an otherwise conventional and pure LELC that showed, in a localized area that constituted approximately 25% of the overall tumor volume, a two to six fold variation in nuclear size, including multinucleated tumor cells. These pleomorphic areas were set in the same lymphoplasmacytic infiltrate as their conventional counterparts, and similarly displayed cellular syncytia. We performed a detailed immunophenotypic comparison between the conventional areas and the pleomorphic areas. No significant differences were found between the 2 areas in overall lymphoplasmacytic or histiocytic density, lymphocytic CD4/CD8 ratio, and lymphoplasmacytic kappa/lambda ratio. Similarly, both displayed similar qualitative and quantitative staining indices for p53, Ki67, cytokeratin AE1/AE3 and p16(INKa). Scattered cells were cytoplasmically beta-catenin positive exclusively in the pleomorphic areas; however these cells were not notably larger than the cells in the conventional areas. Both components were immunohistochemically negative for HMB-45, CD1a, the estrogen receptor, Epstein-Barr virus, CD117, D2-40, CD56, cytokeratin 20 and chromogranin. Clinicopathologic analysis of a series of cases is required to establish if there is any significance to nuclear pleomorphism in LELC. However, the phenotypic similarity between the 2 areas in this case, the intimate admixture of the pleomorphic cells with the lymphoplasmacytic infiltrate, and their syncytial pattern of growth, all suggest that pure LELC may display marked nuclear pleomorphism, and that this finding may not, in of itself, be a valid basis for removing a case from the "pure" group.
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PMID:Pleomorphic lymphoepithelioma-like carcinoma of the urinary bladder. 1907 56

An 11-year old Caucasian female with a remote history of urticaria pigmentosa presented with a neck mass. A biopsy demonstrated a large intradermal nodule composed of unusually large epithelioid mast cells, including a prominent subset with bi-lobed and multi-lobed nuclei. By immunohistochemistry, the cells expressed CD117 (C-Kit), mast cell tryptase, CD68, and CD25, and were negative for CD163, CD1a, and S-100, confirming the diagnosis of mastocytoma. Equally prominent was an admixed infiltrate of CD68 and CD163-positive xanthomatous histiocytes that included Touton-type giant cells. Eosinophils were abundant. At 7 months follow-up, there was no recurrence of the lesion following complete excision. However, given the unusual cytologic features, close clinical observation is warranted, as the long-term biologic potential of mastocytoma with this degree of cytologic atypia is uncertain. Awareness of this unusual morphologic variant is also important as the histologic features may mimic such childhood neoplasms as juvenile xanthogranuloma and Langerhans cell histiocytosis.
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PMID:Histiocyte-rich pleomorphic mastocytoma: an uncommon variant mimicking juvenile xanthogranuloma and Langerhans cell histiocytosis. 1960 70

Atypical fibroxanthoma (AFX) is a rare skin tumor that generally pursues an indolent course despite its alarming histological appearances. It is important for the pathologist to distinguish this neoplasm from more aggressive lesions that may show very similar histological features. Recently, it has been suggested that demonstration of CD117 is of value in identifying AFX. To test this hypothesis, 50 cases of AFX were stained immunohistochemically for CD117 to determine the diagnostic value of this antibody. Cases were also stained for tryptase to identify mast cells, which are CD117 positive. In addition, S100 and CD1a stains were performed to assess any possible contribution of melanocytes or Langerhans cells to CD117 staining. Only 1 of 50 AFXs (2%) showed CD117 positivity in the neoplastic cells, but all tumors demonstrated included CD117- and tryptase-positive mast cells in similar distribution. CD117 is only rarely stainable in the neoplastic cells of AFX and is therefore not useful in identifying these tumors. Mast cells are also CD117 positive, frequently present in AFX, and can lead to misinterpretation. Using immunohistochemistry for mast cell tryptase may be of value where there is doubt as to the nature of CD117-positive cells in neoplasms.
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PMID:CD117 is not a useful marker for diagnosing atypical fibroxanthoma. 2052 72

It is sometimes difficult to differentiate between type B3 thymoma from thymic carcinoma histologically. Given the rarity of these tumours, studies have been limited. A series of 66 thymic neoplasms were reviewed and classified according to the World Health Organization (WHO) scheme. We performed a tissue microarray analysis of surgically resected thymic tumour specimens including 12 thymic carcinomas, 17 type B3 thymomas and 37 thymomas of other types. Percentage and staining intensity of immunohistochemical markers were recorded. Tumour eosinophilia was recorded positive if at least one eosinophilic cell identified. Positive staining of the following markers significantly differentiated type B3 thymoma from thymic carcinoma: cytokeratin 5/6 (15 vs. 3), Mesothelin (0 vs. 5), cytoplasmic androgen receptor (10 vs. 0), CD57 (9 vs. 0), CD5 (0 vs. 7), TdT (lymphocytic) (14 vs. 1), CD1a (lymphocytic) (14 vs. 2), CD117 (1 vs. 9), MOC31 (2 vs. 6), p21 (2 vs. 8), cytoplasmic Survivin (0 vs. 4), and tumour eosinophilia (1 vs. 11). Combining two or three markers was able to differentiate these two tumours with area under the curve percentage of at least 92%. Tumour eosinophilia combined with a panel of immunohistochemistry could differentiate type B3 thymoma from thymic carcinoma.
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PMID:Tumour eosinophilia combined with an immunohistochemistry panel is useful in the differentiation of type B3 thymoma from thymic carcinoma. 2104 86


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