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Unique Markers (unique + marker)

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Medical Sciences100%

Selected Abstracts

Immunoreactivity of CD99 in invasive malignant melanoma

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 10 2006
Anne E. Wilkerson
Background:, CD99, also known as p30/32, is a glycoprotein product of the MIC2 gene. It was originally utilized in immunohistochemistry as a unique marker for Ewing sarcoma, other primitive neuroectodermal tumors, and subsequently in other tumors. Its expression in malignant melanoma (MM) has not been well documented, with just two isolated cases of MM recently reported. Recent studies have documented CD99 expression in a significant percentage of atypical fibroxanthomas (AFX), posing potential diagnostic problems in differentiating these two entities. As mistaking MM for AFX based on immunohistochemical staining pattern has significant consequences, we sought to determine the percentage of invasive MM in our archives that have this staining pattern. Methods:, Seventy-eight cases of invasive melanoma were retrieved from our files. Each case was stained with mouse anti-human CD99 and evaluated for membranous expression. Results:, Our evaluation revealed that 47 of 78 MM cases (60%) stain positive for CD99. Conclusion:, This study is the first to demonstrate, in a large series, the prevalence of CD99 expression in primary cutaneous melanoma. Additionally, this introduces in the histologic differential diagnosis of CD99 expressing dermal spindle cell lesions. [source]

CD99 Immunoreactivity in Metastatic Malignant Melanoma

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2005
AE Wilkerson
CD99, also known as p30/32, is a glycoprotein product of the MIC2 gene, which is located on the short arm of both chromosome X and Y. This transmembrane protein was originally utilized in immunohistochemistry as a unique marker for Ewing sarcoma, other primitive neuroectodermal tumors, and more recently in a wide variety of tumors. It's expression in malignant melanoma (MM) has not been well documented. A recent study at our institution demonstrated membranous staining in approximately 61% of primary MM. As CD99 is expressed by hematopoeitic cells, it has been proposed as a mechanism for lymphocytes to gain access to the vasculature.1 This study is designed to determine if CD99 expression in melanoma cells has a similar role using cases of metastatic MM from our archives. Our evaluation shows that 13 of 28 cases (46.4%) demonstrated membranous CD99 staining. A case of this magnitude has not been previously reported. Reference: 1. Shenkel AR, Mamdouh Z, Chen X, Liebman RM, Muller WA. CD99 plays a major role in the migration of monocytes through endothelial junctions. Nature Immunol 2002;3:143,150. [source]

ORIGINAL ARTICLE: Correlation Between Natural Cytotoxicity Receptors and Intracellular Cytokine Expression of Peripheral Blood NK Cells in Women with Recurrent Pregnancy Losses and Implantation Failures

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 6 2009
Atsushi Fukui
Problem, Natural cytotoxicity receptors (NCRs) are unique markers, which regulate NK cell cytotoxicity and cytokine production. We investigated whether women with recurrent pregnancy losses (RPLs) and implantation failures have aberrant correlation between NCRs and intracellular cytokine expression of NK cells. Method of study, Peripheral blood NK cells (CD56dim and CD56bright) were analyzed for NCRs (NKp46, NKp44 and NKp30) and cytokine expression (TNF-,, IFN-,, IL-4, IL-10) using flow cytometry in RPL (n = 22), implantation failures (n = 23) or controls (n = 15). Results, In type 1 cytokine studies, CD56bright/NKp30+ cells in controls (r = 0.696, P < 0.05) were positively correlated with CD56bright/IFN-,+/TNF-,+ cells. CD56bright/NKp46+ cells in implantation failures (r = ,0.76, P < 0.01) were negatively correlated with CD56bright/IFN-,+/TNF-,, cells. RPL did not have any correlation. In type 2 cytokine studies, CD56+/NKp46+ cells (r = 0.758, P < 0.01) and CD56+/NKp30+ cells (r = 0.637, P < 0.05) were positively correlated with CD56bright/IL-4+/IL-10+ cells in controls. CD56+/NKp30+ cells in implantation failures (r = ,0.778, P < 0.05) were negatively correlated with CD56bright/IL-10+/IL-4+ cells. There were no correlations in RPL. Conclusion, Recurrent pregnancy losses and implantation failures have lack of, or negative correlation between NCRs and intracellular cytokines expression. This observation suggests that excessive pro-inflammatory cytokine expression in NK cells in RPL and implantation failures may be exerted through the NCRs or interruption of signal transduction processes. [source]

1141154113 Expression of natural cytotoxicity receptors in peripheral blood NK cell subsets of women with recurrent spontaneous abortions (RSA) or implantation failures

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 6 2006
A Fukui
Problem:, Natural Cytotoxicity Receptors (NCRs) are unique markers of NK cells and regulate NK cell cytotoxicity and cytokine production. a2V-ATPase is expressed in the cell membrane and can regulate the pH of the extracellular environment, which might facilitate NK cell killing or cytokine secretion. In this preliminary study we evaluated the expression of NCRs and a2V-ATPase in peripheral blood NK cells of women with RSA or implantation (IVF-ET) failures. Method of Study:, Peripheral blood was obtained from women with RSA (n = 10), or IVF-ET failures (n = 9). CD56dim and CD56bright NK cells were analyzed for the expression of NCRs (NKp46, NKp44 and NKp30) and a2V-ATPase using flow cytometry. Results:, For women with RSA, there were significant differences in the expression of NKp46 between CD56dim (36.9 ± 30.2) and CD56bright (76.0 ± 27.5) (P < 0.01), of NKp30 between CD56dim (30.9 ± 25.7) and CD56bright (55.8 ± 29.5) (P < 0.01), and of a2V-ATPase between CD56dim (1.0 ± 0.9) and CD56bright (23.2 ± 15.1) (P < 0.01) NK cells. For women with IVF-ET failures, there were significant differences in the expression of NKp46 between CD56dim (39.5 ± 21.5) and CD56bright (78.8 ± 26.0) (P < 0.01), of NKp30 between CD56dim (27.2 ± 17.9) and CD56bright (45.2 ± 29.8) (P < 0.05), and of a2V-ATPase between CD56dim (1.6 ± 1.4) and CD56bright (21.2 ± 16.5) (P < 0.01) NK cells. Conclusions:, The differential expression of NCRs and a2V-ATPase in NK cell subsets of women with RSA and IVF-ET failures may have an effect in cytotoxicity and cytokine production. Additional studies are currently in effect to evaluate these activities. We suggest that the analysis of NCRs and a2V-ATPase expression in peripheral blood NK cell subsets may contribute to a better understanding in the biology of NK cells in women with RSA or IVF-ET failures. [source]

A Transgenic Insertional Inner Ear Mutation on Mouse Chromosome 1,

THE LARYNGOSCOPE, Issue 4 2000
Rick A. Friedman MD
Abstract Objectives/Hypothesis To clone and characterize the integration site of an insertional inner ear mutation, produced in one of fourteen transgenic mouse lines. The insertion of the transgene led to a mutation in a gene(s) necessary for normal development of the vestibular labyrinth. Study Design Molecular genetic analysis of a transgene integration site. Methods Molecular cloning, Southern and northern blotting, DNA sequencing and genetic database searching were the methods employed. Results The integration of the transgene resulted in a dominantly inherited waltzing phenotype and in degeneration of the pars superior. During development, inner ear fluid homeostasis was disrupted. The integration consisted of the insertion of a single copy of the transgene. Flanking DNA was cloned, and mapping indicated that the genomic DNA on either side of the transgene was not contiguous in the wild-type mouse. Localization of unique markers from the two flanks indicated that both were in the proximal region of mouse chromosome 1. However, in the wild-type mouse the markers were separated by 6.3 cM, indicating a sizable rearrangement. Analysis of the mutant DNA indicated that the entire region between the markers was neither deleted nor simply inverted. Conclusions These results are consistent with a complex rearrangement, including at least four breakpoints and spanning at least 6.3 cM, resulting from the integration of the transgene. This genomic rearrangement disrupted the function of one or more genes critical to the maintenance of fluid homeostasis during development and the normal morphogenesis of the pars superior. [source]