An Immunohistochemical Study of the Expression of Adhesion Molecules in Gallbladder Lesions

Choi, Yoon–La; Xuan, Yan; Shin, Young Kee; Chae, Seoung Wan; Kook, Myeong Cherl; Sung, Rohyun; Youn, Sei Jin; Choi, Jae Woon; Kim, Seok Hyung

doi:10.1177/002215540405200504

Cited by 46 publications

(34 citation statements)

References 45 publications

(43 reference statements)

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“…CD99 down-regulation was clearly associated with increased direct tumor invasion and nodal metastasis. This agrees well with our previous clinicopathologic study for the loss of CD99 expression in gallbladder carcinomas (23). Notably, the CD99-overexpressing AGS cell line showed reduced migration and proliferation, and CD99 knockdown in MKN74 increased migration.…”

Section: Discussionsupporting

confidence: 92%

“…Recently, it was proposed that CD99 downregulation, induced by the EBV-encoded latent membrane protein-1, in B cells is involved in the pathogenesis of Hodgkin's disease (17). Furthermore, the increased or decreased expression of CD99 has been also suggested to act as a marker of various kinds of tumors, including Ewing's sarcoma/ primitive neuroectodermal tumor (18), lymphoblastic lymphoma/leukemia (19), some rhabdomyosarcomas (20), granulose cell tumor and sertoli-leydig cell tumor of the ovary (21), pancreatic endocrine tumors (22), gallbladder carcinoma (23), and stomach carcinoma (24). Based on these previous reports, we speculated that altered CD99 expression could also be a prognostic marker for gastric carcinoma patients.…”

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confidence: 99%

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Clinical Significance of CD99 Down-Regulation in Gastric Adenocarcinoma

Lee

Kim

Wang

et al. 2007

Clinical Cancer Research

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Purpose: CD99 is a cell adhesion molecule associated with human tumors. The aim of the present study was to characterize its role in the development and progression of human gastric adenocarcinoma. Experimental Design: The expression of CD99 was investigated in 283 gastric adenocarcinomas and related lesions and 9 gastric carcinoma cell lines.We also analyzed the methylation status of CD99 gene by using methylation-specific PCR and examined loss of heterozygosity (LOH) of this gene locus by using an intragenic marker. Moreover, we assessed whether SP1, a positive transcription factor for CD99, is expressed in these samples. Results: We found that the decreased expression of CD99 was strongly associated with poor survival and unfavorable clinicopathologic variables. Promoter region methylation (15 of 89, 16.9%) and LOH (21 of 74, 28.4%) were observed and significantly associated with CD99 down-regulation (P < 0.05). In addition, most of the gastric adenocarcinoma cases with CD99 down-regulation had reduced expression of SP1 (47 of 103, 45.6%; P < 0.01). This relationship between CD99 and SP1was consolidated by using SP1small interfering RNA transfection experiment and CD99 promoter luciferase assay. Furthermore, we showed that CD99 down-regulation was associated with proliferation and migration in gastric carcinoma cell line. Conclusion: These observations suggest that CD99 down-regulation is a critical event in the progression of gastric adenocarcinoma, and CD99 promoter methylation, CD99 LOH, and SP1 down-regulation were responsible for the down-regulation of CD99.

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Section: Discussionsupporting

confidence: 92%

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confidence: 99%

Clinical Significance of CD99 Down-Regulation in Gastric Adenocarcinoma

Lee

Kim

Wang

et al. 2007

Clinical Cancer Research

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“…In the diagnostic armamentarium, CD56 is a specific histological immune marker for malignant nervous tumors like medulloblastoma and astrocytoma, malignant NK/T-cell lymphomas (NK/T-NHLs), and neuroendocrine carcinoma. Its over expression in malignant cells is linked with an aggressive tumor type, insufficient therapeutic response, and a reduced survival time in different malignancies including lymphoblastic and myeloid leukemias (ALLs/AML), malignant melanoma (Johnson, 1999;Abbott et al, 2004), and different cancers (Pujol et al, 1993;Zoltowska et al, 2001;Daniel et al, 2003Choi et al, 2004Cho et al, 2006;Evans et al, 2006;). It has been reported in different types of epithelial malignancies and sarcomas like Ewings /PNET (McKenzie et al, 1981;Lipinski et al, 1987;Gardner et al, 1998;Farinola et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Is the Tumor Infiltrating Natural Killer Cell (NK-TILs) Count in Infiltrating Ductal Carcinoma of Breast Prognostically Significant?

Rathore

Goel²,

Makker³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Asian Pac J Cancer Prev, 15 (8), 3757-3761 IntroductionBreast cancer is the most common cause of cancer death in women worldwide (Key et al., 2001), and represents the leading or second most leading cancer in females in India (Ferlay et al., 2010;D'Souza et al., 2013a;2013b). Currently, two major challenges of breast cancer research are; to understand the interrelation between breast cancer and anti-tumor immunity, and to identify candidates whose targeting would contribute to enhance anti-tumor efficiency (Mamessier et al., 2012).The cancer tissue is invaded by a mixed population of immune cells, including T-cells, B-cells, natural killer (NK) cells and macrophages. For a long time NK cells were considered merely as relatively primitive killers, but now they are seen not only as bonafide actors in innate immunity but are also important cells that shape and influence the adaptive immune responses (Poli et al., 2009). NK cells are effector lymphocytes of innate immune system that act by limiting the growth and dissemination of the tumor and are known to have an immunoregulatory role.An established marker for NK cells, CD56, is an AbstractPurpose: The aim of this study was to investigate the prognostic significance of the CD56+NK-TIL count in infiltrating ductal carcinoma (IDC) of breast. Material and Methods: Immunohistochemistry (IHC) was performed using antibodies specific for CD56 on formalin-fixed and paraffin-embedded tissue sections of 175 infiltrating ductal carcinomas (IDC) of breast. Distribution of intratumoral and stromal CD56+NK-TILs was assessed semi-quantitatively. Results: A low intratumoral CD56+count showed significant and inverse associations with tumor grade, stage, and lymph node status, whereas it had significant and direct association with response to treatment indicating good prognosis. These patients had better survival (χ 2 =4.80, p<0.05) and 0.52 fold lower death rate (HR=0.52, 95% CI=0.28-0.93) as compared to patients with high CD56+ intratumoral count. The association of survival was insignificant with low CD56 stromal count as compared to high CD56 stromal count (χ 2 =1.60, p>0.05). Conclusion: To conclude, although NK-TIL count appeared as a significant predictor of prognosis, it alone may not be sufficient for predicting the outcome considering the fact that there exists a crosstalk between NK-TILs and the other immune infiltrating TILs.

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“…13 NCAM expression is a marker for neuroendocrine carcinomas of the lung 14,15 and in other organs. 16,17 Aberrant expression has also been detected in renal cell carcinoma, 18 pancreatic adenocarcinoma and b cell tumors, 19,20 in tumors of the salivary gland 21 and gall bladder, 22 and cases of breast and colon carcinoma. 23,24 In line with the adhesive functions of NCAM, low or absent NCAM expression in carcinomas was correlated with a metastatic phenotype and poor survival rates.…”

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Blockade of natural killer cell‐mediated lysis by NCAM140 expressed on tumor cells

Jarahian

Watzl

Issa

et al. 2007

Intl Journal of Cancer

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Expression of the neural cell adhesion molecule (NCAM) on malignant cells of neuroendocrine, epithelial and hematopoeitic origin has been reported, but its role for tumor cell recognition by the immune system remained uncertain so far. We have studied the cytotoxicity of the natural killer (NK) cell line NK92 and polyclonal NK cells from different donors, against NCAM-deficient and NCAM-transfected tumors. While the pancreatic carcinoma PANC-1 and the glioblastoma T98G showed no enhanced susceptibility to NK lysis after NCAM transfection, de novo NCAM expression in HeLa cervical carcinoma, SHEP neuroblastoma and the multiple myeloma lines RPMI-8226 and LP-1 was associated with significantly decreased lysis by NK cells. Binding of an NCAM-specific monoclonal antibody to NCAM-positive target cells was able to reverse the reduced lysis susceptibility. Conjugate formation of NCAM-expressing tumor cells with NK cells was blocked and could be restored by anti-NCAM. NK cell-expressed NCAM molecules which might engage in homotypic cis-or trans-interactions had no apparent inhibitory function. The known cis-ligands of NCAM, heparan sulfate proteoglycan and L1-CAM, were also not directly involved in NK inhibition. ICAM-1 mRNA and cell surface expression was downmodulated in NCAM-transfected HeLa cells. ICAM-1 is involved in killer cell immune synapse formation. Its downmodulation may therefore contribute to the reduced lysis of NCAM-expressing target cells. We conclude that aberrant expression of NCAM on tumor cells of different histogenetic origin can lead to inhibition of target cell recognition and lysis by NK cells. ' 2007 Wiley-Liss, Inc.

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An Immunohistochemical Study of the Expression of Adhesion Molecules in Gallbladder Lesions

Cited by 46 publications

References 45 publications

Clinical Significance of CD99 Down-Regulation in Gastric Adenocarcinoma

Clinical Significance of CD99 Down-Regulation in Gastric Adenocarcinoma

Is the Tumor Infiltrating Natural Killer Cell (NK-TILs) Count in Infiltrating Ductal Carcinoma of Breast Prognostically Significant?

Blockade of natural killer cell‐mediated lysis by NCAM140 expressed on tumor cells

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