c-erbB-2 and episialin challenge host immune response by HLA class I expression in human non-small-cell lung cancer.

c-erbB-2 and episialin challenge host immune response by HLA class I expression in human non-small-cell lung cancer. Research Abstract Details 

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c-erbB-2 and episialin challenge host immune response by HLA class I expression in human non-small-cell lung cancer. Abstract Text:

M I Koukourakis,A Giatromanolaki,F Guddo,L Kaklamanis,M Vignola,S Kakolyris,H Turley,V Georgoulias,G Bonsignore,K C Gatter,A L Harris,

The role of major histocompatibility complex expression in cancer prognosis and pathogenesis is contradictory. The aim of the current study was to compare the expression of HLA class I molecules and of oncoproteins that may be sources of peptides presented by HLA class I antigens in non-small-cell lung cancer. For this purpose, the expression of HLA class I antigen and TAP-1 molecule (a transporter in the antigen-processing 1 transport protein) were studied with epidermal growth factor, receptor; c-erbB-2; episialin; wild-type and mutant p53; bcl-2 oncoprotein expression; and angiogenic factor expression (vascular endothelial growth factor and thymidine phosphorylase). The degree of lymphocytic stromal infiltration and of platelet-endothelial cell adhesion molecule-expressing lymphocytes was also studied. A strong association of c-erbB-2 and MUC1 (episialin) expression with HLA class I expression was observed (p = 0.005 and 0.009, respectively). Intense CD31-positive lymphocytic infiltration was also more frequent in HLA class I-positive cases (p = 0.05). Although there was no association of HLA class I expression with survival, loss of the HLA class I expression in MUC1 or c-erbB-2 overexpressing cases conferred a poorer clinical outcome (p = 0.04). Both c-erbB-2 and MUC1 are well-known targets of T-cell-mediated cytotoxicity and cell-cell or cell-matrix adhesion-regulating proteins. The authors provide evidence that the sequence of cell adhesion-disrupting oncoprotein expression, HLA class I induction, and enhanced epitope presentation followed by lymphocytic response is an important pathogenetic three-step sequence of events that define, in part, the clinical outcome in non-small-cell lung cancer.

c-erbB-2 and episialin challenge host immune response by HLA class I expression in human non-small-cell lung cancer. Publishing Authors By Initials

MI Koukourakis,A Giatromanolaki,F Guddo,L Kaklamanis,M Vignola,S Kakolyris,H Turley,V Georgoulias,G Bonsignore,KC Gatter,AL Harris,

For similar persons: patients: survivors research abstracts see: persons: patients: survivors research

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c-erbB-2 and episialin challenge host immune response by HLA class I expression in human non-small-cell lung cancer. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of immunotherapy (Hagerstown, Md. : 1997)

VOLUME: 23

Page Numbers: 104-14

Journal Abbreviation: J. Immunother.

ISSN: 1524-9557

DAY: 1

MONTH: Jan

YEAR: 2000

c-erbB-2 and episialin challenge host immune response by HLA class I expression in human non-small-cell lung cancer. Information

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LANGUAGE: eng

NlmUniqueID: 9706083

c-erbB-2 and episialin challenge host immune response by HLA class I expression in human non-small-cell lung cancer. Keywords Mesh Terms:

KEYWORDS: Survivors

MESH TERMS: immunology

Chemical & Substance for Abstract: c-erbB-2 and episialin challenge host immune response by HLA class I expression in human non-small-cell lung cancer. Information

Substance Name: Receptor, erbB-2

Registry Number: EC 2.7.1.112

Grant and Affiliation Information for c-erbB-2 and episialin challenge host immune response by HLA class I expression in human non-small-cell lung cancer.

AFFILIATION: Department of Radiotherapy/Oncology, University Hospital of Iraklion, Crete, Greece. targ@her.forthnet.gr

Country: UNITED STATES

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MEDLINETA: J Immunother (1997)

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