Home FOR AUTHORS Neoplasma 2008 Neoplasma Vol.55, No.3, p.266-272, 2008

Journal info


6 times a year.
Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

Published in English

Editorial Info
Abstracted and Indexed
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Neoplasma Vol.55, No.3, p.266-272, 2008

Title: Prevalent expression of MHC class I chain-related molecule A in human osteosarcoma
Author: SM. LU, P. XIAO, L. XUE, LH. CHE, P. YANG, Y. LI, H. QIAO

Abstract: MHC class I chain-related molecule A (MICA) is one of the major ligands for activating immune-receptor NKG2D which is expressed on NK cells and cytotoxic T lymphocytes. The release and sustained expression of MICA protein can impair NKG2D-mediated cytotoxic activity by reducing NKG2D receptor on immune effector cells. The aim of the study was to investigate the expression and release of MICA in human osteosarcoma. RT-PCR, immunohistochemistry, western blotting and flow cytometry were used in analyzing the expression of MICA. Serum level of soluble MICA was quantitated by ELISA. Our data showed that MICA is prevalently expressed in osteosarcoma both in mRNA and protein level. Upregulation of MICA was found in osteosarcoma compared with benign tumors and normal bone tissues. Higher level of soluble MICA in serum can be detected in osteosarcoma patients. In conclusion, prevalent expression of MICA and higher serum level of soluble MICA may suggest a deficiency of MICA-NKG2D mediated immunosurveillance in osteosarcoma patients. Restoring the expression of NKG2D receptor on immune effector cells may contribute to a therapeutic strategy for human osteosarcoma.

Keywords: osteosarcoma; MICA; NKG2D; sMICA
Year: 2008, Volume: 55, Issue: 3 Page From: 266, Page To: 272

Price: 16.80 €






© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.