| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Department of Medical Oncology [C. B., Y. A. L.], Department of Histopathology [C. C.], Ludwig Institute for Cancer Research (LondonSt. George's Group), London [Y. A. L.]; St. George's Hospital Medical School, Cranmer Terrace, London, SW17 ORE; and Department of Surgery, St. George's Hospital, Blackshaw Road, London, SW17 OQT [I. P.], United Kingdom
Expression of mRNA-encoding transforming growth factors
and ß (TGF
and ß), epidermal growth factor receptor (EGFR), and platelet-derived growth factors (PDGF) A and B chains was examined in 63 human gastric biopsies. Despite considerable individual variation, transcript levels were generally higher in 16 paired gastric tumors compared with surrounding epithelium. Marked increases were observed for the TGFs and c-sis, whereas EGFR mRNA was poorly expressed; there was no correlation with pathological staging of the cancers. In the nonneoplastic tissues, 14 had normal histology and 27 displayed superficial (SG) or atrophic gastritis (AG). Transcript levels
+ were similar between these categories for all the growth factors, but were about 50% higher for EGFR in the tissues with gastritis.
Concurrent expression of TGF
and EGFR (
+ level) was more frequent in the paired tumors (38%) than in adjacent nonmalignant tissue (6%) and was seen in only one of 14 (7%) normal samples, in three of 19 (16%) of those with AG, and none of eight of those displaying SG.
High levels of TGFß and PDGFA mRNA were expressed in gastric ulcers, with little or no TGF
and EGFR transcripts; in contrast both TGFs and EGFR message were found in normal oesophagus.
Stomach tissues are thus capable of synthesizing a variety of growth factors. These may be associated with nonneoplastic hyperplasia and/or malignant proliferation. Coexpression of TGF
/EGFR supports the possibility of an autocrine loop sustaining tumor growth which is different from the mechanisms responsible for normal cellular proliferation.
1 Supported by a grant from the South West Thames Regional Authority for Organized Research.
2 To whom requests for reprints should be addressed.
Received 5/16/88. Revised 11/28/88. Accepted 1/23/89.
This article has been cited by other articles:
![]() |
I. Garcia, F. Vizoso, A. Martin, L. Sanz, O. Abdel-Lah, P. Raigoso, and J.L. Garcia-Muniz Clinical Significance of the Epidermal Growth Factor Receptor and HER2 Receptor in Resectable Gastric Cancer Ann. Surg. Oncol., April 1, 2003; 10(3): 234 - 241. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Moragoda, R. Jaszewski, P. Kulkarni, and A. P. N. Majumdar Age-associated loss of heterozygosity of tumor suppressor genes in the gastric mucosa of humans Am J Physiol Gastrointest Liver Physiol, June 1, 2002; 282(6): G932 - G936. [Abstract] [Full Text] [PDF] |
||||
![]() |
H.-M. Lee, V. Udupi, E. W. Englander, S. Rajaraman, R. J. Coffey Jr., and G. H. Greeley Jr. Stimulatory Actions of Insulin-Like Growth Factor-I and Transforming Growth Factor-{alpha} on Intestinal Neurotensin and Peptide YY Endocrinology, September 1, 1999; 140(9): 4065 - 4069. [Abstract] [Full Text] |
||||
![]() |
H. Ishikawa, D. Carrasco, E. Claudio, R.-P. Ryseck, and R. Bravo Gastric Hyperplasia and Increased Proliferative Responses of Lymphocytes in Mice Lacking the COOH-terminal Ankyrin Domain of NF-kappa B2 J. Exp. Med., October 6, 1997; 186(7): 999 - 1014. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |