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위암에서의 Transforming Growth Factor-B의 발현에 대한 연구
구자영(Ja Young Koo),공덕경(Deuk Kyung Kong),박종남(Jeong Nam Park),박선자(Seon Ja Park),정숙금(Seuk Kum Chung),허만하(Man Ha Huh) 대한소화기학회 1996 대한소화기학회지 Vol.28 No.3
N/A Background/Aims: Transforming growth factor-g(TGF-g), mutifanctional cytokine, has been suggested to have many actions related to tumor progression and tumor cell behavior, because of its increased expression in cancer cells. Only small number of studies were done for its role in gastric carcinoma, and we have conducted this study to elucidate in depth the role of TGF-/3 in gastric carcinoma progression. Methods: Expression of TGF-/3, epidermal growth factor(EGF), p53 and proliferating cell nuc1ear antigen(PCNA) in gastric carcinoma was studied by immunohi- stochemical method applied to paraffin-embedded tissue sections of endoscopic biopsy materials of 71 cases of gastric carcinoma(24 early and 47 advanced) and imrnunoreactivity of antigens was correlated with histological differentintion of carcinoma, degree of tumor infiltration of mononu- clear cells, serum levels of alphafetoprotein(AFP) and carcinoembryonic antigen(CEA), and pre- sence of distant metastases. Results: TGF-0 in carcinoma tissue was expressed in 31 cases(43.7%) of total 71 cases, and immunopositivity of TGF-0 in advanced gastric carcinoma(AGCj was 55.3%, which was much higher than that(20.8%) of early gastric carcinoma(EGC)(pC0.05). 1here was no significant difference in imrnunopositivity of TGF-0 between different differentiation group. There was negative correlation between expression of TGF-g and degree of tumor infiltration of mono- nuclear cells(p0.05). Immunopositivity of TGF-0 in AGC group was significantly higher in the cases with elevated serum AFP level(82.6%) than that with normal serum AFP leve1(29.1%)(p. 0.05), and also was significantly higher in the cases with elevated serum CEA level(87.6%) than that with normal serum CEA level(40.6%)(pw0.05). There was no correlation between expression of TGF-g and presence of distant metastases or metastatic sites. There was significant positive correlation between expression of TGF-g and EGF(p=0.004), TGF-g and p53(p=0.02) but no correlation between expression of TGF-g and PCNA. Conclusions: Above data indicate that TGF-f3 rnay contributes to gastric carcinoma progression by immunosuppressive action and fibrosis, by growth-stimulatory action via EGF modulation, and that loss of growth-inhibitory effects of TGF-0 on gastric carcinoma, which is related to p53 mutation, may be a critical factor in gastric carcinoma progression. (Korean J Gastroenterol 1996;28:336 - 348)