Zhonghua nei ke za zhi · 2004
[Proliferative changes of human gastric mucosa cells in different pathological lesions and their clinical significance].
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Liu Zheng-xin, Chen Bao-wen, Yang Gui-bin, Liu Ping, Zhang Xi-quan, Li Jiang, Jia Bo-qi
Аннотация
OBJECTIVE: To investigate the variation of cell proliferation and growth in different pathological lesions of gastric mucosa and to assess the possible roles of expression of epidermal growth factor receptor (EGFR), transforming growth factor beta receptor type I and type II (TGF(beta)RI, TGF(beta)RII).
METHODS: The proliferating cell nuclear antigen (PCNA), EGFR, TGF(beta)RIand TGF(beta)RII were studied in chronic superficial gastritis (CSG, n = 30), chronic atrophic gastritis (CAG, n = 26), intestinal metaplasia (IM,n = 40), Dysplasia (DYS, n = 22), early gastric cancer (EGC, n = 22), advanced gastric cancer (AGC, n = 26) by immunohistochemical methods and their relations with carcinogenesis were analyzed.
RESULTS: (1) In different gastric mucosa lesions (CSG, CAG, IM, DYS, EGC, AGC), there were significantly different expression of PCNA (chi2 = 91.06, P < 0.0001), EGFR (chi2 = 52.82, P < 0.0001), TGF(beta)RI (chi2 = 15.93, P = 0.007) and TGF(beta)RII (chi2 = 40.48, P < 0.0001), PCNA and EGFR were increased, TGF(beta)RI and TGF(beta)RII were decreased. (2) In DYS stage, PCNALI (40.00 +/- 16.34) was higher than in CSG (16.63 +/- 10.52), CAG (16.92 +/- 8.50) and IM (23.25 +/- 18.64), but lower than EGC (53.09 +/- 13.51) and AGC (57.54 +/- 16.88) (P < 0.0001); (3) EGFR expression in IM (55.0%) and DYS (72.7%) were higher than in CSG (10.0%) and CAG (3.8%) (P < 0.0001), but no different with EGC (59.1%) and AGC (73.1%). (4) TGF(beta)RI expression in EGC (50.0%) and AGC (30.8%) were lower than in CSG (73.3%) (P = 0.007). (5) TGF(beta)RII expression in AGC (26.9%) was lower than in CSG (83.3%), CAG (82.8%), IM (65.0%), DYS (54.5%) and EGC (45.5%) significantly (P < 0.0001). (6) The expression of EGFR had positive correlation with PCNA, TGF(beta)RI and TGF(beta)RII had negative correlation with PCNA respectively, TGF(beta)RI and TGF(beta)RII had positive correlation.
CONCLUSIONS: DYS is the key link in the change of cell proliferation during gastric carcinogenesis; The increase of EGFR and the decrease of TGF(beta)R may play important roles in promoting gastric carcinogenesis by affecting gastric cell proliferation.
METHODS: The proliferating cell nuclear antigen (PCNA), EGFR, TGF(beta)RIand TGF(beta)RII were studied in chronic superficial gastritis (CSG, n = 30), chronic atrophic gastritis (CAG, n = 26), intestinal metaplasia (IM,n = 40), Dysplasia (DYS, n = 22), early gastric cancer (EGC, n = 22), advanced gastric cancer (AGC, n = 26) by immunohistochemical methods and their relations with carcinogenesis were analyzed.
RESULTS: (1) In different gastric mucosa lesions (CSG, CAG, IM, DYS, EGC, AGC), there were significantly different expression of PCNA (chi2 = 91.06, P < 0.0001), EGFR (chi2 = 52.82, P < 0.0001), TGF(beta)RI (chi2 = 15.93, P = 0.007) and TGF(beta)RII (chi2 = 40.48, P < 0.0001), PCNA and EGFR were increased, TGF(beta)RI and TGF(beta)RII were decreased. (2) In DYS stage, PCNALI (40.00 +/- 16.34) was higher than in CSG (16.63 +/- 10.52), CAG (16.92 +/- 8.50) and IM (23.25 +/- 18.64), but lower than EGC (53.09 +/- 13.51) and AGC (57.54 +/- 16.88) (P < 0.0001); (3) EGFR expression in IM (55.0%) and DYS (72.7%) were higher than in CSG (10.0%) and CAG (3.8%) (P < 0.0001), but no different with EGC (59.1%) and AGC (73.1%). (4) TGF(beta)RI expression in EGC (50.0%) and AGC (30.8%) were lower than in CSG (73.3%) (P = 0.007). (5) TGF(beta)RII expression in AGC (26.9%) was lower than in CSG (83.3%), CAG (82.8%), IM (65.0%), DYS (54.5%) and EGC (45.5%) significantly (P < 0.0001). (6) The expression of EGFR had positive correlation with PCNA, TGF(beta)RI and TGF(beta)RII had negative correlation with PCNA respectively, TGF(beta)RI and TGF(beta)RII had positive correlation.
CONCLUSIONS: DYS is the key link in the change of cell proliferation during gastric carcinogenesis; The increase of EGFR and the decrease of TGF(beta)R may play important roles in promoting gastric carcinogenesis by affecting gastric cell proliferation.