Expression of beta-catenin, Glut-1, PTEN proteins in uterine endometrioid adenocarcinoma and its precursor lesions / 中华病理学杂志

<p><b>OBJECTIVE</b>To explore the expression of beta-catenin, Glut-1, PTEN in uterine endometrioid adenocarcinoma and their roles in tumorigenesis.</p><p><b>METHODS</b>A total of 83 cases of endometrial hyperplasia were selected and reclassified according to EIN diagnostic criteria. Expressions of beta-catenin, Glut-1 and PTEN proteins were investigated by immunohistochemistry in 10 proliferative endometrium, 83 endometrial hyperplasia and 24 endometrioid adenocarcinoma.</p><p><b>RESULTS</b>(1) 24 EIN (28.9%) lesions were reclassified among 83 previously diagnosed endometrial hyperplasia, of which, 16 of 24 EIN cases (66.7%) had a prior diagnosis of complex atypical hyperplasia. The relation between EIN diagnosis and grade of atypical hyperplasia was not obvious (P > 0.05). (2) Normal (membranous) expression of beta-catenin was present in 10 cases of proliferative endometrium. Abnormal (marked membranous/cytoplasmic, cytoplasmic and/or nuclear or negative) expression rates of beta-catenin in EIN lesions (50%, 12/24) and endometrioid adenocarcinoma (66.7%, 16/24) were significantly higher than that of benign hyperplasia (10.2%, 6/59) respectively (P < 0.01). However, the difference was not significant between EIN lesions and endometrioid adenocarcinomas (P > 0.05). (3) Low level expressions of Glut-1 was present in proliferative endometrium and benign hyperplasia. Overexpression of Glut-1 was present in 58.3% (14/24) of EIN and 70.8% (17/24) of endometrioid adenocarcinoma, respectively, and statistically not significant (P > 0.05). (4) Percentages of loss of PTEN expression showed no difference between EIN lesions (37.5%, 9/24) and proliferative endometrium (2/10), benign hyperplasia (28.8%, 17/59), endometrioid adenocarcinoma (62.5%, 15/24; P > 0.05). However, loss of PTEN expression in endometrioid adenocarcinoma was significantly higher than those in proliferative endometrium and benign hyperplasia (P < 0.05).</p><p><b>CONCLUSIONS</b>Abnormal expression of beta-catenin and overexpression of Glut-1 may be the early events in tumorigenesis of endometrioid adenocarcinoma. The expression of both markers may be useful in distinguishing a benign hyperplasia from EIN and endometrioid adenocarcinoma. Lack of PTEN expression may be the earliest event in endometrial carcinogenesis. However, it can not be used yet as a diagnostic marker for the EIN lesion.</p>

Expression of NFkappaB p65 and its target genes in gastric cancer and precancerous lesions / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the expression of NFkappaB p65 and its target genes in intestinal metaplasia (IM), dysplasia (Dys), gastric cancer (GC) infected with Helicobacter pylori (Hp) and explore the mechanism of infection by cytotoxin-associated antigen A expressing Hp (CagA(+)Hp) in the development of gastric cancer.</p><p><b>METHODS</b>CagA antibody in blood sample of 289 patients was determined by ELISA. Hp was detected by rapid urease test and Warthin starry staining. Expression of NFkappaB p65 and its target genes in IM, Dys and GC was examined by immunohistochemistry.</p><p><b>RESULTS</b>In IMI approximately II, IMIII, DysI, DysII approximately III and GC, the expression of NFkappaB p65 was significantly higher in patients with CagA(+)Hp infection than those without CagA Hp infection. In IMIII and DysII approximately III, the expression of NFkappaB p65, c-myc, CyclinD(1) and bcl-xl was significantly higher in patients with CagA Hp infection than those without CagA Hp infection. In gastric cancer infected with CagA(+)Hp, the expression of NFkappaB p65, c-myc, CyclinD(1) and bcl-xl was significantly higher in intestinal type than in diffuse type.</p><p><b>CONCLUSION</b>There are different mechanisms in intestinal type and diffuse type in the development of gastric cancer. The occurrence of intestinal type gastric cancer is associated with CagA(+)Hp infection which by NFkappaB p65 upregulating the expression of c-myc, CyclinD(1),bcl-xl in patients with IMIII, DysII approximately III. It may be an effective method to prevent gastric cancer by inhibiting NFkappaB p65.</p>