[Expressions of aromatase protein and sex hormone receptor in endometrial lesions].

OBJECTIVE: To investigate the expression of aromatase protein, estrogen receptor (ER), progesterone receptor (PR) and nuclear antigen associated with cell proliferation Ki67 in endometrial diseases and their clinical significance in diagnosis and endocrine therapy of endometrial diseases. METHOD: Expressions of aromatase, ER, PR and Ki-67 were detected with immunohistochemistry technic (streptavidin-peroxidase-biotin, SP) in 148 cases including 30 of endometrial hyperplasia, 30 of atypical proliferation and 88 of endometrial adenocarcinoma as observational group and 15 cases of proliferative endometrium and 15 cases of secretory endometrium as control group. RESULTS: Expression of aromatase protein and ER, PR, Ki67 in endometrial hyperplasia, atypical proliferation had no significant difference comparing with the proliferative endometrium group (P > 0.05). In endometrial adenocarcinoma, the expression of aromatase protein increased obviously (64%, 56/88), which was higher than in benign diseases [atypical proliferation group was 23% (7/30), endometrial hyperplasia group was 13% (4/30)] and control group significantly (P < 0.01). The positive expression of ER, PR in endometrial adenocarcinoma decreased [22% (19/88), 19% (17/88)], and Ki67 increased (41%, 36/88) and there was a significant difference compared with control group (P < 0.01). The positive rate of aromatase protein did not increase with the progress of clinical stage or grade of cellular differentiation. Aromatase was not consistent with ER, PR and Ki67 in endometrial adenocarcinoma. CONCLUSION: Aromatase protein is related to the incidence of endometrial adenocarcinoma, and the expression of proteins (aromatase, ER, PR and Ki67) provides theoretical basis for understanding biological behavior of endometrial adenocarcinoma.

[Study of tissue morphology and vascular endothelial growth factor and matrix metalloproteinase-9 gene expressions in nude mouse endometriosis model].

OBJECTIVE: To establish an experimental endometriosis model using nude mouse as a xenographic host for relative biological behavior study of endometriosis. METHODS: Nude mice of experimental group were implanted with the late secretory endometrium of patients with endometriosis (n = 24) or without endometriosis (n = 24) into pelvic and abdominal cavities. Nude mice of control group (n = 3) were implanted with the greater omentum. Nude mice were killed at 5, 15 and 30 d randomly to observe the growth of endometriotic lesions. The morphological changes of endometriotic lesions from different sources and at different time points of growth were examined by light microscopy and electron microscopy; the expressions of vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) of eutopic endometrium and endometriotic lesions were detected by RT-PCR method, and the expressions of steroid hormone receptors by immunohistochemistry method. RESULTS: Endometriotic lesions were found from 5 d with rich blood supply, endometrial glands and stroma under light microscope. And the adhesion to mouse tissues became more severe with time. Under electron microscope, proliferation and infiltration of inflammatory cells were most striking at 15 d. At 30 d the organellae of gland cells were disappeared and there was nuclear chromatin aggregation with apoptosis tendency, but secretory granules still could be seen. The expressions of VEGF and MMP-9 mRNA were increased in endometriotic lesions compared with eutopic endometrium (P < 0.05), and were strongest at 15 d (EM group: 1.11 +/- 0.13/1.00 +/- 0.11; NEM group: 1.10 +/- 0.11/0.99 +/- 0.08) and decreased at 30 d (EM group: 0.85 +/- 0.11/0.77 +/- 0.13; NEM group: 0.86 +/- 0.14/0.76 +/- 0.11). Immunochemistry revealed the positive rate of estrogen and progestogen receptors at 30 d (EM group: 4/8 and 4/8; NEM group: 5/8 and 4/8) was lower than that at 5 d (EM group: 7/8 and 7/8; NEM group: 8/8 and 7/8) and 15 d (EM group: 7/8 and 7/8; NEM group: 7/8 and 8/8), and the expressions of steroid hormone receptors were mostly weak. There was no differences in expression of VEGF and MMP-9 mRNA, estrogen and progestogen between endometriotic lesions implanted with normal endometrium and endometrium from patients with endometriosis. CONCLUSIONS: The nude mouse is an appropriate model for the study of the early phase of endometriosis, and the genesis and development of endometriotic lesions are similar to that of human endometriosis. Endometriosis is associated with multiple factors.