Lack of correlation between leptin receptor expression and PI3-K/Akt signaling pathway proteins immunostaining in endometrioid-type endometrial carcinomas.
A number of studies published recently focused on the putative role of leptin in the pathogenesis of various primary human malignancies. Current study was aimed at investigating ObR, PI3-kinase, phospho-Akt kinase and PTEN proteins expression in forty-five primary human endometrioid-type endometrial carcinomas (EC). ObR immunostaining was detected in 21 of 45 (47%) ECs, presented in almost 60% of well- and moderately-differentiated tumors compared to only 17% of poorly-differentiated neoplasms (P<0.05). Semi-quantitative histological score (H-score) ObR values were inversely correlated with patients' body mass index (R=-0.35; P=0.019). ObR expression was significantly higher in normal weight compared to overweight and obese patients (P=0.024). All slides displayed intense PI3-kinase immunoreactivity, whereas phospho-Akt kinase expression was reported in 96% (43 out of 45) cases. Fifteen (33%) ECs were negative for PTEN expression, nine (20%) showed heterogeneous immunostaining pattern, whereas 21 (47%) were PTEN-positive. There was a trend towards a higher phospho-Akt kinase intensity immunostaining in PTEN-negative compared to PTEN-positive cases, but the difference was not significant. There was no significant association between each PI3-K/Akt signaling pathway proteins immunostaining in endometrioid-type ECs. In conclusion, ObR expression is associated with histological grading and the weight of women affected by EC. The components of PI3-K/Akt kinase signaling pathway are expressed in most of the primary endometrioid-type endometrial neoplasms.
Bogusiewicz
Michał
M
2nd Department of Gynecology, Lublin University School of Medicine, 8 Jaczewski street, 20-954, Lublin, Poland.
Semczuk
Andrzej
A
Gogacz
Marek
M
Skomra
Danuta
D
Jakowicki
Jerzy A
JA
Rechberger
Tomasz
T
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D018269:Carcinoma, Endometrioid / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D016889:Endometrial Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008875:Middle Aged; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000378:metabolism*; D054411:Receptors, Leptin; D015398:Signal Transduction
D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; C515448:LEPR protein, human