Effect of progestin therapy on steroid receptor status and cellular proliferation in low-grade endometrial adenocarcinoma

2021 ◽  
Vol 162 ◽  
pp. S146
Author(s):  
Britt Erickson ◽  
Anne Eaton ◽  
Jaswinder Chalia ◽  
Mahmoud Khalifa ◽  
Carol Lange
1995 ◽  
Vol 5 (4) ◽  
pp. 275-281 ◽  
Author(s):  
H. Kerner ◽  
E. Sabo ◽  
M. Friedman ◽  
D. Beck ◽  
O. Samare ◽  
...  

The immunoperoxidase stain for estrogen and progesterone receptor content in endometrial adenocarcinoma was correlated with the grade and stage, level of myometrial invasion, age and survival of the patients. Anti-estrogen and anti-progesteone receptor monoclonal antibodies were applied to paraffin-embedded tissue from hysterectomy specimens of 100 patients with adenocarcinoma of the endometrium. In 34 of the cases the receptors were studied in the endometrium adjacent to the tumor and compared to the nuclear receptor content in the carcinoma. There was a high inverse correlation between the estrogen receptor status and the grade of tumor (R= − 0.45,P= 0.006). The estrogen receptor measured in the endometrium near the tumor showed a negative correlation with the grade of the tumor (R= −0.42,P= 0.013). The estrogen, but not the progesterone, receptor content, was positively related to the age of the patient (P< 0.05). No significant correlation of the receptor status with the depth of myometrial invasion was found, despite the obvious interdependence between the grade and myometrial invasion. The progesterone receptor staining index appeared to be a distinct independent prognostic factor in endometrial cancer. The immunohistochemical analysis of the steroid hormone status in endometrial cancer therefore offers an alternative to the quantitative ligand-binding assay.


1992 ◽  
Vol 28 (1) ◽  
pp. 112-115 ◽  
Author(s):  
Dario Giuffrida ◽  
Lorenzo Lupo ◽  
Gianfranco A. La Porta ◽  
Giacomo L. La Rosa ◽  
Giuseppa Padova ◽  
...  

2018 ◽  
Vol 20 (4) ◽  
pp. 632-640 ◽  
Author(s):  
Georg Alexander Gihr ◽  
Diana Horvath-Rizea ◽  
Nikita Garnov ◽  
Patricia Kohlhof-Meinecke ◽  
Oliver Ganslandt ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Jakub Karczmarski ◽  
Krzysztof Goryca ◽  
Jacek Pachlewski ◽  
Michalina Dabrowska ◽  
Kazimiera Pysniak ◽  
...  

Accumulation of allelic variants in genes that regulate cellular proliferation, differentiation, and apoptosis may result in expansion of the aberrant intestinal epithelium, generating adenomas. Herein, we compared the mutation profiles of conventional colorectal adenomas (CNADs) across stages of progression towards early carcinoma. DNA was isolated from 17 invasive adenocarcinomas (ACs) and 58 large CNADs, including 19 with low-grade dysplasia (LGD), 21 with LGD adjacent to areas of high-grade dysplasia and/or carcinoma (LGD-H), and 28 with high-grade dysplasia (HGD). Ion AmpliSeq Comprehensive Cancer Panel libraries were prepared and sequenced on the Ion Proton. We identified 956 unique allelic variants; of these, 499 were considered nonsynonymous variants. Eleven genes (APC, KRAS, SYNE1, NOTCH4, BLNK, FBXW7, GNAS, KMT2D, TAF1L, TCF7L2, and TP53) were mutated in at least 15% of all samples. Out of frequently mutated genes, TP53 and BCL2 had a consistent trend in mutation prevalence towards malignancy, while two other genes (HNF1A and FBXW7) exhibited the opposite trend. HGD adenomas had significantly higher mutation rates than LGD adenomas, while LGD-H adenomas exhibited mutation frequencies similar to those of LGD adenomas. A significant increase in copy number variant frequency was observed from LGD through HGD to malignant samples. The profiling of advanced CNADs demonstrated variations in mutation patterns among colorectal premalignancies. Only limited numbers of genes were repeatedly mutated while the majority were altered in single cases. Most genetic alterations in adenomas can be considered early contributors to colorectal carcinogenesis.


1991 ◽  
Vol 1 (6) ◽  
pp. 513-523 ◽  
Author(s):  
Nancy Kreiger ◽  
Will D. King ◽  
Lynn Rosenberg ◽  
E.Aileen Clarke ◽  
Julie R. Palmer ◽  
...  

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