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Could Obesity be a Triggering Factor for Endometrial Tubal Metaplasia to be a Precancerous Lesion?

ABSTRACT: Background & Aims:Endometrial tubal metaplasia (ETM) is mostly described in conjunction with unopposed estrogen levels, and its association with endometrial hyperplasia and endometrial carcinoma (EC) is striking. Obesity is a risk factor for endometrial hyperplasia and EC development. The aim of this study is to investigate the impact of BMI and serum estradiol level on expression of PAX-2, H-TERT, P16, Ki-67, and P53 in studied ETM in reference to benign endometrium and EC. Methods:The study was conducted on the following groups: group (1) consists of 57 cases that had endometrial biopsies with histologically demonstrable ETM (typical or atypical) and all were subjected to serum estradiol levelling and body mass index (BMI) evaluation; group (2) had adjacent benign endometrial tissue as control; group (3) consists of 52 cases of conventional endometrial carcinoma and 16 serous carcinoma paraffin blocks which were collected and reevaluated. All included groups were immunostained for PAX-2, H-TERT, p16, ki67, and p53. Results:The relation between BMI and serum estradiol level in group 1 and PAX-2, H-TERT, P16, and p53 was statistically significant, while their relation with atypia and ki67 expression was insignificant. Twenty-three ETM cases (40.4%) out of group 1 were all (100%) obese, 87% had high serum estradiol level, and 73.9% were postmenopausal and had a similar immunohistochemical profile as EC cases (group 3). Conclusions:The presence of ETM regardless of the histologic atypia in obese postmenopausal patients with high serum estradiol level is an alarming sign. This implies that ETM might not be as benign as generally accepted, as under certain clinical conditions, it may turn into a potential premalignant lesion.

SUBMITTER: El-Saka AM

PROVIDER: S-EPMC7136792 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Could Obesity be a Triggering Factor for Endometrial Tubal Metaplasia to be a Precancerous Lesion?

El-Saka Ayman M AM Zamzam Yomna A YA Zamzam Yosra A YA El-Dorf Ayman A

Journal of obesity 20200320

<h4>Background & aims</h4>Endometrial tubal metaplasia (ETM) is mostly described in conjunction with unopposed estrogen levels, and its association with endometrial hyperplasia and endometrial carcinoma (EC) is striking. Obesity is a risk factor for endometrial hyperplasia and EC development. The aim of this study is to investigate the impact of BMI and serum estradiol level on expression of PAX-2, H-TERT, P16, Ki-67, and P53 in studied ETM in reference to benign endometrium and EC.<h4>Methods</ ...[more]

PMID: 32300484

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Project description:The identification as well as the molecular characterization of breast precancerous lesions in terms of increased risk of progression and/or recurrence is becoming a critical issue today as improved non-surgical procedures are detecting cancer at an earlier stage. The strategy we have been pursuing to identify early apocrine breast lesions is based on the postulate that invasive apocrine carcinomas evolve from epithelial cells in terminal duct lobular units (TDLUs) in a stepwise manner that involves apocrine metaplasia of normal breast epithelia, hyperplasia, atypia, and apocrine carcinoma in situ. First, we identify specific protein biomarkers for benign apocrine metaplasia and thereafter we search for biomarkers that are highly overexpressed by pure invasive apocrine carcinomas. Here we present studies in which we have used antibodies against components of a benign apocrine signature that includes 15-prostaglandin dehydrogenase (15-PGDH), a protein that is expressed by all benign apocrine lesions, and markers that are highly overexpressed by pure invasive apocrine carcinomas such as MRP14 (S100A9), psoriasin (S100A7), and p53 to identify precancerous lesions in sclerosing adenosis (SA) with apocrine metaplasia. The latter is a benign proliferative lesion of the breast that exhibits an increase in the size of the TDLUs and characterized by retained two-cell lining, and myoepithelial (ME) and stromal hyperplasia. SA with apocrine metaplasia, i.e. apocrine adenosis (AA), presents with a higher degree of atypical apocrine hyperplasia, and these lesions are believed to be precursors of apocrine carcinoma, in situ and invasive. Analysis of 24 selected SA samples with apocrine metaplasia revealed non-obligate putative apocrine precancerous lesions that displayed some, or in same cases all the three markers associated with pure invasive apocrine carcinomas. These studies also revealed p53 positive, non-apocrine putative precancerous lesions as well as novel phenotypes for ME and some luminal cells characterized by the expression of cytokeratin 15.

Project description:BACKGROUND:Studies on relationship between tubal ligation and endometrial cancer have led to contradictory findings. In several studies, however, a reduced endometrial cancer risk was suggested following tubal ligation. Therefore, a systematic review and meta-analysis was conducted to examine the relationship between tubal ligation and endometrial cancer risk. METHODS:In this systematic review and meta-analysis, PubMed/Medline, Web of Science, Scopus, Embase, and Google Scholar were searched for relevant studies published up to May 30th, 2018. We compared endometrial cancer risk in women with and without tubal ligation in retrieved studies. RESULTS:Two hundred nine studies were initially retrieved from the data bases. After exclusion of duplicates and studies which did not meet inclusion criteria, ten cohort and case-control studies, including 6,773,066 cases, were entered into the quantitative meta-analysis. There was 0.90% agreement between two researchers who searched and retrieved the studies. The summary OR (SOR) was reported using a random effect model. Begg's test suggested that there was no publication bias, but a considerable heterogeneity was observed (I2 =?95.4%, P?=?0.001). We pooled the raw number of tables cells (i.e. a, b, c, and d) of eight studies. The SOR suggested that tubal ligation was significantly associated with a lower risk of endometrial cancer (SOR?=?0.577, 95% CI?=?0.420-0.792). Also, given the rare nature of endometrial cancer (<?5%), different effect sizes were considered as comparable measures of risk. Therefore we pooled ten studies and SOR of these studies revealed that tubal ligation was significantly associated with a lower risk of endometrial cancer (SOR?=?0.696, 95% CI?=?0.425-0.966). Besides that, we pooled eight studies in which adjusted effect sizes were reported and a subsequent analysis revealed that the summary estimate of adjusted odds ratio (SAOR) was significant (SAOR?=?0.862, 95% CI?=?0.698-1.026). CONCLUSIONS:This study revealed a protective effect of tubal ligation on endometrial cancer risk (approximately 42% lower risk of cancer). It is recommended that studies should be designed to reveal mechanisms of this relationship.

Dataset Information

Could Obesity be a Triggering Factor for Endometrial Tubal Metaplasia to be a Precancerous Lesion?

Publications

Could Obesity be a Triggering Factor for Endometrial Tubal Metaplasia to be a Precancerous Lesion?

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