Pathology of the Female Genital Tract

Blaustein, Ancel

doi:10.1097/00000478-197803000-00012

Cited by 74 publications

(13 citation statements)

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“…17. In our study follicularcysts (37.15%) were most common followed by simple serous(30%), endometriotic cysts (9.37%), corpusluteal cysts (7.80%).…”

Section: Non Neoplasticsupporting

confidence: 48%

Scenario of ovarian mass lesions at a teaching hospital in Andhra Pradesh, India

Soumini

Sarella

Chaveli

et al. 2015

Int J Reprod Contracept Obstet Gynecol

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“…17. In our study follicularcysts (37.15%) were most common followed by simple serous(30%), endometriotic cysts (9.37%), corpusluteal cysts (7.80%).…”

Section: Non Neoplasticsupporting

confidence: 48%

Scenario of ovarian mass lesions at a teaching hospital in Andhra Pradesh, India

Soumini

Sarella

Chaveli

et al. 2015

Int J Reprod Contracept Obstet Gynecol

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“…The human endometrium consists of glandular and surface epithelia, a surrounding stroma, and a vascular system found only in menstruating species (55). Throughout the childbearing years, the endometrium undergoes cycles of rapid growth, remodeling, differentiation, and angiogenesis.…”

Section: The Inflammation-cancer Linkmentioning

confidence: 99%

Inflammation and Endometrial Cancer: A Hypothesis

Modugno

Ness

Chen

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

231

201

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Endometrial cancer is the most common gynecologic malignancy in the United States. Substantial epidemiologic data implicate an imbalance of estrogens and progestogens in the etiology of this disease. We propose that inflammation also plays a role in endometrial cancer development. Emerging laboratory data suggest that elevated levels of prostaglandin E 2 may underlie the transformation of normal endometrium to neoplastic tissue and that in vitro nonsteroidal anti-inflammatory drugs may inhibit endometrial cancer cell growth. In this review, we suggest that the risk factors for endometrial cancer-unopposed estrogens, anovulation, polycystic ovary syndrome, excessive menstruation, early menarche, and late menopause-may be viewed as factors increasing the exposure of the endometrium to inflammation, whereas pregnancy and smoking, two likely protective factors, have the opposite effect. Chronic inflammation can induce rapid cell division, increasing the possibility for replication error, ineffective DNA repair, and subsequent mutations. A proinflammatory milieu can also directly increase estrogen production. Hence, inflammation may work in conjunction with or in addition to estrogen exposure in the development of endometrial cancer. (Cancer Epidemiol Biomarkers Prev 2005;14 (12):2840 -7)

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“…1 Ectopic endometrial tissue is identified as endometrial glands and stromal tissue generally accompanied by hemosederin laden histiocytes. Endometriosis frequently involves the female reproductive system.…”

Section: Introductionmentioning

confidence: 99%