1986
DOI: 10.1002/1097-0142(19860401)57:7<1385::aid-cncr2820570724>3.0.co;2-v
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Progesterone receptors in two groups of endometrial carcinoma

Abstract: A previous study evaluated two types of endometrial carcinoma: one with, the other without, associated adenomatous hyperplasia (Groups 1 and 2, respectively). On the basis of histologic observations, the study concluded that Group 1 tumors were likely to be estrogen-dependent, whereas Group 2 tumors appeared to represent a hormone-independent type of cancer. The authors present quantitative biochemical data to support the proposition that Group 1 tumors are likely to be under the influence of estrogen. Progest… Show more

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Cited by 46 publications
(15 citation statements)
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“…The distinction between these two types was later utterly refined by histopathological subtyping and immunohistochemical profiling: high proportion of endometrioid histological subtype, estrogen and progesterone receptors positivity in Type I cancers while Type II cancers were dominated by non-endometrioid histological subtypes including serous papillary, clear cell and undifferentiated subtypes, and loss of hormone receptors. 13,14 Excess estrogen relative to progesterone stimulates endometrial-cell proliferation, inhibits apoptosis and promotes angiogenesis 5,15 , all processes in favour of carcinogenesis. Conditions leading to long-term estrogen overexpression relative to the expression of progesterone promote increased risk of Type I endometrial cancer: obesity, persistent anovulation, nulliparity, tamoxifen use and HRT without concomitant progestin substitution.…”
Section: Etiology and Risk Factorsmentioning
confidence: 99%
“…The distinction between these two types was later utterly refined by histopathological subtyping and immunohistochemical profiling: high proportion of endometrioid histological subtype, estrogen and progesterone receptors positivity in Type I cancers while Type II cancers were dominated by non-endometrioid histological subtypes including serous papillary, clear cell and undifferentiated subtypes, and loss of hormone receptors. 13,14 Excess estrogen relative to progesterone stimulates endometrial-cell proliferation, inhibits apoptosis and promotes angiogenesis 5,15 , all processes in favour of carcinogenesis. Conditions leading to long-term estrogen overexpression relative to the expression of progesterone promote increased risk of Type I endometrial cancer: obesity, persistent anovulation, nulliparity, tamoxifen use and HRT without concomitant progestin substitution.…”
Section: Etiology and Risk Factorsmentioning
confidence: 99%
“…The intensity of the response correlates with the receptor levels (28,29). This therapy produces an arrest of glandular proliferation, with secretory changes in the glands and decidual reaction in the stroma.…”
Section: Antineoplastic Hormone Therapymentioning
confidence: 99%
“…The former may be separated from the main group of nonendometrioid carcinomas and considered together with the G 1 endometrioid carcinomas not solely on the basis of an almost excellent prognosis, but also on histological groundthey have an architectural resemblance with well-differentiated endometrioid adenocarcinomas which is typified by a glandular pattern and a low nuclear grade. [43][44][45][46] With regard to the propensity of adenosquamous carcinomas to run an indolent clinical course, 45,[47][48][49][50] this leaves us with little justification for its continued taxonomic separation from adenoacanthoma-the two are frequently classed into a single entity of G 1 endometrioid adenocarcinoma with squamous differentiation.…”
mentioning
confidence: 99%