Estrogen and Progesterone Receptors in Colon Tumors

Department of Family and Preventive Medicine, University of Utah, Salt Lake City, USA.
American Journal of Clinical Pathology (Impact Factor: 2.51). 04/2000; 113(3):364-8. DOI: 10.1309/5MHB-K6XX-QV50-PCJQ
Source: PubMed

ABSTRACT Existing data suggest that there is a hormonal basis to the cause of colon cancer. In the present study, we evaluated the presence of estrogen receptors (ERs) and progesterone receptors (PRs) in colonic tumors from 156 women diagnosed with colon cancer in Utah from September 1991 through September 1994. Immunohistochemical staining with antibodies to ERs and PRs was performed on histologic sections prepared from paraffin blocks. None of the tumors were considered ER-positive; 1 tumor was PR-positive. Use of hormone replacement therapy was not associated with PR-positive tumors. These data do not support previous reports that suggest that colon tumors frequently have receptors for estrogen, progesterone, or both.

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Available from: Martha Slattery, Sep 28, 2015
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    • "Maybe the increased levels of estrogen and progesterone during pregnancy stimulate the growth of tumoral cells with such receptors; however, all reports did not support this hypothesis. Slattery et al. in a study found only one case with positive progesterone receptor among 156 pregnant cases with CRC [20]. e elevated amounts of Cox-2 in CRC patients has raised the hypothesis of its association with colorectal cancer; however, there are little evidences to elucidate its carcinogenic role. "
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    ABSTRACT: The incidence of colorectal cancer (CRC) during pregnancy is so rare. Herein we present a case of colorectal cancer that was missed by pregnancy all over the pregnancy period. The patient was a 37-year-old woman (gravid 4, para 2) referred with the complaints of vaginal discharge and suspicious rupture of membrane (ROM). The patient was pale and the initial physical examination revealed dilation of two fingers, effacement about 30%. She underwent emergent cesarean section which showed adhesions surrounding the uterus, the bladder, and the abdominal wall. Forty days postoperatively, the patient presented with abdominal pain in the left upper quadrant (LUQ). Imaging confirmed a mass in LUQ. Partial colectomy of transverse colon (20 cm) was performed. Postoperative histopathologic study revealed a 7 ∗ 6 ∗ 5 cm mass in transverse colon compatible to stage IIa of the Duck class (T3, N0, Mx). Adjuvant chemotherapy was applied and the patient showed improvements during 7 months followup after surgery. Colorectal cancer in pregnancy is associated with diagnostic and therapeutic challenges which mostly lead to late diagnosis in advanced stages and poor prognosis. A targeted program to improve the general population knowledge and the establishment of a national consultant and screening program particularly for women with a planned pregnancy in the high risk group might be beneficial.
    01/2013; 2013:626393. DOI:10.1155/2013/626393
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    • "Some investigators have reported that normal colonic tissue as well as colorectal cancers express PR mRNA [16] or show progesterone binding capacity [17]. In contrast, work by others suggests that few colon cancers express PR and expression is low [18] or find no evidence for PR expression, at least in the epithelium [19]. PR expression has been documented in colon cancer cell lines and data on growth inhibition of these cell lines by progestins points towards a role for progestins as being antiproliferative [20]. "
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    ABSTRACT: Clinical data suggest that progestins have chemopreventive properties in the development of colorectal cancer. We set out to examine a potential protective effect of progestins and progesterone signaling on colon cancer development. In normal and neoplastic intestinal tissue, we found that the progesterone receptor (PR) is not expressed. Expression was confined to sporadic mesenchymal cells. To analyze the influence of systemic progesterone receptor signaling, we crossed mice that lacked the progesterone receptor (PRKO) to the Apc(Min/+) mouse, a model for spontaneous intestinal polyposis. PRKO-Apc(Min/+) mice exhibited no change in polyp number, size or localization compared to Apc(Min/+). To examine effects of progestins on the intestinal epithelium that are independent of the PR, we treated mice with MPA. We found no effects of either progesterone or MPA on gross intestinal morphology or epithelial proliferation. Also, in rats treated with MPA, injection with the carcinogen azoxymethane did not result in a difference in the number or size of aberrant crypt foci, a surrogate end-point for adenoma development. We conclude that expression of the progesterone receptor is limited to cells in the intestinal mesenchyme. We did not observe any effect of progesterone receptor signaling or of progestin treatment in rodent models of intestinal tumorigenesis.
    PLoS ONE 07/2011; 6(7):e22620. DOI:10.1371/journal.pone.0022620 · 3.23 Impact Factor
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    ABSTRACT: Oestrogen/oestrogen receptor (ER) and vitamin D/vitamin D receptor (VDR) systems have been implicated in the pathogenesis of colorectal cancers. The expression of erbB-2 and epidermal growth factor receptor (EGFR) in colorectal cancers has been suggested to have diagnostic and prognostic significance. In our study, XbaI and PvuII polymorphisms of the ER gene and the BsmI polymorphism of the VDR gene were studied in 56 Caucasian patients with rectal cancer. The relationship between the ER and VDR genotypes and the expression of oncogenes was also investigated. The presence of the x allele of ER gene significantly correlated with the overexpression of the erbB-2 and EGFR oncogenes. Significantly increased erbB-2 expression was observed in patients with the VDR B allele. The XXbb allelic combination of the ER/VDR genes was associated with a significantly lower erbB-2 expression, whereas in the other genotypes significantly higher oncogene expression was seen. Our data raise the possibility that ER/VDR gene polymorphisms accompanied by variable oncogene expression might influence the pathogenetic processes of colorectal cancers.
    European Journal of Cancer 09/2001; 37(12):1463-8. DOI:10.1016/S0959-8049(01)00139-3 · 5.42 Impact Factor
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