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[Cancer Research 51, 1227-1233, February 15, 1991]
© 1991 American Association for Cancer Research

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Sex Steroid and 1,25-Dihydroxyvitamin D3 Receptors in Human Colorectal Adenocarcinoma and Normal Mucosa1

Farid Meggouh2, Patrice Lointier and Simone Saez

Laboratoire de Biologie Médicale, Centre Léon Bérard, Rue Laënnec, 69373 Lyon [F. M., S. S.], and Service de Chirurgie Générale and Digestive, Hotel-Dieu, BP 69, 63003, Clermont-Ferrand [P. L.], France

In order to determine the potential role of sex steroid and 1,25-dihydroxyvitamin D3 in the spreading of colorectal cancer, previously hypothesized from epidemiological and experimental data, specific androgen (AR, n = 94), estrogen (ER, n = 60), progesterone (PGR, n = 50), and 1,25-dihydroxyvitamin D3 receptors (VDR, (n = 111) were investigated in human colorectal adenocarcinoma (AC) and compared with the normal adjacent mucosa (NM).

Scatchard analysis and competition studies of binding data did not reveal any difference between the biochemical behavior (affinity, specificity, and sedimentation coefficient) of the normal and tumoral tissue receptors. For ARs and ERs, high incidences were found (92 of 94 and 90 of 94 in NM versus 46 of 60 and 40 of 60 in AC, respectively) in both classes of tissues, while they were low for progesterone (7 of 50 and 5 of 50 in NM versus AC). While for sex steroid receptors the incidences did not vary with sex and age of the patients or the location and histopathological grade of the tumor, the VDR incidence was lower in AC (35 of 111) than in NM (99 of 111) and decreased significantly from the right colon to the rectum in adenocarcinoma. Binding capacities were similar in NM and AC for ERs and VDRs, whereas AR levels in NM were significantly higher than in AC.

The expression of VDRs in some colorectal tumors suggests a possible clinical significance. No known function for sex steroid receptors is related to their presence in human colorectal tissues and their pattern in carcinoma does not support any hypothesis previously raised in the case of chemically induced colonic tumors in rodents.

1 This work was supported by grants from Fédération Nationale des Centres de Lutte contre le Cancer and Ligue Nationale Française contre le Cancer.

2 To whom requests for reprints should be addressed, at Laboratoire de Biologie Médicale, Centre Léon Bérard, Rue Laënnec, 69373 Lyon, France.

Received 6/20/90. Accepted 12/ 4/90.




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Copyright © 1991 by the American Association for Cancer Research.