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[Cancer Research 61, 1652-1658, February 15, 2001]
© 2001 American Association for Cancer Research

Tumor Biology

Identification of CGA as a Novel Estrogen Receptor-responsive Gene in Breast Cancer: An Outstanding Candidate Marker to Predict the Response to Endocrine Therapy1

Ivan Bièche, Béatrice Parfait, Vivianne Le Doussal, Martine Olivi, Marie-Christine Rio, Rosette Lidereau and Michel Vidaud2

Laboratoire de Génétique Moléculaire–UPRES JE 2195, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, F-75006 Paris [I. B., B. P., M. O., M. V.]; Laboratoire d’Oncogénétique-Institut National de la Santé et de la Recherche Médicale (INSERM) E0017 [I. B., R. L.] and Laboratoire d’Anatomo-Cytopathologie [V. L. D.], Centre René Huguenin, F-92211 St-Cloud; and Institut de Génétique et de Biologie Moléculaire et Cellulaire-INSERM U184, Université Louis Pasteur, F-67404 Illkirch Cedex [M-C. R.], France

The estrogen receptor (ER) status of breast tumors is used to identify patients who may respond to endocrine agents such as tamoxifen. However, ER status alone is not perfectly predictive, and there is a pressing need for more reliable markers of endocrine responsiveness.

Here, we identified the well-known CGA gene (coding for the {alpha} subunit of glycoprotein hormones) as a new ER{alpha}-responsive gene in human breast cancer cells. We used a real-time quantitative reverse transcription-PCR assay to quantify CGA mRNA copy numbers in a large series of breast tumors. CGA overexpression (>10 SD above the mean for normal breast tissues) was observed in 44 of 131 (33.6%) breast tumor RNAs, ranging from 20 to 16,500 times the level in normal breast tissues; the highest levels of CGA gene expression were close to those observed in placenta.

Significant links were observed between CGA gene overexpression and Scarff-Bloom-Richardson histopathological grade I+II (P = 0.015), and progesterone (P = 0.0009) and estrogen (P < 10-7) receptor positivity, which suggested that CGA is a marker of low tumor aggressiveness. We observed CGA mRNA overexpression in 44 of 90 (48.9%) ER{alpha}-positive tumors and in none of the 41 ER{alpha}-negative tumors. Immunohistochemical studies demonstrated that human chorionic gonadotropin {alpha} protein was strictly limited to ER{alpha}-positive tumor cells. Overexpression of the CGA gene was not accompanied by overexpression of the CGB gene.

Our results also suggest that CGA could be a more reliable marker than PS2 and PR for ER{alpha} functionality and, thus, for endocrine responsiveness. Moreover, the CGA marker has the added value of dichotomizing ER{alpha}-positive patients into two subgroups of similar size. Specific antibodies directed to secreted human chorionic gonadotropin {alpha} protein are commercially available, thus facilitating the future application of this marker to the clinical management of breast cancer.




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