Early growth response gene 1 (EGR1) is deleted in estrogen receptor‐negative human breast carcinoma

BACKGROUND Patients with estrogen receptor (ER)‐positive and ER‐negative breast carcinomas differ in terms of disease progression, treatment regimens, and prognosis. The mechanism underlying the biologic differences of the two groups is understood poorly. Array comparative genome hybridization (CGH) on breast carcinoma subtypes demonstrated a consistent association between loss in regions of chromosome 5q and ER‐negative tumors. It was shown previously that early growth response gene 1 (EGR1) on 5q acts like a tumor‐suppressor gene, with its expression repressed in breast carcinomas. METHODS To test the hypothesis that EGR1 is deleted differentially in ER‐negative versus ER‐positive breast carcinomas, fluorescence in situ hybridization was employed in this study to determine the EGR1 deletion status in 50 breast carcinoma specimens. Deletion status was measured by the signal ratio of EGR1/chromosome 5. Linear regression was used to assess the results. RESULTS The mean EGR1/chromosome 5 ratio for the ER‐negative group was significantly lower compared with the same ratio for the ER‐positive group (P < 0.001). Although grade alone was not significant for predicting the ratio, the interaction between ER status and grade was significant (P < 0.01): For ER‐negative specimens, the higher the grade, the lower the EGR1/chromosome 5 ratio. CONCLUSIONS The EGR1 gene appeared to be deleted in ER‐negative human breast carcinomas. Egr‐1 may contribute to the pathogenesis of ER‐negative breast carcinomas versus ER‐positive breast carcinomas. Cancer 2005. © 2005 American Cancer Society. Fluorescence in situ hybridization studies on 50 human breast carcinoma specimens suggested that early growth response gene 1 (EGR1), a proposed tumor‐suppressor gene, was deleted in estrogen receptor‐negative breast carcinoma. No deletion was observed in estrogen receptor‐positive breast carcinomas.