engleski

HER2 overexpression in breast ductal invasive carcinomas according to immunophenotypic subtypes and steroid hormone receptors expression.

Background: If HER2 overexpression results from epigenetic selection during repeated or sustained tissue repair that favors cells sensitive to EGFR ligands, breast cancer phenotypes dependent on tissue repair should have increased shares of HER2 3+, reduced number of HER2 1+ or 2+ tumors and unaltered number of tumors without any HER2. Methods: IHC data of 1169 consecutive patients with ductal invasive breast carcinomas (IDBC) at Osijek Univ Med Center, Croatia were distributed in subgroups (four grades of HER2 (0+, 1+, 2+ and 3+) and three ER/PgR phenotypes (ER+PgR+, ER+PgR- and ER-PgR-)). Results: The table shows detected differences among our patients, according to the tumor type (upper two rows, χ2=65.25), or to ER/PgR phenotypes (bottom three rows, χ2=76.95). Shares of HER2 0+ tumors in all subgroups are obviously near the expected values, suggesting that almost no epigenetic selection due to tissue repair has affected breast cancers lacking HER2 molecules. Tumor migration toward HER2 overexpression (reduced share of 2+ and increased share of 3+ tumors) is noted only among ER and PgR negative tumors (shown in the 2nd row as “triple- negative or pure HER2" and in the last row as “ER-PgR-“). When considering Ki-67 values among 125 pts with ER-PgR- HER2 3+ tumors vs. other HER2 3+ phenotypes, found in 198 pts, difference was significant (Mann- Whitney p<0.00001). Medians of Ki-67 values were 35% for the former and 23% for the latter. Conclusions: Results suggest that repeated or sustained tissue reparation is important in the occurrence of ER-PgR- HER2 3+ IDBC and this might be the reason while their share among steroid receptor negative cancers is above the expected value. Elucidating this possibility by analyzing other features related to tumor biology in these tumors further seems warranted.

breast cancer ; HER2 ; Ki67

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