Evaluation of the expression of P16INK4A by immunohistochemistry in post-neoadjuvant chemotherapy hormone receptor negative breast cancer specimens.

CONCLUSION: NAC induced the accumulation of P16INK4a(+)cells in nonneoplastic breast tissues more pronounced in patients with a complete pathologic response. Therapy-induced senescence is a potential marker of bystander damage due to NAC. P16INK4a loss and CD-44 gain may represent a phenotype of chemoresistance in residual HRNBCs. PMID: 31839602 [PubMed - as supplied by publisher]
Source: Breast Disease - Category: Cancer & Oncology Tags: Breast Dis Source Type: research