Advances from targeted therapy for non-metastatic HER2-positive inflammatory breast cancer
Jessica A. Steadman
Department of Surgery, Division of Breast and Melanoma Surgical Oncology, Mayo Clinic, Rochester, Minnesota, USA
Search for more papers by this authorCorresponding Author
Tina J. Hieken
Department of Surgery, Division of Breast and Melanoma Surgical Oncology, Mayo Clinic, Rochester, Minnesota, USA
Correspondence Tina J. Hieken, Department of Surgery, Division of Breast and Melanoma Surgical Oncology, Mayo Clinic, 200 1st St SW, Rochester, MN 55905, USA.
Email: [email protected]; Twitter: @TJH0828
Search for more papers by this authorJessica A. Steadman
Department of Surgery, Division of Breast and Melanoma Surgical Oncology, Mayo Clinic, Rochester, Minnesota, USA
Search for more papers by this authorCorresponding Author
Tina J. Hieken
Department of Surgery, Division of Breast and Melanoma Surgical Oncology, Mayo Clinic, Rochester, Minnesota, USA
Correspondence Tina J. Hieken, Department of Surgery, Division of Breast and Melanoma Surgical Oncology, Mayo Clinic, 200 1st St SW, Rochester, MN 55905, USA.
Email: [email protected]; Twitter: @TJH0828
Search for more papers by this authorAbstract
Among inflammatory breast cancer (IBC) patients, over one-third have HER2-overexpressing (HER2+) tumors. Pathologic complete response (pCR) rates to neoadjuvant targeted and chemotherapy for patients with HER2+ non-metastatic IBC now apporach 60% and favorable long-term survival rates are being reported for those with a pCR. Immune mechanisms contributing to this phenomenon include antibody-mediated immune activation and induction of memory T-cell reponses which may explain the sustained antitumor response seen after discontinuation of targeted therapies.
Open Research
DATA AVAILABILITY STATEMENT
All data used for this review article are from literature referenced in the text and publicly available.
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