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P06.06 Adoptive cell therapy of triple negative breast cancer with redirected cytokine-induced killer cells
  1. R Sommaggio1,
  2. E Cappuzzello2,
  3. A Dalla Pietà2,
  4. P Palmerini2,
  5. A Tosi2,
  6. D Carpanese1,
  7. L Nicolè3 and
  8. A Rosato2,4
  1. 1Veneto Institute of Oncology, IOV – IRCCS, Padova, Italy
  2. 2Department of Surgery, Oncology and Gastroenterology, Immunology and Oncology Section, University of Padua, Padova, Italy
  3. 3Department of Medicine, Surgical Pathology and Cytopathology Unit, University of Padua, Padova, Italy
  4. 4Veneto Institute of Oncology IOV – IRCCS, Padova, Italy


Background Cytokine-Induced Killer (CIK) cells share several functional and phenotypical properties of both T and natural killer (NK) cells, and represent an attractive approach for cell-based immunotherapy as they do not require antigen-specific priming for tumor cell recognition, and can be efficiently and rapidly expanded in vitro. We recently reported that CIK cells have a relevant expression of FcγRIIIa (CD16a), which can be exploited in combination with clinical-grade monoclonal antibodies (mAbs) to redirect their lytic activity in an antigen-specific manner. Here, we report the assessment and the efficacy of this combined approach against triple negative breast cancer (TNBC), an aggressive tumor that still requires reliable therapeutic options.

Materials and methods Different primitive and metastatic TNBC cancer mouse models were established in NSG mice, either by implanting patient-derived TNBC samples or MDA-MB-231 cells subcutaneously or orthotopically into the mammary fat pad, or by injecting MDA-MB-231 cells intravenously. The combined treatment consisted in the repeated intratumoral or intravenous injection of CIK cells and cetuximab, while the mAb alone or CIK cells plus Rituximab served as control treatments. Tumor growth and metastasis were monitored by bioluminescence or immunohistochemistry, and survival was recorded.

Results CIK cells plus cetuximab significantly restrained primitive tumor growth in mice, either implanted with TNBC patient-derived tumor xenografts or injected with MDA-MB-231 TNBC cell line. Moreover, in both experimental and spontaneous metastatic models the combined approach almost completely abolished metastasis spreading and dramatically improved survival. The antigen-specific mAb favored tumor and metastasis tissue infiltration by CIK cells, and in particular led to an enrichment of the CD16a+ subset.

Conclusions Data highlight the potentiality of a novel immunotherapy approach where a non-specific cytotoxic cell population can be converted into tumor-specific effectors with clinical-grade antibodies, thus providing not only a therapeutic option for TNBC but also a valid alternative to more complex approaches based on chimeric antigen receptor-engineered cells.

Disclosure Information R. Sommaggio: None. E. Cappuzzello: None. A. Dalla Pietà: None. P. Palmerini: None. A. Tosi: None. D. Carpanese: None. L. Nicolè: None. A. Rosato: None.

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