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June 30th, 2025
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University of California San Diego
cancer biology
biorxiv

CD47 blockade enhances immunoradiotherapy response in head and neck squamous cell carcinoma

Monther, A.Open in Google Scholar•Al-Msari, R.Open in Google Scholar•Saddawi-Konefka, R.Open in Google Scholar•Fassardi, S.Open in Google Scholar•Tang, C.Open in Google Scholar•Philips, C.Open in Google Scholar•Sen, P.Open in Google Scholar•Mohammadzadeh, P.Open in Google Scholar•Decker, K.Open in Google Scholar•Miyauchi, S.Open in Google Scholaret al.

Head and neck squamous cell carcinoma (HNSCC) is a significant cause of morbidity and mortality worldwide, with limited treatment options for patients with locally advanced disease. CD47 immune checkpoint inhibitors have been used to block the CD47/SIRPa interaction that inhibits antigen-presenting cell phagocytosis, thereby enhancing antigen presentation to cytotoxic T-cells, and have shown promise in combination with anti-PD1 immunotherapy in tumors, including recurrent/metastatic HNSCC. We found that CD47 expression is associated with poor prognosis in HNSCC and explored the anti-tumor activity of CD47 blockade in combination with anti-PD1 and lymphatic-sparing radiotherapy in a locally advanced HNSCC model. Using the 4MOSC1 orthotopic, syngeneic murine model of HPV-negative HNSCC, treatment with an engineered CD47-blocking SIRP fusion protein (ALX301) similarly induced complete tumor regression in combination with anti-PD1, and a partial response as a standalone therapeutic. An anti-PD1 immune checkpoint inhibitor in a CD47-null tumor background led to complete tumor regression confirming a key role for CD47 in tumor immunity. Anti-CD47 treated mice demonstrated increased MHC-II expression on dendritic cells within the tumor and upregulation of CD86 co-stimulatory molecule on dendritic cells within the tumor, sentinel lymph nodes, and contralateral lymph nodes. Combination ALX301 and anti-PD1 treatment in an anti-PD1 resistant 4MOSC2 model demonstrated significant tumor regression, enhanced survivability, improved response with neoadjuvant radiotherapy, and greater retention of CD8+ T-cells within the tumor microenvironment. Notably, T-cell receptor sequencing revealed increased shared clonality between the tumor and sentinel lymph nodes of anti-CD47 treated mice. These data demonstrate that a combination of CD47 blockade and anti-PD1 therapy enhances tumor antigen presentation and immune cell infiltration, while further improving anti-tumor responses in combination with tumor-targeted radiotherapy. This study provides support for the rational design of combinatorial immunoradiotherapy, using anti-CD47 inhibitors and anti-PD1 therapy, in a clinical trial targeting locally advanced HPV-negative HNSCC.

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