Pancreatic cancer (PC) lacks effective therapies for advanced disease and has a 10% 5-year survival rate. Given the genomic heterogeneity of PC1, personalized medicine approaches are a promising strategy to improve outcomes. We have previously shown that ROCK signalling plays an important role in the promotion of chemoresistance and desmoplasia of PC2,3,4. Here, we present promising pre-clinical data on the efficacy of selective, orally administered ROCK2 inhibitors (ROCK2-i) as a way of sensitising pancreatic cancer to both contemporary chemotherapy and immunotherapy-based approaches.
Comprehensive analyses of pancreatic tumours isolated from the syngeneic KPC PC model revealed positive changes to ECM composition post-ROCK2-i treatment, specifically decreased levels of collagen I and reduced collagen fibril maturity, indicative of a looser matrix. Further immunohistochemical and immunofluorescence analysis of the tumour immune microenvironment revealed positive changes in the components of both innate (macrophage) and adaptive immunity (CD8+ T cell infiltration) in ROCK2-i treated tumours. Excitingly, ROCK2-i extended survival in combination with anti-PD1 immunotherapy compared to anti-PD1 treatment alone in the same model. This may indicate a role for ROCK2 signalling in the regulation of the immune microenvironment in PDAC, as seen in other cancer types5,6.
Furthermore, ROCK2-i improves overall survival in clinically relevant regimens in combination with current standard-of-care chemotherapies, Gemcitabine/Abraxane or FOLFIRINOX in a range of chemoresistant and metastatic patient-derived models of PC.
ROCK2-i therefore shows strong translational potential to combat chemoresistance and potentially sensitise pancreatic tumours to immunotherapy. Ongoing work includes identification of tumour and stromal biomarkers of response to ROCK2-i using single cell transcriptomics. Building on these preclinical data, a Phase I clinical study is currently being planned to assess the safety of ROCK2-i in combination with chemotherapy as frontline treatment of metastatic PC.