Innovative Treatments for Liver & Pancreatic Tumors

Immunological and physical barriers within the organ and the tumor microenvironment (TME) often limit the efficacy of immunotherapies in the liver and pancreas. The TriSalus™ integrated approach aims to address two of the most significant barriers to treatment, potentially enabling more patients to benefit from checkpoint inhibitors and other immunotherapeutic agents.

Liver and Pancreatic Tumors Are Difficult to Treat

Despite progress in cancer treatment, tumors in the liver and pancreas remain challenging to treat and patients have extremely poor outcomes.1,2 Few patients with liver or pancreatic cancers benefit from immunotherapy drugs such as checkpoint inhibitors and CAR-T therapies.3–7

While multiple factors play a role in immunotherapy resistance, a clear understanding of the biological and physical barriers to therapy efficacy in liver and pancreatic cancers is paramount to developing effective solutions.

Scientific illustration of a torso with the two organs TriSalus focuses on: the liver and pancreas.

Immunological & Physical Barriers

At TriSalus, we believe that poor outcomes in liver and pancreatic cancers are due to the lack of attention paid to the organ-specific TME and its role in preventing consistent and durable treatment responses.

Immunosuppressive mechanisms in the liver (which are amplified in the TME) and intratumoral pressure are two important barriers to the treatment of tumors in the liver.8–13

Scientific illustration of a tumor in the liver and a small drug delivery device approaching the tumor via the main blood vessels supplying the liver.

Pancreatic ductal adenocarcinomas (PDAC) have a highly fibrotic TME and high immunosuppressive cell infiltration, limiting the efficacy of immunotherapy.14,15

Scientific illustration of a tumor in the pancreas and a small delivery device approaching the tumor via the venous system.

An Integrated Approach

By aiming to address both immunosuppression and intratumoral pressure within the TME, our approach has the potential to overcome two of the most significant barriers that limit treatment success for liver and pancreatic tumors.10,14–21

Immunosuppression within liver and pancreatic tumors allows cancer cells to grow and multiply. Our investigational immunotherapeutic is designed to reactivate the immune system within the TME.

Tumor growth leads to increased pressure within the tumor and causes blood vessels in the surrounding area to collapse.10,21–23 We believe we can optimize intravascular therapeutic delivery by modulating pressure and flow to enhance local drug concentrations.

Scientific illustration of a myeloid-derived suppressor cells reprogramming a macrophage.
Scientific illustration of a collapsed blood vessel restricting blood flow, and restoration of blood flow after the vessel is reopened.

Immunosuppression within liver and pancreatic tumors allows cancer cells to grow and multiply. Our investigational immunotherapeutic is designed to reactivate the immune system within the TME.

Scientific illustration of a myeloid-derived suppressor cells reprogramming a macrophage.

Tumor growth leads to increased pressure within the tumor and causes blood vessels in the surrounding area to collapse.10,21–23 We believe we can optimize intravascular therapeutic delivery by modulating pressure and flow to enhance local drug concentrations.

Scientific illustration of a collapsed blood vessel restricting blood flow, and restoration of blood flow after the vessel is reopened.

CITATIONS

  1. Llovet JM, et al. Nat Rev Clin Oncol. 2018;15(10):599-616.
  2. Villanueva A. New England Journal of Medicine. 2019;11(380(15)):1450-1462.
  3. Finn RS, et al. Journal of Clinical Oncology. 2021;39(3 suppl):267
  4. Job S, et al. Hepatology. 2020;72(3):965-981.
  5. Morrison AH, et al. Trends Cancer. 2018;4(6):418-428.
  6. Park W, et al. JAMA. 2021;326(9):851-862.
  7. Yeo D, et al. Mol Ther Oncolytics. 2022;24:561-576. 
  8. Chai LF, et al. Cancer Gene Ther. 2020;27(7-8):528-538.
  9. DaSilva NA, et al. Cell Death Discov. 2021;7(1):232.
  10. Stylianopoulos T, et al. Cancer Res. 2013;73(13):3833-3841.
  11. Zhang X, et al. PLoS ONE. 2019;14(12):e0225327.
  12. Loeuillard E, et al. J Clin Invest. 2020;130(10):5380-5396.
  13. Thorn M, et al. Cancer Gene Ther. 2016;23(6):188-198.
  14. Feig C, et al. Clin Cancer Res. 2012;18(16):4266-4276.
  15. Looi CK, et al. J Exp Clin Cancer Res. 2019;38(1):162.
  16. Li X, et al. Nat Rev Cancer. 2021;21(9):541-557.
  17. Brodt P. et al. Clin Cancer Res. 2016;22(24):5971-5982.
  18. Arepally A, et al. Cardiovasc Intervent Radiol. 2021;44(1):141-149.
  19. Guha P, et al. Oncogene. 2019;38(4):533-548.
  20. Chai LF, et al. Vaccines (Basel). 2021;9(8):807.
  21. Shankara Narayanan JS, et al. Surgery. 2020;168(3):448-456.
  22. Jain RK, et al. Annu Rev Biomed Eng. 2014;16:321-346.
  23. Hardaway JC, et al. SITC Annual Meeting. 2018.

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