Propanc Biopharma Concludes PRP Could Become an Effective Chemosensitizer Agent Against Pancreatic Cancer

Propanc Biopharma, Inc. (OTC Pink: PPCB) (“Propanc” or the “Company”), a biopharmaceutical company developing novel cancer treatments for patients suffering from recurring and metastatic cancer, today announced that Chief Scientific Officer and Co-Founder, Dr. Julian Kenyon MD, MB, ChB, has recently come to the conclusion that PRP could become an effective chemosensitizer agent against pancreatic cancer. Chemotherapy activates certain growth factors, which directly activate cancer-associated fibroblasts (CAFs) to induce collagen deposits in pancreatic ductal adenocarcinoma, thus increasing tumor resistance and becoming unresponsive to treatment, according to Kim, et al., Nature Communications, journal, October 22, 2022. Pancreatic adenocarcinoma (PDAC) accounts for 80% of pancreatic cancers and has a 5-year survival rate of less than 8%. According to Dr. Kenyon, chemotherapy-induced fibrosis in PDAC highlights an “opportunity for a combinatorial therapeutic strategy to treat these resistant tumors.”

Cancer-associated fibroblasts (CAFs) are one of the abundant cell types in the external fibrous walls of tumors, which is the major source of the extracellular matrix within the tumor microenvironment (TME). Emerging evidence indicates that the dense collagen matrix increases resistance to standard anti-PDAC therapies. Furthermore, activated CAFs stimulate cellular signals that promote tumor growth through angiogenesis (blood vessel formation) and immunosuppression. As a result, various therapeutic targets have been identified to support CAF activation, reduce tumor resistance, and improve patient prognosis. Despite extensive efforts, none of these attempts has received FDA approval for the treatment of PDAC due to limited efficacy. One reason for the frustrating outcome could be due to the genetic variability of the CAF population within the TME, making genetic sequencing and targeting difficult. Therefore, the key is to target genetic variations which are less subject to mutation. Another option is to enforce CAFs to express different cellular signaling pathways, which re-educates the cell instead of targeting eradication, leading to decreasing the influence of the TME in drug uptake, immune evasion, tumor progression and further tumor dispersion.