The impact of KMT2D on treatment response of pancreatic cancer – UROP Symposium

The impact of KMT2D on treatment response of pancreatic cancer

Ali Ahmad Mohammad

Research Mentor(s): Jiaqi Shi
Program: CCSFP
Authors: Ali Mohammad, Jiaqi Shi, M.D. PhD, Shungang, PhD, Suny Kim, PhD

Abstract

Pancreatic ductal adenocarcinoma (PDAC) has proven to be one of the most fatal types of cancer. With all the failing types of immunotherapy, it does not make it easy to recover from PDAC. Previous investigations have revealed that the difficulty in effectively treating pancreatic cancer may stem from the suppressive nature of the tumor microenvironment, which impedes or delays the immune system’s ability to mount a proper response, especially when the cancer spreads to other organs. Our study aims to explore the reasons behind the lower survival rate and heightened resistance to treatment observed in this particular cancer type. Specifically, we are focused on unraveling the role of the KMT2D gene and its potential implications for immunotherapeutic interventions. To achieve this, we rely on cell culture techniques and CRISPR-Cas9 procedures to generate KMT2D knockout cell lines. Subsequently, both in vitro experiments and in vivo assays involving mice will be conducted to examine these cells and assess tumor growth. Following this, we will administer chemotherapy and/or immune checkpoint inhibitors to the mice and closely monitor tumor growth to gather data and evaluate treatment response disparities. By establishing a connection between the KMT2D gene and the response to cancer treatment, we aim to gain valuable insights into the role of KMT2D in the development of pancreatic cancer and its resistance to treatment. These findings hold the potential to enhance our understanding of the biology of pancreatic cancer and identify novel strategies for effectively treating patients affected by this disease.

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