New study establishes that ATM activity poses a major barrier to the development of cancer in the pancreas by maintaining genomic stability.

A new study published by our 2014-15 Seed Grant recipient, Yiannis Drosos, PhD has uncovered information that can help diagnose and treat pancreatic cancer tumors. 

Research from St. Jude Children’s Research Hospital examined how ATM-deficiency increases genomic instability, which promotes highly metastatic pancreatic cancer.

Approximately 5% of patients with hereditary pancreatic cancer carry genetic alterations in a gene known as ATM. This gene is responsible for synthesizing a protein that is necessary to preserve the stability of the genome as it helps repair DNA damage.

This study reveals that ATM-deficiency leads to persistent DNA damage in both precancerous lesions and primary tumors. The study found that when ATM alterations occurred in combination with Kras mutations (the most common mutation shown in pancreatic cancer patients) highly metastatic pancreatic cancer tumors developed due to un-repaired DNA and genomic instability. However, these tumors showed high sensitivity to low doses of radiation, providing insight into potential treatment option.

This study establishes that ATM activity poses a major barrier to the development of cancer in the pancreas by maintaining genomic stability. The results of this study hold clinical relevance to understanding how pancreatic cancer spreads and potential treatment options. The Hirshberg Foundation is proud to support studies such as this in order to uncover information that will help the diagnosis and/or treatment of pancreatic tumors.

To read the full article: https://www.ncbi.nlm.nih.gov/pubmed/28894253