Northwestern University Feinberg School of Medicine

Beatriz Sosa-Pineda Lab

Genomic Instability in Pancreatic Cancer

Recent GWAS studies identified deleterious mutations in ATM (encoding a kinase involved with DNA damage responses) in about 20% of patients afflicted with Familial Pancreatic Cancer, and about 10% of sporadic cases of pancreatic cancer. We generated a mouse model of widely metastatic pancreatic cancer carrying deficiency in Atm (manuscript in preparation). Follow-up studies will use our generated Atm mouse models and primary pancreatic cancer cell lines to study fundamental aspects of tumor biology, to explore how Atm function poses a barrier to tumor formation, and to investigate the contribution of genomic instability to pancreatic cancer. Potential therapeutic opportunities will be explored using the former valuable resources as well.

Partial or total Atm loss increase KrasG12D-driven pancreatic oncognesis


Pancreatic cancer cells lacking Atm have increased chromosomal alterations


Cell lines from primary tumors (arrow) or liver metastases (arrowheads) that lack Atm exhibit radiosensitivity.

Figure 3c
Figure 3d