The use of MR and/or ultrasound imaging to systematically surveil individuals at high risk of developing pancreatic ductal adenocarcinoma (PDAC) due to their carrying of a mutation in the CDNK2A gene has proven worthwhile, as researchers in a European study were able to detect most PDACs at a resectable stage.

The same type of surveillance as applied to individuals with a family history of pancreatic cancer but no gene mutation was less impressive.

Lead author Hans Vasen, MD, PhD, of Leiden University Medical Center in the Netherlands and colleagues published their results online April 25 in the Journal of Clinical Oncology.

After collecting screening outcomes from three European centers that offer prospective screening for high-risk groups—including families with histories of pancreatic cancer as well as those with the CDNKA gene defect—the researchers annually imaged 411 asymptomatic participants using MRI, MR cholangiopancreatography and/or endoscopic ultrasound.

The participants, who were surveilled from four to 15 years, included 178 CDKN2A mutation carriers and 214 individuals with FPC (as well as 19 BRCA1/2 or PALB2 mutation carriers).

PDAC turned up in 13 (7.3 percent) of 178 CDKN2A mutation carriers. The resection rate was 75 percent, and the 5-year survival rate was 24 percent.

Two CDKN2A mutation carriers (1 percent) underwent surgical resection for low-risk precursor lesions.  

In the familial pancreatic cancer (FPC) cohort, two individuals (0.9 percent) had a pancreatic tumor, including one advanced PDAC and one early grade 2 neuroendocrine tumor.

Some 13 patients with FPC (6.1 percent) underwent surgical resection for a suspected precursor lesion, but only four (1.9 percent) had high-risk lesions (such as high-grade intraductal papillary mucinous neoplasms or grade 3 pancreatic intraepithelial neoplasms).

In their discussion, Vasen and co-authors conclude that surveillance of CDNK2A mutation carriers “was relatively successful, detecting most PDACs at a resectable stage. The value of surveillance of FPC is still not clear, and the main effect seems to be prevention of PDAC by removal of PRLs.”

In an accompanying article, Teresa Brentnall, MD, a gastroenterologist and cancer researcher at the University of Washington Medical Center in Seattle, does not withhold her enthusiasm over the overall thrust of the findings.  

Brentnall writes that the results reported by Vasen et al. “represent a remarkable and encouraging step forward for better management of PDAC, a disease that has not had a significant improvement in survival in the last 50 years.”

Brentnall adds that the long-term, prospective study “highlights the prognostic value and clinical need for developing better biomarkers and molecular imaging tests for the earlier detection of PDAC.”

The Journal of Clinical Oncology has posted the full study and Brentnall’s accompanying commentary.