Pancreatic ductal adenocarcinoma (PDAC) is the most common form of pancreatic cancer, accounting for over 90% of cases. It remains difficult to treat and has a high mortality rate. According to the Global Cancer Observatory 2022 report, pancreatic cancer ranks as the sixth most common cancer in Japan, with more than 47,000 new cases and over 40,000 deaths reported. This makes it the fourth leading cause of cancer-related deaths in the country.
Researchers at Tokyo University of Science have focused on the gene CTD nuclear membrane phosphatase 1 (CTDNEP1) as a potential tumor suppressor in PDAC. Ms. Mayuka Nii, a doctoral student, and Professor Tadayoshi Hayata led the study published in Cancer Genomics & Proteomics on January 1, 2026.
"PDAC is one of the most difficult cancers to treat and has a very high mortality rate. To find new treatments, it is important to identify genes involved in cancer progression. Our research points to CTDNEP1 as a possible tumor-suppressing gene that could help slow the cancer," says Prof. Hayata.
The team analyzed genetic and clinical data from The Cancer Genome Atlas (TCGA) and Pan-Cancer Atlas involving 184 PDAC patients. They also used online resources such as TIMER2.0 and UALCAN to examine how CTDNEP1 relates to patient survival, its biological functions, and its interaction with immune cells within tumors.
Their results showed that CTDNEP1 expression was lower in PDAC tissues compared to healthy tissues, especially during early disease stages. Tumors with low CTDNEP1 were more likely to have mutations in key genes like KRAS and TP53. Patients whose tumors had low levels of this gene had poorer survival rates, particularly those diagnosed at stage II.
The researchers found that reduced CTDNEP1 expression contributed to an environment where tumors could evade immune detection and fostered chronic inflammation around tumors—factors known to support tumor growth. In contrast, higher levels of CTDNEP1 were linked with greater metabolic activity within tumors and increased infiltration by immune cells.
"These results suggest that CTDNEP1 low expression occurs early in pancreatic cancer and may play a role in disease progression and malignancy," explains Prof. Hayata. He adds that this gene might help detect pancreatic cancer earlier or serve as an indicator for predicting disease severity: "Personally, I have several acquaintances who died very young from pancreatic cancer. Hence, I undertook this research and it is my mission and personal desire as a researcher to translate this research into medical care."
Following these findings, further laboratory studies are underway at Tokyo University of Science to clarify how CTDNEP1 affects cell growth, spread of disease (metastasis), and interactions with immune responses in both test tubes (in vitro) and living organisms (in vivo). The goal is also to understand what controls CTDNEP1 expression so new treatment strategies can be developed.
While clinical applications are still being explored for this gene’s role in pancreatic cancer detection or therapy development, researchers believe their data provide useful directions for future studies aimed at improving outcomes for patients facing this challenging disease.
