Pancreatic Cancer Research beyond DNA Mutations

Hiromichi Sato, Kazuki Sasaki, Tomoaki Hara, Yoshiko Tsuji, Yasuko Arao, Chihiro Otsuka, Yumiko Hamano, Mirei Ogita, Shogo Kobayashi, Eric di Luccio, Takaaki Hirotsu, Yuichiro Doki, Hidetoshi Eguchi, Taroh Satoh, Shizuka Uchida*, Hideshi Ishii*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

5 Downloads (Pure)


Pancreatic ductal adenocarcinoma (PDAC) is caused by genetic mutations in four genes: KRAS proto-oncogene and GTPase (KRAS), tumor protein P53 (TP53), cyclin-dependent kinase inhibitor 2A (CDKN2A), and mothers against decapentaplegic homolog 4 (SMAD4), also called the big 4. The changes in tumors are very complex, making their characterization in the early stages challenging. Therefore, the development of innovative therapeutic approaches is desirable. The key to overcoming PDAC is diagnosing it in the early stages. Therefore, recent studies have investigated the multifaced characteristics of PDAC, which includes cancer cell metabolism, mesenchymal cells including cancer-associated fibroblasts and immune cells, and metagenomics, which extend to characterize various biomolecules including RNAs and volatile organic compounds. Various alterations in the KRAS-dependent as well as KRAS-independent pathways are involved in the refractoriness of PDAC. The optimal combination of these new technologies is expected to help treat intractable pancreatic cancer.
Original languageEnglish
Article number1503
Issue number10
Publication statusPublished - Oct 2022


  • Carcinoma, Pancreatic Ductal/metabolism
  • Cyclin-Dependent Kinases/metabolism
  • DNA/therapeutic use
  • Humans
  • Mutation
  • Pancreatic Neoplasms/metabolism
  • Proto-Oncogene Proteins p21(ras)/genetics
  • Tumor Suppressor Protein p53/metabolism
  • Volatile Organic Compounds
  • RNA
  • pancreatic ductal adenocarcinoma
  • sequencing
  • cancer metabolism
  • mutations


Dive into the research topics of 'Pancreatic Cancer Research beyond DNA Mutations'. Together they form a unique fingerprint.

Cite this