• Shuji Suzuki, Yuko Omori, Yusuke Ono, Katsuya Hirose, Taito Itoh, Hidenori Karasaki, Mitsugi Shimoda, Yuichi Nagakawa, Ryota Higuchi, Itaru Endo, Toshiki Rikiyama, Michiaki Unno, Tsutomu Fujii, Yuki Sunagawa, Hidetoshi Eguchi, Hideki Sasanuma, Takahiro Akahori, Keiichi Okano, Masaji Tani, Satoshi Hirano, Yasuhiro Shimizu, Minoru Kitago, Shugo Mizuno, Tomohisa Yamamoto, Masayuki Furukawa, Masayuki Ohtsuka, Motokazu Sugimoto, Akira Matsushita, Kenichi Hakamada, Hisato Igarashi, Tamotsu Kuroki, Satoshi Tanno, Yoshihisa Tsuji, Atsushi Masamune, Kazuhiro Mizumoto, Yoshiki Hirooka, Hiroki Yamaue, Kazuichi Okazaki, Sohei Satoi, Yoshifumi Takeyama, Yusuke Mizukami, and Toru Furukawa.
• Department of Gastroenterological Surgery, Ibaraki Medical Center, Tokyo Medical University, Ami, 300-0395, Japan.
• Ann. Surg. 2024 Jul 17.

ObjectiveThis study aimed to clarify the molecular mechanism of remnant pancreatic cancer (PC) development after primary PC resection.Summary Background DataMolecular mechanisms of the development of remnant PCs following primary PC resection are largely unknown.MethodsForty-three patients undergoing remnant PC resection after primary PC resection between 2001 and 2017 at 26 institutes were retrospectively analyzed. Clinicopathological features and molecular alterations detected by targeted amplicon sequencing of 36 PC-associated genes were evaluated.ResultsThese patients showed significantly lower body mass indices and higher hemoglobin A1c values at remnant PC resection than at primary PC resection. A comparison of the molecular features between primary and remnant PCs indicated that remnant PCs were likely to develop via three different molecular pathways: successional, showing identical and accumulated alterations (n=14); phylogenic, showing identical and distinct alterations (n=26); and distinct, showing independent distinctive alterations (n=3). The similarity of gene alterations was associated with time to the remnant PC development (r=－0.384, P=0.0173). Phylogenic pathways were significantly associated with the intraductal spread of carcinoma (P=0.007). Patient survival did not differ significantly depending on these molecular pathways.ConclusionMolecular profiling uncovered three pathways for the development of remnant PCs, namely, successional, phylogenic, and distinct pathways. The vast majority of remnant PCs are likely to be molecularly associated with primary PCs either in the successional or phylogenic way. This information could impact the design of a strategy for monitoring and treating remnant PCs.Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.

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