TY - JOUR
T1 - Plasma KRAS mutations predict the early recurrence after surgical resection of pancreatic cancer
AU - Ako, Soichiro
AU - Kato, Hironari
AU - Nouso, Kazuhiro
AU - Kinugasa, Hideaki
AU - Terasawa, Hiroyuki
AU - Matushita, Hiroshi
AU - Takada, Saimon
AU - Saragai, Yosuke
AU - Mizukawa, Sho
AU - Muro, Shinichiro
AU - Uchida, Daisuke
AU - Tomoda, Takeshi
AU - Matsumoto, Kazuyuki
AU - Horiguchi, Shigeru
AU - Nobuoka, Daisuke
AU - Yoshida, Ryuichi
AU - Umeda, Yuzo
AU - Yagi, Takahito
AU - Okada, Hiroyuki
N1 - Publisher Copyright:
© 2021 Taylor & Francis Group, LLC.
PY - 2021
Y1 - 2021
N2 - Background: The technique to analyze circulating tumor DNA (ctDNA) in body fluid (so-called “liquid biopsy”) is recently developed. Aims: Our aim was to assess the utility of liquid biopsy for predicting progression of pancreatic ductal adenocarcinoma (PDAC) after surgical resection or chemotherapy. Methods: A total of 72 patients with PDAC were retrospectively enrolled for this study, 33 treated surgically and 39 given chemotherapy, either FOLFIRINOX (oxaliplatin/irinotecan/fluorouracil/leucovorin) or gemcitabine plus nab-paclitaxel. Prior to treatment, patients were screened for the presence of KRAS mutations (G12D and G12V) in plasma using droplet digital polymerase chain reaction, and outcomes were compared. Results: KRAS mutations were identified in plasma samples of 12 patients (36%) underwent surgical resection. Patients with plasma KRAS mutations had significantly shorter disease-free survival (DFS) and overall survival (p < .01 and p = .01, respectively). Of 10 clinical variables analyzed, plasma KRAS mutation was the factor predictive of DFS in multivariate analysis (RR = 3.58, 95% CI: 1.36–9.60; p = .01). Although 12 patients (31%) given chemotherapy tested positive for plasma KRAS mutations, there was no demonstrable relation between plasma KRAS mutations and progression-free survival (PFS) or overall survival (OS) (p = .35 and p = .68, respectively). Conclusions: In patients with PDAC, detection of KRAS mutations in plasma proved independently predictive of early recurrence after surgical resection but did not correlate with PFS following chemotherapy.
AB - Background: The technique to analyze circulating tumor DNA (ctDNA) in body fluid (so-called “liquid biopsy”) is recently developed. Aims: Our aim was to assess the utility of liquid biopsy for predicting progression of pancreatic ductal adenocarcinoma (PDAC) after surgical resection or chemotherapy. Methods: A total of 72 patients with PDAC were retrospectively enrolled for this study, 33 treated surgically and 39 given chemotherapy, either FOLFIRINOX (oxaliplatin/irinotecan/fluorouracil/leucovorin) or gemcitabine plus nab-paclitaxel. Prior to treatment, patients were screened for the presence of KRAS mutations (G12D and G12V) in plasma using droplet digital polymerase chain reaction, and outcomes were compared. Results: KRAS mutations were identified in plasma samples of 12 patients (36%) underwent surgical resection. Patients with plasma KRAS mutations had significantly shorter disease-free survival (DFS) and overall survival (p < .01 and p = .01, respectively). Of 10 clinical variables analyzed, plasma KRAS mutation was the factor predictive of DFS in multivariate analysis (RR = 3.58, 95% CI: 1.36–9.60; p = .01). Although 12 patients (31%) given chemotherapy tested positive for plasma KRAS mutations, there was no demonstrable relation between plasma KRAS mutations and progression-free survival (PFS) or overall survival (OS) (p = .35 and p = .68, respectively). Conclusions: In patients with PDAC, detection of KRAS mutations in plasma proved independently predictive of early recurrence after surgical resection but did not correlate with PFS following chemotherapy.
KW - Chemotherapy
KW - disease-free survival
KW - droplet digital polymerase chain reaction
KW - progression-fee survival
KW - surgical resection
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U2 - 10.1080/15384047.2021.1980312
DO - 10.1080/15384047.2021.1980312
M3 - Article
C2 - 34632919
AN - SCOPUS:85116764296
SN - 1538-4047
JO - Cancer Biology and Therapy
JF - Cancer Biology and Therapy
ER -