Serum DUPAN-2 could be an Alternative Biological Marker for CA19-9 Nonsecretors with Pancreatic Cancer.


Journal

Annals of surgery
ISSN: 1528-1140
Titre abrégé: Ann Surg
Pays: United States
ID NLM: 0372354

Informations de publication

Date de publication:
01 Jun 2023
Historique:
medline: 29 11 2023
pubmed: 27 1 2022
entrez: 26 1 2022
Statut: ppublish

Résumé

This study investigates the use of serum DUPAN-2 in predicting the PC progression in CA19-9 nonsecretors. Although we previously reported that serum CA19-9 >500U/ mL is a poor prognostic factor and an indication for enhanced neoadjuvant treatment, there is not a biomarker surrogate that equivalently predicts prognosis for CA19-9 nonsecretors. We evaluated consecutive PC patients who underwent pancreatectomy from 2005 to 2019. All patients were categorized as either nonsecretor or secretor (CA19-9 ≤ or >2.0U/mL). Of the 984 resected PC patients, 94 (9.6%) were nonsecretors and 890 (90.4%) were secretors. The baseline characteristics were not statistically different between the 2 groups except for the level of DUPAN-2 (720 vs. 100U/mL, P < 0.001). Survival curves after resection were similar between the 2 groups (29.4 months vs. 31.3 months, P = 0.900). Survival curves of patients with DUPAN-2 >2000U/mL in the nonsecretors and patients with CA19-9 >500U/mL in the secretors were nearly equivalent as well (hazard ratio 2.08 vs. 1.89). In the multivariate analysis, DUPAN-2 >2000U/mL (hazard ratio 2.53, P = 0.010) was identified as independent prognostic factor after resection. DUPAN-2 >2000U/mL in CA19-9 nonsecretors can be an unfavorable factor that corresponds to CA19-9 >500U/mL in CA19-9 secretors which is an indicator for enhanced neoadjuvant treatment. The current results shed light on the subset of nonsecretors with poor prognosis that were traditionally categorized in a group with a more favorable prognosis group.

Sections du résumé

OBJECTIVE OBJECTIVE
This study investigates the use of serum DUPAN-2 in predicting the PC progression in CA19-9 nonsecretors.
BACKGROUND BACKGROUND
Although we previously reported that serum CA19-9 >500U/ mL is a poor prognostic factor and an indication for enhanced neoadjuvant treatment, there is not a biomarker surrogate that equivalently predicts prognosis for CA19-9 nonsecretors.
METHODS METHODS
We evaluated consecutive PC patients who underwent pancreatectomy from 2005 to 2019. All patients were categorized as either nonsecretor or secretor (CA19-9 ≤ or >2.0U/mL).
RESULTS RESULTS
Of the 984 resected PC patients, 94 (9.6%) were nonsecretors and 890 (90.4%) were secretors. The baseline characteristics were not statistically different between the 2 groups except for the level of DUPAN-2 (720 vs. 100U/mL, P < 0.001). Survival curves after resection were similar between the 2 groups (29.4 months vs. 31.3 months, P = 0.900). Survival curves of patients with DUPAN-2 >2000U/mL in the nonsecretors and patients with CA19-9 >500U/mL in the secretors were nearly equivalent as well (hazard ratio 2.08 vs. 1.89). In the multivariate analysis, DUPAN-2 >2000U/mL (hazard ratio 2.53, P = 0.010) was identified as independent prognostic factor after resection.
CONCLUSION CONCLUSIONS
DUPAN-2 >2000U/mL in CA19-9 nonsecretors can be an unfavorable factor that corresponds to CA19-9 >500U/mL in CA19-9 secretors which is an indicator for enhanced neoadjuvant treatment. The current results shed light on the subset of nonsecretors with poor prognosis that were traditionally categorized in a group with a more favorable prognosis group.

Identifiants

pubmed: 35081567
doi: 10.1097/SLA.0000000000005395
pii: 00000658-900000000-93098
doi:

Substances chimiques

CA-19-9 Antigen 0
Antigens, Neoplasm 0
Biomarkers, Tumor 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1278-e1283

Informations de copyright

Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.

Déclaration de conflit d'intérêts

The authors report no conflicts of interest.

Références

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Auteurs

Kojiro Omiya (K)

Division of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.

Atsushi Oba (A)

Division of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.

Yosuke Inoue (Y)

Division of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.

Kosuke Kobayashi (K)

Division of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.

Y H Andrew Wu (YHA)

Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.

Yoshihiro Ono (Y)

Division of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.

Takafumi Sato (T)

Division of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.

Takashi Sasaki (T)

Department of Gastroenterological medicine, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan; and.

Masato Ozaka (M)

Department of Gastroenterological medicine, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan; and.

Naoki Sasahira (N)

Department of Gastroenterological medicine, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan; and.

Hiromichi Ito (H)

Division of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.

Akio Saiura (A)

Department of Hepatobiliary-Pancreatic Surgery, Juntendo University School of Medicine, Tokyo, Japan.

Yu Takahashi (Y)

Division of Hepatobiliary and Pancreatic Surgery, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.

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