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Mutant GNAS drives a pyloric metaplasia with tumor suppressive glycans in intraductal papillary mucinous neoplasia.

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Cell reports 📖 저널 OA 36.1% 2022: 1/1 OA 2024: 6/12 OA 2025: 20/55 OA 2026: 17/54 OA 2022~2026 2025 Vol.44(12) p. 116684
Retraction 확인
출처

PICO 자동 추출 (휴리스틱, conf 2/4)

유사 논문
P · Population 대상 환자/모집단
추출되지 않음
I · Intervention 중재 / 시술
multiplex immunostaining, RNA sequencing, glycosylation profiling, and computational analysis
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
Acting as a glycan rheostat, GNAS elevates LacdiNAcs at the expense of pro-tumorigenic acidic Lewis epitopes, inhibiting cancer cell invasion and disease progression. LacdiNAcs and 3'-sulfo-Le are mutually exclusive and may serve as markers to risk stratify IPMN patients for surgery.

Quoc-Huy Trinh V, Ankenbauer KE, Torbit SM, Taranto CP, Liu J, Batardiere M, Kumar B, Maurer HC, Revetta F, Chen Z, Kruse ARS, Judd AM, Copeland C, Wong J, Ben-Levy O, Jarvis B, Brown M, Brown JW, Das K, Makino Y, Spraggins JM, Lau KS, Azadi P, Maitra A, Tan MCB, DelGiorno KE

📝 환자 설명용 한 줄

Intraductal papillary mucinous neoplasms (IPMNs) are cystic lesions and bona fide precursors of pancreatic ductal adenocarcinoma (PDAC), one of the deadliest solid tumors.

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↓ .bib ↓ .ris
APA Quoc-Huy Trinh V, Ankenbauer KE, et al. (2025). Mutant GNAS drives a pyloric metaplasia with tumor suppressive glycans in intraductal papillary mucinous neoplasia.. Cell reports, 44(12), 116684. https://doi.org/10.1016/j.celrep.2025.116684
MLA Quoc-Huy Trinh V, et al.. "Mutant GNAS drives a pyloric metaplasia with tumor suppressive glycans in intraductal papillary mucinous neoplasia.." Cell reports, vol. 44, no. 12, 2025, pp. 116684.
PMID 41370125 ↗

Abstract

Intraductal papillary mucinous neoplasms (IPMNs) are cystic lesions and bona fide precursors of pancreatic ductal adenocarcinoma (PDAC), one of the deadliest solid tumors. Although ∼90% of IPMNs are detected before PDAC forms, markers distinguishing benign from malignant disease are lacking, resulting in an abundance of unnecessary, invasive surgeries. Recent studies show that pancreatic precancer assumes a pyloric phenotype. To identify the regulators of this plasticity, cell lines, organoids, tumors from mouse models of IPMNs, and patient samples underwent multiplex immunostaining, RNA sequencing, glycosylation profiling, and computational analysis. These data revealed that GNAS drives an indolent phenotype in IPMNs by amplifying a differentiated, pyloric phenotype through SPDEF/CREB3L1, which is characterized by distinct glycans. Acting as a glycan rheostat, GNAS elevates LacdiNAcs at the expense of pro-tumorigenic acidic Lewis epitopes, inhibiting cancer cell invasion and disease progression. LacdiNAcs and 3'-sulfo-Le are mutually exclusive and may serve as markers to risk stratify IPMN patients for surgery.

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