Evidence map›Paper›PMID 40077847›Full record

ArticleMolecular oncology2025

Highly multiplexed digital PCR assay for simultaneous quantification of variant allele frequencies and copy number alterations of KRAS and GNAS in pancreatic cancer precursors.

Junko Tanaka, Tatsuo Nakagawa, Yusuke Ono, Yoshio Kamura, Takeshi Ishida, Hidemasa Kawabata, Kenji Takahashi, Hiroki Sato, Andrew S Liss, Yusuke Mizukami and 1 more

Abstract read
In one paragraph

Article in Molecular oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Junko TanakaCenter for Digital Services - Healthcare, Research & Development Group, Hitachi, Ltd., Tokyo, Japan.ORCID https://orcid.org/0000-0003-2802-1797
Tatsuo NakagawaCenter for Digital Services - Healthcare, Research & Development Group, Hitachi, Ltd., Tokyo, Japan.
Yusuke OnoInstitute of Biomedical Research, Sapporo Higashi Tokushukai Hospital, Japan.
Yoshio KamuraCenter for Digital Services - Healthcare, Research & Development Group, Hitachi, Ltd., Tokyo, Japan.
Takeshi IshidaCenter for Digital Services - Healthcare, Research & Development Group, Hitachi, Ltd., Tokyo, Japan.
Hidemasa KawabataDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, Japan.
Kenji TakahashiDepartment of Advanced Genomic Community Healthcare, Asahikawa Medical University, Japan.ORCID https://orcid.org/0000-0002-6166-6848
Hiroki SatoDivision of Gastroenterology, Department of Medicine, Asahikawa Medical University, Japan.
Andrew S LissDivision of Gastrointestinal and Oncologic Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.ORCID https://orcid.org/0000-0002-4040-9172
Yusuke MizukamiInstitute of Biomedical Research, Sapporo Higashi Tokushukai Hospital, Japan.ORCID https://orcid.org/0000-0002-1068-7024
Takahide YokoiCenter for Digital Services - Healthcare, Research & Development Group, Hitachi, Ltd., Tokyo, Japan.

Funding

Hitachi, Ltd.Japan Society for the Promotion of Science 23K06759Japan Society for the Promotion of Science 24K02431
6 · The paper itself

Abstract

Pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous neoplasms (IPMNs) are pancreatic ductal adenocarcinoma (PDAC) precursor lesions. Detecting these precursors and monitoring their progression are crucial for early PDAC diagnosis. Digital PCR (dPCR) is a highly sensitive nucleic acid quantification technique and offers a cost-effective option for patient follow-up. However, the clinical utility of conventional dPCR is restricted by multiplexing constraints, particularly due to the challenge of simultaneously quantifying multiple mutations and amplifications. In this study, we applied highly multiplexed dPCR and melting curve analysis to simultaneously measure single nucleotide mutations and amplifications of KRAS and GNAS. The developed 14-plex assay included both wild-type and mutant KRAS, a common driver gene in both PanIN and IPMN, and GNAS, which is specifically mutated in IPMN, along with RPP30, a reference gene for copy number alterations (CNAs). This multiplex dPCR method detected all target mutations with a limit of detection below 0.2% while quantifying CNAs. Additionally, the assay accurately quantified variant allele frequencies in liquid biopsy and tissue samples from both pancreatic neoplasm precursor and PDAC patients, indicating its potential for use in comprehensive patient follow-up.

Indexed as

ChromograninsDNA Copy Number VariationsGene FrequencyGTP-Binding Protein alpha Subunits, GsMultiplex Polymerase Chain ReactionPancreatic NeoplasmsProto-Oncogene Proteins p21(ras)Carcinoma, Pancreatic DuctalHumansMutationChromograninsGNAS protein, humanGTP-Binding Protein alpha Subunits, GsKRAS protein, humanProto-Oncogene Proteins p21(ras)copy number alterationsdigital PCRmelting curve analysismultiplexpancreatic cancervariant allele frequency

Identifiers

PMID40077847
PMCPMC12515721

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.