Evidence map›Paper›PMID 37980563›Full record

ArticleCell reports2023

SERPINB3-MYC axis induces the basal-like/squamous subtype and enhances disease progression in pancreatic cancer.

Yuuki Ohara, Wei Tang, Huaitian Liu, Shouhui Yang, Tiffany H Dorsey, Helen Cawley, Paloma Moreno, Raj Chari, Mary R Guest, Azadeh Azizian and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

33 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  3. Fingerprinting the Metabolic and Lipidomic Landscapes of Pancreatic Ductal Adenocarcinoma with MALDI Imaging.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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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

15 authors at 8 institutions in 2 countries.

Yuuki OharaPancreatic Cancer Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: yuuki.oohara.1196@gmail.com.
Wei TangLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA; Data Science & Artificial Intelligence, R&D, AstraZeneca, Gaithersburg, MD 20878, USA.
Huaitian LiuLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Shouhui YangPancreatic Cancer Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Tiffany H DorseyLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Helen CawleyPancreatic Cancer Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Paloma MorenoPancreatic Cancer Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Raj ChariGenome Modification Core, Laboratory Animal Sciences Program, Frederick National Lab for Cancer Research, Frederick, MD 21701, USA.
Mary R GuestGenome Modification Core, Laboratory Animal Sciences Program, Frederick National Lab for Cancer Research, Frederick, MD 21701, USA.
Azadeh AzizianStädtisches Klinikum Karlsruhe, Moltkestraße 90, 76133 Karlsruhe, Germany.
Jochen GaedckeStädtisches Klinikum Karlsruhe, Moltkestraße 90, 76133 Karlsruhe, Germany.
Michael GhadimiDepartment of General, Visceral and Pediatric Surgery, University Medical Center Göttingen, Robert-Koch-Straße 40, 37075 Göttingen, Germany.
Nader HannaDivision of General & Oncologic Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Stefan AmbsLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
S Perwez HussainPancreatic Cancer Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: hussainp@mail.nih.gov.
National Institutes of Health · USCenter for Cancer Research · USFrederick National Laboratory for Cancer Research · USNational Cancer Institute · USStädtisches Klinikum Karlsruhe · DEAstraZeneca (United States) · USUniversity of Göttingen · DEUniversity of Maryland, Baltimore · US

Funding

Molecular Profiling of Pancreatic CancerZIABC011162 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HUSSAIN, SYED PERWEZ · 2009 to 2023
$11.1M
Animal model of Pancreatic CancerZIABC011186 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HUSSAIN, SYED · 2009 to 2012
$1.2M
Intramural NIH HHS ZIA BC011162Intramural NIH HHS ZIA BC011186
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) exhibits distinct molecular subtypes: classical/progenitor and basal-like/squamous. Our study aimed to identify genes contributing to the development of the basal-like/squamous subtype, known for its aggressiveness. Transcriptome analyses revealed consistent upregulation of SERPINB3 in basal-like/squamous PDAC, correlating with reduced patient survival. SERPINB3 transgene expression in PDAC cells enhanced in vitro invasion and promoted lung metastasis in a mouse PDAC xenograft model. Metabolome analyses unveiled a metabolic signature linked to both SERPINB3 and the basal-like/squamous subtype, characterized by heightened carnitine/acylcarnitine and amino acid metabolism, associated with poor prognosis in patients with PDAC and elevated cellular invasiveness. Further analysis uncovered that SERPINB3 inhibited the cysteine protease calpain, a key enzyme in the MYC degradation pathway, and drove basal-like/squamous subtype and associated metabolic reprogramming through MYC activation. Our findings indicate that the SERPINB3-MYC axis induces the basal-like/squamous subtype, proposing SERPINB3 as a potential diagnostic and therapeutic target for this variant.

Indexed as

Carcinoma, Pancreatic DuctalCarcinoma, Squamous CellPancreatic NeoplasmsAnimalsAntigens, NeoplasmDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceProto-Oncogene Proteins c-mycSerpinsAntigens, NeoplasmMYC protein, humanProto-Oncogene Proteins c-mycSerpinssquamous cell carcinoma-related antigenamino acidBBOX1calpaincarnitine/acylcarnitineCP: CancerCP: Metabolismmetabolismmolecular subtypeMYCpancreatic ductal adenocarcinomaserine/cysteine proteinase inhibitor family B member 3SERPINB3/SCCA1

Identifiers

PMID37980563
PMCPMC10842852
OpenAlexW4388793436

What OpenQuestion holds

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Registered trials

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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.