Evidence map›Paper›PMID 42048185›Full record

ArticleCell reports2026

GLIS3 marks a neural-like progenitor cell state that drives metastasis in pancreatic ductal adenocarcinoma.

Dennis Gong, Jimmy A Guo, Jennifer Su, Sueda Cetinkaya, Connor Hennessey, Patrick Yu, Ananya Jambhale, Peter L Wang, Nicholas J Caldwell, Ashley Lam and 14 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

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

24 authors.

Dennis GongCenter for Systems Biology, Krantz Family Center for Cancer Research, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA; Program in Health Sciences and Technology, Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA.
Jimmy A GuoBroad Institute of MIT and Harvard, Cambridge, MA, USA; School of Medicine, University of California, San Francisco, San Francisco, CA, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Jennifer SuBroad Institute of MIT and Harvard, Cambridge, MA, USA; Harvard University, Graduate School of Arts and Sciences, Cambridge, MA, USA.
Sueda CetinkayaDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA; Harvard University, Graduate School of Arts and Sciences, Cambridge, MA, USA.
Connor HennesseyDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Patrick YuBroad Institute of MIT and Harvard, Cambridge, MA, USA.
Ananya JambhaleDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA; Grossman School of Medicine, New York University, New York, NY, USA.
Peter L WangCenter for Systems Biology, Krantz Family Center for Cancer Research, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Nicholas J CaldwellDepartment of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Ashley LamCenter for Systems Biology, Krantz Family Center for Cancer Research, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA; Department of Surgery and Interventional Science Centre for 3D Models of Health and Disease, and Department of Cell and Developmental Biology Consortium for Mitochondrial Research, University College London, London, UK.
Junning WangDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Carina ShiauCenter for Systems Biology, Krantz Family Center for Cancer Research, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA; Harvard Medical School, Boston, MA, USA.
Kevin S KapnerDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Julien DillyDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Laleh AbbassiDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Seema ChughDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Shatavisha DasguptaImaging Platform, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Jonathan NowakDepartment of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Brian M WolpinDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
M Lisa ZhangDepartment of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Mari Mino-KenudsonDepartment of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Tyler JacksKoch Institute for Integrative Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA.
Andrew J AguirreBroad Institute of MIT and Harvard, Cambridge, MA, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA. Electronic address: andrew_aguirre@dfci.harvard.edu.
William L HwangCenter for Systems Biology, Krantz Family Center for Cancer Research, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Electronic address: whwang1@mgh.harvard.edu.

Funding

Elucidating cancer-intrinsic mechanisms of perineural invasion in pancreatic cancerK08CA270417 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI William L Hwang · 2022 to 2026
$1.6M
NCI NIH HHS K08 CA270417
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) frequently recurs and metastasizes despite intensive therapy. The neural-like progenitor (NRP) transcriptional program is enriched in residual disease after neoadjuvant chemotherapy and radiotherapy, but its basis has remained unclear. We hypothesized that NRP represents a regeneration program co-opted by tumors recovering from cytotoxic injury. NRP signatures were strongly enriched in normal pancreatic injury and regeneration, and NRP cancer cells co-expressed transcription factors involved in pancreatic development. Our data support cell-intrinsic contributions and implicate IL-1β-associated inflammatory signaling as a plausible microenvironmental driver of elevated NRP expression. To enable direct phenotypic comparison with other cancer cell states, we established isogenic mouse organoid overexpression models for transcription factors linked to NRP, classical, and basal-like states. Glis3 emerged as a key NRP-associated factor, promoting clonogenicity, tumor growth, and metastasis. These findings identify a clinically relevant developmental regeneration program that emerges in PDAC after treatment.

Indexed as

Carcinoma, Pancreatic DuctalNeoplastic Stem CellsNeural Stem CellsPancreatic NeoplasmsTranscription FactorsAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceNeoplasm MetastasisTranscription Factorscell stateschemoresistanceCP: cancerGlis3neural-like progenitorpancreatic cancerresidual disease

Identifiers

PMID42048185
PMCPMC13479318

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.