Evidence map›Paper›PMID 40001347›Full record

ArticleThe Journal of pathology2025

Tumor immune microenvironment alterations associated with progression in human intraductal papillary mucinous neoplasms.

Kevin T Jamouss, Alexander Ioannis Damanakis, Abigail C Cornwell, Martine Jongepier, Maria A Trujillo, Michael Johannes Pflüger, Ryan Kawalerski, Alexandre Maalouf, Katsuya Hirose, Shalini Datta and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors.

Kevin T Jamouss *Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0001-5039-6013
Alexander Ioannis Damanakis *Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Abigail C Cornwell *Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-2932-9032
Martine JongepierDepartment of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Maria A TrujilloDepartment of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Michael Johannes PflügerDepartment of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-4932-4829
Ryan KawalerskiMolecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Alexandre MaaloufDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Katsuya HiroseDepartment of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Shalini DattaDepartment of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Abigail SipesDepartment of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Brian A PedroDepartment of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0003-1898-3458
Emma GudmundssonDepartment of Physiology, University of Maryland, Baltimore, MD, USA.
Naziheh AssarzadeganDepartment of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Logan EngleBloomberg Kimmel Institute, Tumor Microenvironment Technology Development Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Robert B ScharpfDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Satomi KawamotoRussell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Elizabeth D ThompsonDepartment of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Laura D WoodDepartment of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0003-3096-652X

Funding

Characterization of the Molecular Determinants of High-Grade Dysplasia in Pancreatic Cancer Precursor LesionsK08DK107781 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI WOOD, LAURA DELONG · 2016 to 2020
$846k
AACR-Bristol-Myers Squibb Midcareer Female InvestigatorBuffone Family Gastrointestinal Cancer Research FundDennis Troper and Susan WojcickiIPMN Global FoundationJoseph C. Monastra Foundation for Pancreatic Cancer ResearchNCI NIH HHS P50 CA62924NIDDK NIH HHS K08 DK107781Rolfe Pancreatic Cancer FoundationSol Goldman Pancreatic Cancer Research CenterThe Gerald O Mann Charitable Foundation
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) poses a significant challenge due to late-stage diagnoses. To improve patient outcomes, early intervention in precursor lesions such as intraductal papillary mucinous neoplasm (IPMN) is crucial. However, early intervention must be balanced against overtreatment of low-risk lesions that are unlikely to progress, underscoring the need to better understand molecular alterations in neoplastic cells and changes in the tumor microenvironment (TME) that drive the progression of IPMNs. In this study, we characterized alterations in the TME of IPMNs as they progressed to high-grade dysplasia, using immunohistochemistry to quantify immune cell density and activation status in more than 100 well-characterized human IPMN samples. Analyses revealed progression to a more immunosuppressive TME in high-grade IPMN compared with low-grade IPMN, characterized by elevated expression of immune checkpoint molecules (PD-L1, TIM3, VISTA), increased density of macrophages, and decreased density of cytotoxic T cells. Intriguingly, the alterations in macrophages were limited to focal regions of high-grade dysplasia, while T-cell alterations affected the entire IPMN. Additionally, elevated VISTA expression was associated with poorer clinical outcome after IPMN resection in an independent cohort. These findings provide important insights into the interplay between the immune microenvironment and IPMN progression, highlighting potential targets to modify the TME for cancer interception. © 2025 The Pathological Society of Great Britain and Ireland.

Indexed as

Adenocarcinoma, MucinousCarcinoma, Pancreatic DuctalPancreatic Intraductal NeoplasmsPancreatic NeoplasmsTumor MicroenvironmentAgedBiomarkers, TumorDisease ProgressionFemaleHumansLymphocytes, Tumor-InfiltratingMaleMiddle AgedBiomarkers, Tumorcancer immunologyimmune checkpointimmune evasionimmunosuppressive microenvironmentintraductal papillary mucinous neoplasmlymphocyte infiltrationpancreatic ductal adenocarcinomatumor heterogeneitytumor immune microenvironmenttumor progression

Identifiers

PMID40001347
PMCPMC13014305

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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.