Evidence map›Paper›PMID 38874979›Full record

ArticleTissue engineering. Part A2024

Hematoxylin and Eosin Architecture Uncovers Clinically Divergent Niches in Pancreatic Cancer.

Jason L Guo, David M Lopez, Shamik Mascharak, Deshka S Foster, Anum Khan, Michael F Davitt, Alan T Nguyen, Austin R Burcham, Malini S Chinta, Nicholas J Guardino and 8 more

Abstract read
In one paragraph

Article in Tissue engineering. Part A, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Understanding and targeting the tumour matrisome.Nature reviews. Clinical oncology · 2026
    Review
  2. Article
  3. Article
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

18 authors.

Jason L GuoHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
David M LopezHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Shamik MascharakHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Deshka S FosterHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Anum KhanCell Sciences Imaging Facility, Stanford University, Stanford, California, USA.
Michael F DavittHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Alan T NguyenHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Austin R BurchamHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Malini S ChintaHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Nicholas J GuardinoHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Michelle GriffinHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Elisabeth MillerDepartment of Pathology, University of Virginia School of Medicine, Charlottesville, Virginia, USA.
Michael JanuszykHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Shyam S RaghavanDepartment of Pathology, University of Colorado Anschutz Medical Center, Aurora, Colorado, USA.
Teri A LongacreDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Daniel J DelittoHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Jeffrey A NortonHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.
Michael T LongakerHagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, California, USA.

Funding

Translational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI Vittorio Sebastiano · 2007 to 2026
$71.4M
Mechanoresponsive Engrailed-1-negative fibroblasts activate Engrailed-1 to promote fibrosis in wound healingR01GM136659 · NIGMS · STANFORD UNIVERSITY · PI LONGAKER, MICHAEL T · 2020 to 2023
$1.3M
Spatiotemporal Atlas of Cellular Networks and Ultrastructural States Mediating the Progression and Resolution of Pulmonary FibrosisF32HL167318 · NHLBI · STANFORD UNIVERSITY · PI GUO, JASON LIWEI · 2023 to 2024
$146k
NCI NIH HHS P30 CA124435NHLBI NIH HHS F32 HL167318NIGMS NIH HHS R01 GM136659
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) represents one of the only cancers with an increasing incidence rate and is often associated with intra- and peri-tumoral scarring, referred to as desmoplasia. This scarring is highly heterogeneous in extracellular matrix (ECM) architecture and plays complex roles in both tumor biology and clinical outcomes that are not yet fully understood. Using hematoxylin and eosin (H&E), a routine histological stain utilized in existing clinical workflows, we quantified ECM architecture in 85 patient samples to assess relationships between desmoplastic architecture and clinical outcomes such as survival time and disease recurrence. By utilizing unsupervised machine learning to summarize a latent space across 147 local (e.g., fiber length, solidity) and global (e.g., fiber branching, porosity) H&E-based features, we identified a continuum of histological architectures that were associated with differences in both survival and recurrence. Furthermore, we mapped H&E architectures to a CO-Detection by indEXing (CODEX) reference atlas, revealing localized cell- and protein-based niches associated with outcome-positive versus outcome-negative scarring in the tumor microenvironment. Overall, our study utilizes standard H&E staining to uncover clinically relevant associations between desmoplastic organization and PDAC outcomes, offering a translatable pipeline to support prognostic decision-making and a blueprint of spatial-biological factors for modeling by tissue engineering methods.

Indexed as

Eosine Yellowish-(YS)HematoxylinPancreatic NeoplasmsAgedCarcinoma, Pancreatic DuctalExtracellular MatrixFemaleHumansMaleMiddle AgedTumor MicroenvironmentEosine Yellowish-(YS)Hematoxylinarchitecturedesmoplasiafibrosismachine learningpancreatic ductal adenocarcinomaspatial biology

Identifiers

PMID38874979
PMCPMC12919455

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.