Evidence map›Paper›PMID 40425415›Full record

ReviewTrends in cell biology2025

Tumor-stromal metabolic crosstalk in pancreatic cancer.

Ravi Thakur, Nicholas J Mullen, Kamiya Mehla, Pankaj K Singh

Abstract readReview
In one paragraph

Review in Trends in cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Review
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  5. Hypoxia Impairs CD8Cancers · 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

4 authors.

Ravi ThakurDepartment of Oncology Science, University of Oklahoma College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Nicholas J MullenEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA.
Kamiya MehlaDepartment of Oncology Science, University of Oklahoma College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA; OU Health Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Pankaj K SinghDepartment of Oncology Science, University of Oklahoma College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA; OU Health Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: pankaj-singh@ouhsc.edu.

Funding

Tissue Core-UNMC Rapid Autopsy ProgramU54CA274329 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Paul M Grandgenett · 2022 to 2026
$7.8M
CHEMICAL CARCINOGENESIS &CANCER BIOLOGYT32CA009476 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Jennifer D. Black · 1988 to 2026
$6.2M
Targeting Tumor-Stromal Metabolic Cross-Talk in Pancreatic CancerR01CA163649 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Pankaj Kumar Singh · 2012 to 2026
$5.4M
Mitochondrial calcium signaling in pancreatic cancer metastasis and progressionR01CA256911 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI Pankaj Kumar Singh, Shengyu Yang · 2022 to 2026
$3.2M
Molecular Basis of ME2-mediated Tumor Suppression in Pancreatic CancerR01CA270234 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Pankaj Kumar Singh · 2022 to 2026
$2.2M
Vitamin B6 Modulates NK Cell Metabolism in Pancreatic CancerR37CA276924 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Kamiya Mehla · 2023 to 2026
$1.5M
NCI NIH HHS R01 CA163649NCI NIH HHS R01 CA256911NCI NIH HHS R01 CA270234NCI NIH HHS R37 CA276924NCI NIH HHS T32 CA009476NCI NIH HHS U54 CA274329
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a dire prognosis. Standard-of-care chemotherapy regimens offer marginal survival benefit and carry risk of severe toxicity, while immunotherapy approaches have uniformly failed in clinical trials. Extensive desmoplasia in the PDAC tumor microenvironment (TME) disrupts blood flow to and from the tumor, thereby creating a nutrient-depleted, hypoxic, and acidic milieu that suppresses the function of antitumor immune cells and imparts chemotherapy resistance. Additionally, recent seminal studies have demonstrated crucial roles for metabolic crosstalk - the exchange of metabolites between PDAC cells and stromal cell populations in the TME - in establishing and maintaining core malignant behaviors of PDAC: tumor growth, metastasis, immune evasion, and therapy resistance. In this review, we provide a conceptual overview of metabolic crosstalk and how it evolves under various selection pressures in the TME, analyze the landscape of proposed tumorigenic metabolic crosstalk pathways, and highlight potentially druggable nodes.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsStromal CellsTumor MicroenvironmentAnimalsHumanshypoxiametabolic competitionpancreatic cancerstromal diversitytherapy resistancetumor–stromal metabolic crosstalk

Identifiers

PMID40425415
PMCPMC12353458

What Socratic 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 Socratic graph.