Evidence map›Paper›PMID 33122631›Full record

ReviewSignal transduction and targeted therapy2020

Beyond just a tight fortress: contribution of stroma to epithelial-mesenchymal transition in pancreatic cancer.

Ashenafi Bulle, Kian-Huat Lim

Open access · goldAbstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 5 pooled it
8.0field-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

142 citing papers in PubMed, 5 syntheses or guidelines pooled it, 183 citations in OpenAlex.

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  4. Changes in Tissue Fluidity Predict Tumor Aggressiveness In Vivo.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
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82 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Ashenafi BulleDivision of Oncology, Department of Internal Medicine, Barnes-Jewish Hospital and The Alvin J. Siteman Comprehensive Cancer Center, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Kian-Huat LimDivision of Oncology, Department of Internal Medicine, Barnes-Jewish Hospital and The Alvin J. Siteman Comprehensive Cancer Center, Washington University School of Medicine, St. Louis, MO, 63110, USA. kian-huat.lim@wustl.edu.ORCID 0000-0002-2766-200X
Barnes-Jewish Hospital · US

Funding

Washington University PDX Development and Trial Center - Evaluation of Abemaciclib in Combination with Olaparib in Ovarian Cancer and Breast Cancer Patient-derived Xenograft ModelsU54CA224083 · NCI · WASHINGTON UNIVERSITY · PI Li Ding · 2017 to 2026
$13.0M
Washington University SPORE in Pancreatic CancerP50CA196510 · NCI · WASHINGTON UNIVERSITY · PI FIELDS, RYAN C · 2016 to 2020
$10.9M
IRAK4 AS A NOVEL IMMUNOTHERAPEUTIC TARGET IN PANCREATIC DUCTAL ADENOCARCINOMAR37CA219697 · NCI · WASHINGTON UNIVERSITY · PI LIM, KIAN H · 2018 to 2024
$2.4M
Evaluation of IRAK4 As A Novel Therapeutic Target in Colorectal CancerR21CA223112 · NCI · WASHINGTON UNIVERSITY · PI LIM, KIAN H · 2018 to 2019
$359k
NCI NIH HHS P50 CA196510NCI NIH HHS R21 CA223112NCI NIH HHS R37 CA219697NCI NIH HHS U54 CA224083
6 · The paper itself

Abstract

Novel effective treatment is direly needed for patients with pancreatic ductal adenocarcinoma (PDAC). Therapeutics that target the driver mutations, especially the KRAS oncoprotein and its effector cascades, have been ineffective. It is increasing clear that the extensive fibro-inflammatory stroma (or desmoplasia) of PDAC plays an active role in the progression and therapeutic resistance of PDAC. The desmoplastic stroma is composed of dense extracellular matrix (ECM) deposited mainly by the cancer-associated-fibroblasts (CAFs) and infiltrated with various types of immune cells. The dense ECM functions as a physical barrier that limits tumor vasculatures and distribution of therapeutics to PDAC cells. In addition, mounting evidence have demonstrated that both CAFs and ECM promote PDAC cells aggressiveness through multiple mechanisms, particularly engagement of the epithelial-mesenchymal transition (EMT) program. Acquisition of a mesenchymal-like phenotype renders PDAC cells more invasive and resistant to therapy-induced apoptosis. Here, we critically review seminal and recent articles on the signaling mechanisms by which each stromal element promotes EMT in PDAC. We discussed the experimental models that are currently employed and best suited to study EMT in PDAC, which are instrumental in increasing the chance of successful clinical translation.

Indexed as

Epithelial-Mesenchymal TransitionSignal TransductionAnimalsCarcinoma, Pancreatic DuctalDesmosomesHumansPancreatic Neoplasms

Identifiers

PMID33122631
PMCPMC7596088
OpenAlexW3097893749

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.