Evidence map›Paper›PMID 37452870›Full record

ReviewCellular and molecular life sciences : CMLS2023

Intrapancreatic fat, pancreatitis, and pancreatic cancer.

Anna C Lilly, Igor Astsaturov, Erica A Golemis

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
13.3field-weighted citation impact, top 1% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Anna C LillyProgram in Cancer Signaling and Microenvironment, Fox Chase Cancer Center, 333 Cottman Ave., Philadelphia, PA, 19111, USA.
Igor AstsaturovProgram in Cancer Signaling and Microenvironment, Fox Chase Cancer Center, 333 Cottman Ave., Philadelphia, PA, 19111, USA.
Erica A GolemisProgram in Cancer Signaling and Microenvironment, Fox Chase Cancer Center, 333 Cottman Ave., Philadelphia, PA, 19111, USA. Erica.Golemis@fccc.edu.ORCID http://orcid.org/0000-0003-3618-3673
Fox Chase Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Dietmar J Kappes · 1985 to 2026
$138.8M
Neoadjuvant Stroma Modification in Pancreatic CancerR21CA252535 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI ASTSATUROV, IGOR, DOTAN, EFRAT · 2021 to 2022
$460k
NCI NIH HHS P30 CA006927NCI NIH HHS R21 CA252535
6 · The paper itself

Abstract

Pancreatic cancer is typically detected at an advanced stage, and is refractory to most forms of treatment, contributing to poor survival outcomes. The incidence of pancreatic cancer is gradually increasing, linked to an aging population and increasing rates of obesity and pancreatitis, which are risk factors for this cancer. Sources of risk include adipokine signaling from fat cells throughout the body, elevated levels of intrapancreatic intrapancreatic adipocytes (IPAs), inflammatory signals arising from pancreas-infiltrating immune cells and a fibrotic environment induced by recurring cycles of pancreatic obstruction and acinar cell lysis. Once cancers become established, reorganization of pancreatic tissue typically excludes IPAs from the tumor microenvironment, which instead consists of cancer cells embedded in a specialized microenvironment derived from cancer-associated fibroblasts (CAFs). While cancer cell interactions with CAFs and immune cells have been the topic of much investigation, mechanistic studies of the source and function of IPAs in the pre-cancerous niche are much less developed. Intriguingly, an extensive review of studies addressing the accumulation and activity of IPAs in the pancreas reveals that unexpectedly diverse group of factors cause replacement of acinar tissue with IPAs, particularly in the mouse models that are essential tools for research into pancreatic cancer. Genes implicated in regulation of IPA accumulation include KRAS, MYC, TGF-β, periostin, HNF1, and regulators of ductal ciliation and ER stress, among others. These findings emphasize the importance of studying pancreas-damaging factors in the pre-cancerous environment, and have significant implications for the interpretation of data from mouse models for pancreatic cancer.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsPancreatitisAcinar CellsAnimalsMicePancreasTumor MicroenvironmentCiliaDuctal cellsLipidsPancreatic steatosisPDAC

Identifiers

PMID37452870
PMCPMC10349727
OpenAlexW4384405948

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.