Evidence map›Paper›PMID 26658038›Full record

ReviewPancreas2016

Phosphatidylinositol 3-Kinase: A Link Between Inflammation and Pancreatic Cancer.

Chiara Birtolo, Vay Liang W Go, Andrzej Ptasznik, Guido Eibl, Stephen J Pandol

Open access · greenAbstract readReview
In one paragraph

Review in Pancreas, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 36% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
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

5 authors at 3 institutions in 2 countries.

Chiara BirtoloFrom the *Department of Medicine, Cedars Sinai Medical Center, Los Angeles, CA; †Department of Internal Medicine, S. Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy; Departments of ‡Medicine and §Surgery, David Geffen School of Medicine at UCLA; and ∥VA Greater Los Angeles Health Care System, Los Angeles, CA.
Vay Liang W Go
Andrzej Ptasznik
Guido Eibl
Stephen J Pandol
Cedars-Sinai Medical Center · USPoliclinico S.Orsola-Malpighi · ITUniversity of Bologna · IT

Funding

The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANNA S. GUKOVSKAYA · 1999 to 2026
$45.8M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Vector and Human Acinar CoreP01DK098108 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PANDOL, STEPHEN J. · 2014 to 2018
$8.1M
Targeting diet-induced promotion of Kras-initiated pancreatic adenocarcinomaP01CA163200 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PANDOL, STEPHEN J. · 2012 to 2016
$6.2M
Pathophysiology, Epidemiology, and Prevention of Pancreatogenic Diabetes - Administrative SupplementU01DK108314 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI Mark Goodarzi, Stephen J. Pandol · 2015 to 2026
$6.1M
UCLA Center for Excellence in Pancreatic DiseasesP01AT003960 · NCCIH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HINES, OSCAR JOE · 2007 to 2011
$5.6M
NCCIH NIH HHS P01 AT003960NCCIH NIH HHS P01AT3960NCI NIH HHS P01 CA163200NIAAA NIH HHS P50 AA011999NIAAA NIH HHS P50 AA11999NIDDK NIH HHS P01 DK098108NIDDK NIH HHS P30 DK041301NIDDK NIH HHS U01 DK108314
6 · The paper itself

Abstract

Even though a strong association between inflammation and cancer has been widely accepted, the underlying precise molecular mechanisms are still largely unknown. A complex signaling network between tumor and stromal cells is responsible for the infiltration of inflammatory cells into the cancer microenvironment. Tumor stromal cells such as pancreatic stellate cells (PSCs) and immune cells create a microenvironment that protects cancer cells through a complex interaction, ultimately facilitating their local proliferation and their migration to different sites. Furthermore, PSCs have multiple functions related to local immunity, angiogenesis, inflammation, and fibrosis. Recently, many studies have shown that members of the phosphoinositol-3-phosphate kinase (PI3K) family are activated in tumor cells, PSCs, and tumor-infiltrating inflammatory cells to promote cancer growth. Proinflammatory cytokines and chemokines secreted by immune cells and fibroblasts within the tumor environment can activate the PI3K pathway both in cancer and inflammatory cells. In this review, we focus on the central role of the PI3K pathway in regulating the cross talk between immune/stromal cells and cancer cells. Understanding the role of the PI3K pathway in the development of chronic pancreatitis and cancer is crucial for the discovery of novel and efficacious treatment options.

Indexed as

AnimalsCell Transformation, NeoplasticHumansInflammation MediatorsPancreatic NeoplasmsPancreatic Stellate CellsPancreatitis, ChronicPhosphatidylinositol 3-KinasePrognosisRisk FactorsSignal TransductionInflammation MediatorsPhosphatidylinositol 3-Kinase

Identifiers

PMID26658038
PMCPMC4859755
OpenAlexW2203590148

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.