Evidence map›Paper›PMID 31134894›Full record

ArticleeLife2019

Human pancreatic cancer cell exosomes, but not human normal cell exosomes, act as an initiator in cell transformation.

Karoliina Stefanius, Kelly Servage, Marcela de Souza Santos, Hillery Fields Gray, Jason E Toombs, Suneeta Chimalapati, Min S Kim, Venkat S Malladi, Rolf Brekken, Kim Orth

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 2 pooled it
5.4field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 2 syntheses or guidelines pooled it, 107 citations in OpenAlex.

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3 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

10 authors at 3 institutions in 1 country.

Karoliina StefaniusDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, United States.ORCID 0000-0002-9456-1954
Kelly ServageDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, United States.ORCID 0000-0001-7183-2865
Marcela de Souza SantosDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, United States.
Hillery Fields GrayDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, United States.
Jason E ToombsDivision of Surgical Oncology, Department of Surgery, Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, United States.
Suneeta ChimalapatiDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, United States.
Min S KimDepartment of Bioinformatics, University of Texas Southwestern Medical Center, Dallas, United States.
Venkat S MalladiDepartment of Bioinformatics, University of Texas Southwestern Medical Center, Dallas, United States.
Rolf BrekkenDivision of Surgical Oncology, Department of Surgery, Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, United States.ORCID 0000-0003-2704-2377
Kim OrthDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, United States.ORCID 0000-0002-0678-7620
Howard Hughes Medical Institute · USThe University of Texas Southwestern Medical Center · USNational Institutes of Health · US

Funding

Exploitation of RAS signaling to develop therapy and early detection strategies for PDAR01CA192381 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI BREKKEN, ROLF A, WILKIE, THOMAS M · 2015 to 2019
$2.2M
Proteostasis, AMPylation and the Unfolded Protein repsonse (UPR)R01GM115188 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI ORTH, KIM · 2015 to 2018
$1.2M
NCI NIH HHS R01 CA192381NIGMS NIH HHS R01 GM115188NIH HHS CA192381NIH HHS GM115188Welch Foundation I-1561
6 · The paper itself

Abstract

Cancer evolves through a multistep process that occurs by the temporal accumulation of genetic mutations. Tumor-derived exosomes are emerging contributors to tumorigenesis. To understand how exosomes might contribute to cell transformation, we utilized the classic two-step NIH/3T3 cell transformation assay and observed that exosomes isolated from pancreatic cancer cells, but not normal human cells, can initiate malignant cell transformation and these transformed cells formed tumors in vivo. However, cancer cell exosomes are unable to transform cells alone or to act as a promoter of cell transformation. Utilizing proteomics and exome sequencing, we discovered cancer cell exosomes act as an initiator by inducing random mutations in recipient cells. Cells from the pool of randomly mutated cells are driven to transformation by a classic promoter resulting in foci, each of which encode a unique genetic profile. Our studies describe a novel molecular understanding of how cancer cell exosomes contribute to cell transformation. Editorial note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that major issues remain unresolved (see decision letter).

Indexed as

AnimalsCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalExosomesGenomicsHumansMiceNeoplasm TransplantationNIH 3T3 CellsPancreatic NeoplasmsProteomicscancercancer biologycell biologyexosomesmousepancreatic cancerproteomicstransformation

Identifiers

PMID31134894
PMCPMC6538373
OpenAlexW2947836829

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.