Evidence map›Paper›PMID 23463345›Full record

ArticleInternational journal of cancer2013

Dysfunctional endothelial cells directly stimulate cancer inflammation and metastasis.

Joseph W Franses, Natalia C Drosu, William J Gibson, Vipul C Chitalia, Elazer R Edelman

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
0.1field-weighted citation impact, top 45% 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

75 citing papers in PubMed, 10 citations in OpenAlex.

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  16. Cellular and molecular characteristics of the premetastatic niches.Animal models and experimental medicine · 2023
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  20. Article

15 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

5 authors at 3 institutions in 1 country.

Joseph W FransesInstitute of Medical Engineering and Science, MIT, E25-438, Cambridge, MA, USA.
Natalia C Drosu
William J Gibson
Vipul C Chitalia
Elazer R Edelman
Massachusetts Institute of Technology · USBoston University · USBrigham and Women's Hospital · US

Funding

Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0M
Vascular Drug Delivery - Supplement for EquipmentR01GM049039 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI EDELMAN, ELAZER R · 1994 to 2019
$8.9M
BIOLOGY OF TISSUE ENGINEERED ENDOTHELIAL IMPLANTSR01HL060407 · NHLBI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI EDELMAN, ELAZER R · 1999 to 2002
$1.2M
Role of Wnt signaling in uremia-induced entothelial dysfunctionK08DK080946 · NIDDK · BOSTON MEDICAL CENTER · PI CHITALIA, VIPUL C · 2009 to 2013
$746k
NHLBI NIH HHS R01 HL060407NIDDK NIH HHS 1K08DK080946NIDDK NIH HHS K08 DK080946NIGMS NIH HHS R01 GM049039NIGMS NIH HHS R01 GM49039NIGMS NIH HHS T32 GM007753NIGMS NIH HHS T32GM007753
6 · The paper itself

Abstract

Although the influence of context-dependent endothelial cell (EC) regulation of vascular disease and repair is well-established, the privileged roles ECs play as paracrine regulators of tumor progression has only recently become appreciated. We hypothesized that if the same endothelial physiology governs vascular and cancer biology then EC control in cancer should follow endothelial regulation of vascular health. Healthy ECs promote vascular repair and inhibit tumor invasiveness and metastasis. Dysfunctional ECs have the opposite effects in vascular disease, and we now ask if dysfunctionally activated ECs will promote cancer cell inflammatory signaling and aggressive properties. Indeed, while factors released from quiescent ECs induce balanced inflammatory signaling, correlating with decreased proliferation and invasiveness, factors released from dysfunctional ECs robustly activated NF-κB and STAT3 signaling within cancer cells, correlating with increased in vitro invasiveness and decreased proliferation and survival. Furthermore, matrix-embedded dysfunctional ECs stimulated intratumoral pro-inflammatory signaling and spontaneous metastasis, while simultaneously slowing primary tumor growth, when implanted adjacent to Lewis lung carcinoma tumors. These studies may broaden our appreciation of the roles of endothelial function and dysfunction, increase understanding and control of the tumor microenvironment, and facilitate optimization of anti-angiogenic and vascular-modifying therapies in cancer and other diseases.

Indexed as

Neoplasm MetastasisAnimalsApoptosisCell ProliferationCells, CulturedEndothelial CellsFemaleHumansInflammationMiceMice, Inbred C57BLNeoplasm InvasivenessNeoplasmsPhenotypeTranscriptomeTumor Microenvironmentangiogenesisendotheliuminflammationmetastasis

Identifiers

PMID23463345
PMCPMC3707950
OpenAlexW1491321564

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.