Evidence map›Paper›PMID 24507936›Full record

ArticleJournal of dermatological science2014

Thrombospondin-2 overexpression in the skin of transgenic mice reduces the susceptibility to chemically induced multistep skin carcinogenesis.

Rainer Kunstfeld, Thomas Hawighorst, Michael Streit, Young-Kwon Hong, Lynh Nguyen, Lawrence F Brown, Michael Detmar

Open access · greenAbstract read
In one paragraph

Article in Journal of dermatological science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 17 citations in OpenAlex.

  1. CD36 and Its Role in Regulating the Tumor Microenvironment.Current oncology (Toronto, Ont.) · 2022
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
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

7 authors at 3 institutions in 4 countries.

Rainer KunstfeldDepartment of Dermatology, Division of General Dermatology, Medical University Vienna, Vienna, Austria; Cutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Thomas HawighorstCutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA; Department of Gynecology and Obstetrics, Georg-August University Goettingen, Goettingen, Germany.
Michael StreitCutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Young-Kwon HongCutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA; Department of Surgery, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles, CA, USA; Department of Biochemistry and Molecular Biology, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles, CA, USA.
Lynh NguyenCutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Lawrence F BrownDepartment of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Michael DetmarCutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA; Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland. Electronic address: michael.detmar@pharma.ethz.ch.
Harvard University · USMassachusetts General Hospital · USETH Zurich · CH

Funding

VPF/VEGF IN NORMAL AND NEOPLASTIC SKIN ANGIOGENESISR01CA069184 · NCI · SWISS FEDERAL INST OF TECH (ETH ZURICH) · PI DETMAR, MICHAEL J. · 1996 to 2008
$1.6M
NCI NIH HHS CA69184NCI NIH HHS R01 CA069184
6 · The paper itself

Abstract

backgroundWe have previously reported stromal upregulation of the endogenous angiogenesis inhibitor thrombospondin-2 (TSP-2) during multistep carcinogenesis, and we found accelerated and enhanced skin angiogenesis and carcinogenesis in TSP-2 deficient mice. GOALS: To investigate whether enhanced levels of TSP-2 might protect from skin cancer development.

methodsWe established transgenic mice with targeted overexpression of TSP-2 in the skin and subjected hemizygous TSP-2 transgenic mice and their wild-type littermates to a chemical skin carcinogenesis regimen.

resultsTSP-2 transgenic mice showed a significantly delayed onset of tumor formation compared to wild-type mice, whereas the ratio of malignant conversion to squamous cell carcinomas was comparable in both genotypes. Computer-assisted morphometric analysis of blood vessels revealed pronounced tumor angiogenesis already in the early stages of carcinogenesis in wild type mice. TSP-2 overexpression significantly reduced tumor blood vessel density in transgenic mice but had no overt effect on LYVE-1 positive lymphatic vessels. The percentage of desmin surrounded, mature tumor-associated blood vessels and the degree of epithelial differentiation remained unaffected. The antiangiogenic effect of transgenic TSP-2 was accompanied by a significantly increased number of apoptotic tumor cells in transgenic mice.

conclusionOur results demonstrate that enhanced levels of TSP-2 in the skin result in reduced susceptibility to chemically-induced skin carcinogenesis and identify TSP-2 as a new target for the prevention of skin cancer.

Indexed as

CarcinogenesisAnimalsApoptosisBiomarkersCarcinoma, Squamous CellCell DifferentiationEpidermisFemaleGenotypeMiceMice, TransgenicNeovascularization, PathologicSkin NeoplasmsThrombospondin 2ThrombospondinsVascular Endothelial Growth Factor ABiomarkersThrombospondin 2ThrombospondinsVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseAngiogenesisCarcinogenesisSkin cancerThrombospondin

Identifiers

PMID24507936
PMCPMC3975683
OpenAlexW2082206952

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.