Evidence map›Paper›PMID 25488971›Full record

ArticleBlood2015

Integrin αvβ3 acting as membrane receptor for thyroid hormones mediates angiogenesis in malignant T cells.

Florencia Cayrol, María Celeste Díaz Flaqué, Tharu Fernando, Shao Ning Yang, Helena Andrea Sterle, Marcela Bolontrade, Mariana Amorós, Blanca Isse, Ricardo Norberto Farías, Haelee Ahn and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 85 citations in OpenAlex.

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  14. Editorial: Thyroid hormone actions in cancer.Frontiers in endocrinology · 2023
    Article
  15. Article
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  18. Three-dimensional models: a novel approach for lymphoma research.Journal of cancer research and clinical oncology · 2022
    Review
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  20. 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

16 authors at 5 institutions in 2 countries.

Florencia CayrolNeuroimmunomodulation and Molecular Oncology Department, Institute for Biomedical Research (BIOMED), National Research Council of Argentina (CONICET), Catholic University of Argentina (UCA), Buenos Aires, Argentina;
María Celeste Díaz FlaquéNeuroimmunomodulation and Molecular Oncology Department, Institute for Biomedical Research (BIOMED), National Research Council of Argentina (CONICET), Catholic University of Argentina (UCA), Buenos Aires, Argentina;
Tharu FernandoDivision of Hematology and Oncology, Department of Medicine, Weill Cornell Medical College, Cornell University, New York, NY;
Shao Ning YangDivision of Hematology and Oncology, Department of Medicine, Weill Cornell Medical College, Cornell University, New York, NY;
Helena Andrea SterleNeuroimmunomodulation and Molecular Oncology Department, Institute for Biomedical Research (BIOMED), National Research Council of Argentina (CONICET), Catholic University of Argentina (UCA), Buenos Aires, Argentina;
Marcela BolontradeLaboratory of Molecular and Cellular Therapy, Foundation Institute Leloir-IIBBA, Buenos Aires, Argentina;
Mariana AmorósLaboratory of Molecular and Cellular Therapy, Foundation Institute Leloir-IIBBA, Buenos Aires, Argentina;
Blanca IsseDepartment of Nutritional Biochemistry, CONICET, National University of Tucumán, and Institute of Biological Chemistry "Dr Bernabé Bloj," San Miguel de Tucumán, Tucumán, Argentina;
Ricardo Norberto FaríasDepartment of Nutritional Biochemistry, CONICET, National University of Tucumán, and Institute of Biological Chemistry "Dr Bernabé Bloj," San Miguel de Tucumán, Tucumán, Argentina;
Haelee AhnDivision of Hematology and Oncology, Department of Medicine, Weill Cornell Medical College, Cornell University, New York, NY;
Ye F TianSibley School of Mechanical and Aerospace Engineering, Cornell University, Ithaca, NY;
Fabrizio TabbòDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, Cornell University, New York, NY; and.
Ankur SinghSibley School of Mechanical and Aerospace Engineering, Cornell University, Ithaca, NY;
Giorgio InghiramiDepartment of Pathology and Laboratory Medicine, Weill Cornell Medical College, Cornell University, New York, NY; and.
Leandro CerchiettiDivision of Hematology and Oncology, Department of Medicine, Weill Cornell Medical College, Cornell University, New York, NY;
Graciela Alicia CremaschiNeuroimmunomodulation and Molecular Oncology Department, Institute for Biomedical Research (BIOMED), National Research Council of Argentina (CONICET), Catholic University of Argentina (UCA), Buenos Aires, Argentina; Radioisotope Laboratory, School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina.
Cornell University · USConsejo Nacional de Investigaciones Científicas y Técnicas · ARPontificia Universidad Católica Argentina · ARFundación Instituto Leloir · ARSibley Memorial Hospital · US

Funding

(PQD5)Biomaterials-based Adaptive Tumor Microenvironments for In Vitro Drug ScreeR21CA185236 · NCI · CORNELL UNIVERSITY · PI CERCHIETTI, LEANDRO C, SINGH, ANKUR · 2014 to 2015
$395k
NCI NIH HHS R21 CA185236
6 · The paper itself

Abstract

The interaction of lymphoid tumor cells with components of the extracellular matrix via integrin αvβ3 allows tumor survival and growth. This integrin was demonstrated to be the membrane receptor for thyroid hormones (THs) in several tissues. We found that THs, acting as soluble integrin αvβ3 ligands, activated growth-related signaling pathways in T-cell lymphomas (TCLs). Specifically, TH-activated αvβ3 integrin signaling promoted TCL proliferation and angiogenesis, in part, via the upregulation of vascular endothelial growth factor (VEGF). Consequently, genetic or pharmacologic inhibition of integrin αvβ3 decreased VEGF production and induced TCL cell death in vitro and in human xenograft models. In sum, we show that integrin αvβ3 transduces prosurvival signals into TCL nuclei, suggesting a novel mechanism for the endocrine modulation of TCL pathophysiology. Targeting this mechanism could constitute an effective and potentially low-toxicity chemotherapy-free treatment of TCL patients.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCell Line, TumorCell MovementCell ProliferationFemaleHumansIntegrin alphaVbeta3Jurkat CellsLymphoma, T-CellMaleMiceMice, SCIDNeoplasm TransplantationNeovascularization, PathologicRNA, Small InterferingCilengitideIntegrin alphaVbeta3RNA, Small InterferingSnake VenomsThyroid HormonesVascular Endothelial Growth Factor A

Identifiers

PMID25488971
PMCPMC4311229
OpenAlexW2021068750

What OpenQuestion holds

Textmetadata
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.