Evidence map›Paper›PMID 22036564›Full record

ArticleCell2011

The Eph-receptor A7 is a soluble tumor suppressor for follicular lymphoma.

Elisa Oricchio, Gouri Nanjangud, Andrew L Wolfe, Jonathan H Schatz, Konstantinos J Mavrakis, Man Jiang, Xiaoping Liu, Joanne Bruno, Adriana Heguy, Adam B Olshen and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 2 pooled it
5.9field-weighted citation impact, top 2% 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

105 citing papers in PubMed, 2 syntheses or guidelines pooled it, 179 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  12. Review
  13. Frontiers in immunology · 2023
    Article
  14. Advances in the multi-omics landscape of follicular lymphoma.International journal of biological sciences · 2023
    Review
  15. The role of EphA7 in different tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  16. Article
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  18. Article
  19. Review
  20. Article

45 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 3 institutions in 1 country.

Elisa OricchioCancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
Gouri Nanjangud
Andrew L Wolfe
Jonathan H Schatz
Konstantinos J Mavrakis
Man Jiang
Xiaoping Liu
Joanne Bruno
Adriana Heguy
Adam B Olshen
Nicholas D Socci
Julie Teruya-Feldstein
Frances Weis-Garcia
Wayne Tam
Rita Shaknovich
Ari Melnick
Juha P Himanen
R S K Chaganti
Hans-Guido Wendel
Memorial Sloan Kettering Cancer Center · USCornell University · USTri-Institutional PhD Program in Chemical Biology · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Transcriptional silencing by the BCL6 oncoproteinR01CA104348 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MELNICK, ARI M. · 2004 to 2014
$2.6M
The contribution of protein translation to tumorigenesisR01CA142798 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI WENDEL, HANS-GUIDO · 2010 to 2014
$1.9M
Epigenetic Mechanisms of Lymphomagenesis.K08CA127353 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI SHAKNOVICH, RITA · 2008 to 2012
$693k
NCI NIH HHS K08 CA127353NCI NIH HHS P30 CA008748NCI NIH HHS P30-CA008748NCI NIH HHS R01 CA104348NCI NIH HHS R01 CA142798NCI NIH HHS R01-CA142798-01NIGMS NIH HHS GM07739NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

Insights into cancer genetics can lead to therapeutic opportunities. By cross-referencing chromosomal changes with an unbiased genetic screen we identify the ephrin receptor A7 (EPHA7) as a tumor suppressor in follicular lymphoma (FL). EPHA7 is a target of 6q deletions and inactivated in 72% of FLs. Knockdown of EPHA7 drives lymphoma development in a murine FL model. In analogy to its physiological function in brain development, a soluble splice variant of EPHA7 (EPHA7(TR)) interferes with another Eph-receptor and blocks oncogenic signals in lymphoma cells. Consistent with this drug-like activity, administration of the purified EPHA7(TR) protein produces antitumor effects against xenografted human lymphomas. Further, by fusing EPHA7(TR) to the anti-CD20 antibody (rituximab) we can directly target this tumor suppressor to lymphomas in vivo. Our study attests to the power of combining descriptive tumor genomics with functional screens and reveals EPHA7(TR) as tumor suppressor with immediate therapeutic potential.

Indexed as

Genes, Tumor SuppressorAnimalsAntibodies, Monoclonal, Murine-DerivedCell Line, TumorChromosomes, Human, Pair 6GenomicsHumansLymphoma, FollicularMaleMiceNeoplasm TransplantationReceptor, EphA7RituximabRNA InterferenceTransplantation, HeterologousAntibodies, Monoclonal, Murine-DerivedReceptor, EphA7Rituximab

Identifiers

PMID22036564
PMCPMC3208379
OpenAlexW2114625470

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.