Evidence map›Paper›PMID 19055724›Full record

ArticleReproductive biology and endocrinology : RB&E2008

Serial analysis of gene expression reveals differential expression between endometriosis and normal endometrium. Possible roles for AXL and SHC1 in the pathogenesis of endometriosis.

Hiroshi Honda, Fermin F Barrueto, Jean Gogusev, Dwight D Im, Patrice J Morin

Open access · goldAbstract read
In one paragraph

Article in Reproductive biology and endocrinology : RB&E, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
7.2field-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

41 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Endometriosis and the Hallmarks of Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Review
  3. Article
  4. Review
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  11. Review
  12. New concepts on the etiology of endometriosis.The journal of obstetrics and gynaecology research · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Hippo Signaling in the Endometrium.International journal of molecular sciences · 2022
    Review
  17. The Role of mTOR and eIF Signaling in Benign Endometrial Diseases.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Article
  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

5 authors at 3 institutions in 2 countries.

Hiroshi HondaLaboratory of Cellular and Molecular Biology, National Institute on Aging, Baltimore MD 21224, USA. h-honda@qg8.so-net.ne.jp
Fermin F Barrueto
Jean Gogusev
Dwight D Im
Patrice J Morin
Mercy Medical Center · USNational Institute on Aging · USInserm · FR

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

backgroundEndometriosis is a clinical condition that affects up to 10% of the women of reproductive age. Endometriosis is characterized by the presence of endometrial tissues outside the uterine cavity and can lead to chronic pelvic pain, infertility and, in some cases, to ovarian cancer.

methodsIn order to better understand the pathogenesis of endometriosis, we have used Serial Analysis of Gene Expression (SAGE) to identify genes differentially in this disease by studying three endometriotic tissues and a normal endometrium sample. Promising candidates (AXL, SHC1, ACTN4, PI3KCA, p-AKT, p-mTOR, and p-ERK) were independently validated by immunohistochemistry in additional normal and endometriotic tissues.

resultsWe identified several genes differentially expressed between endometriosis and normal endometrium. IGF2, ACTN4, AXL, and SHC1 were among the most upregulated genes. Comparison of the endometriosis gene expression profiles with the gene expression patterns observed in normal human tissues allowed the identification of endometriosis-specific genes, which included several members of the MMP family (MMP1,2,3,10,11,14). Immunohistochemical analysis of several candidates confirmed the SAGE findings, and suggested the involvement of the PI3K-Akt and MAPK signaling pathways in endometriosis.

conclusionIn human endometriosis, the PI3K-Akt and MAPK signaling pathways may be activated via overexpression of AXL and SHC1, respectively. These genes, as well as others identified as differentially expressed in this study, may be useful for the development of novel strategies for the detection and/or therapy of endometriosis.

Indexed as

Axl Receptor Tyrosine KinaseEndometriosisEndometriumExtracellular Signal-Regulated MAP KinasesFemaleGene Expression ProfilingGene Expression RegulationHumansOncogene ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptor Protein-Tyrosine KinasesShc Signaling Adaptor ProteinsSignal TransductionSrc Homology 2 Domain-Containing, Transforming Protein 1AXL protein, humanAxl Receptor Tyrosine KinaseExtracellular Signal-Regulated MAP KinasesOncogene ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptor Protein-Tyrosine KinasesSHC1 protein, humanShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1

Identifiers

PMID19055724
PMCPMC2615013
OpenAlexW2141369228

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.