Evidence map›Paper›PMID 25971410›Full record

ArticleOncotarget2015

Tumorigenesis and peritoneal colonization from fallopian tube epithelium.

Sharon L Eddie, Suzanne M Quartuccio, Eoghainin Ó hAinmhir, Georgette Moyle-Heyrman, Dan D Lantvit, Jian-Jun Wei, Barbara C Vanderhyden, Joanna E Burdette

Abstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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

33 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Loss ofOncotarget · 2025
    Article
  5. Article
  6. Loss of phosphatase and tensin homolog (Cancer pathogenesis and therapy · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. In Vivo and Ex Vivo Analysis of Omental Adhesion in Ovarian Cancer.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  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

8 authors.

Sharon L EddieDepartment of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, IL, USA.
Suzanne M QuartuccioDepartment of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, IL, USA.
Eoghainin Ó hAinmhirDepartment of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, IL, USA.
Georgette Moyle-HeyrmanDepartment of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, IL, USA.
Dan D LantvitDepartment of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, IL, USA.
Jian-Jun WeiDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Barbara C VanderhydenDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada.
Joanna E BurdetteDepartment of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, IL, USA.

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
NCI NIH HHS P30 CA060553
6 · The paper itself

Abstract

Ovarian cancer is the most lethal gynecological malignancy, primarily because its origin and initiation factors are unknown. A secretory murine oviductal epithelial (MOE) model was generated to address the hypothesis that the fallopian tube is an origin for high-grade serous cancer. MOE cells were stably altered to express mutation in p53, silence PTEN, activate AKT, and amplify KRAS alone and in combination, to define if this cell type gives rise to tumors and what genetic alterations are required to drive malignancy. Cell lines were characterized in vitro and allografted into mice. Silencing PTEN formed high-grade carcinoma with wide spread tumor explants including metastasis into the ovary. Addition of p53 mutation to PTEN silencing did not enhance this phenotype, whereas addition of KRAS mutation reduced survival. Interestingly, PTEN silencing and KRAS mutation originating from ovarian surface epithelium generated endometrioid carcinoma, suggesting that different cellular origins with identical genetic manipulations can give rise to distinct cancer histotypes. Defining the roles of specific signaling modifications in tumorigenesis from the fallopian tube/oviduct is essential for early detection and development of targeted therapeutics. Further, syngeneic MOE allografts provide an ideal model for pre-clinical testing in an in vivo environment with an intact immune system.

Indexed as

AnimalsCarcinogenesisEpitheliumFallopian TubesFemaleHumansMiceMice, NudeOvarian NeoplasmsPeritoneumAKTfallopian tubehigh-grade serous carcinomaKRASp53PTEN

Identifiers

PMID25971410
PMCPMC4653021

What OpenQuestion holds

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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.