Evidence map›Paper›PMID 24672774›Full record

ArticleFrontiers in oncology2014

A new spontaneously transformed syngeneic model of high-grade serous ovarian cancer with a tumor-initiating cell population.

Curtis W McCloskey, Reuben L Goldberg, Lauren E Carter, Lisa F Gamwell, Ensaf M Al-Hujaily, Olga Collins, Elizabeth A Macdonald, Kenneth Garson, Manijeh Daneshmand, Euridice Carmona and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

45 citing papers in PubMed, 67 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Curtis W McCloskeyDepartment of Cellular and Molecular Medicine, University of Ottawa , Ottawa, ON , Canada ; Centre for Cancer Therapeutics, Ottawa Hospital Research Institute , Ottawa, ON , Canada.
Reuben L GoldbergDepartment of Cellular and Molecular Medicine, University of Ottawa , Ottawa, ON , Canada ; Centre for Cancer Therapeutics, Ottawa Hospital Research Institute , Ottawa, ON , Canada.
Lauren E CarterDepartment of Cellular and Molecular Medicine, University of Ottawa , Ottawa, ON , Canada ; Centre for Cancer Therapeutics, Ottawa Hospital Research Institute , Ottawa, ON , Canada.
Lisa F GamwellDepartment of Cellular and Molecular Medicine, University of Ottawa , Ottawa, ON , Canada ; Centre for Cancer Therapeutics, Ottawa Hospital Research Institute , Ottawa, ON , Canada.
Ensaf M Al-HujailyDepartment of Cellular and Molecular Medicine, University of Ottawa , Ottawa, ON , Canada ; Centre for Cancer Therapeutics, Ottawa Hospital Research Institute , Ottawa, ON , Canada.
Olga CollinsDepartment of Cellular and Molecular Medicine, University of Ottawa , Ottawa, ON , Canada ; Centre for Cancer Therapeutics, Ottawa Hospital Research Institute , Ottawa, ON , Canada.
Elizabeth A MacdonaldDepartment of Cellular and Molecular Medicine, University of Ottawa , Ottawa, ON , Canada ; Centre for Cancer Therapeutics, Ottawa Hospital Research Institute , Ottawa, ON , Canada.
Kenneth GarsonDepartment of Cellular and Molecular Medicine, University of Ottawa , Ottawa, ON , Canada ; Centre for Cancer Therapeutics, Ottawa Hospital Research Institute , Ottawa, ON , Canada.
Manijeh DaneshmandCentre for Cancer Therapeutics, Ottawa Hospital Research Institute , Ottawa, ON , Canada ; Department of Pathology and Laboratory Medicine, University of Ottawa , Ottawa, ON , Canada.
Euridice CarmonaCentre de Recherche du Centre Hospitalier de l'Université de Montréal, Institut du Cancer de Montréal , Montreal, QC , Canada.
Barbara C VanderhydenDepartment of Cellular and Molecular Medicine, University of Ottawa , Ottawa, ON , Canada ; Centre for Cancer Therapeutics, Ottawa Hospital Research Institute , Ottawa, ON , Canada ; Department of Obstetrics and Gynecology, University of Ottawa , Ottawa, ON , Canada.
University of Ottawa · CAOttawa Hospital · CAOttawa Hospital Research InstituteCentre Hospitalier de l’Université de Montréal · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Improving screening and treatment options for patients with epithelial ovarian cancer has been a major challenge in cancer research. Development of novel diagnostic and therapeutic approaches, particularly for the most common subtype, high-grade serous ovarian cancer (HGSC), has been hampered by controversies over the origin of the disease and a lack of spontaneous HGSC models to resolve this controversy. Over long-term culture in our laboratory, an ovarian surface epithelial (OSE) cell line spontaneously transformed OSE (STOSE). The objective of this study was to determine if the STOSE cell line is a good model of HGSC. STOSE cells grow faster than early passage parental M0505 cells with a doubling time of 13 and 48 h, respectively. STOSE cells form colonies in soft agar, an activity for which M0505 cells have negligible capacity. Microarray analysis identified 1755 down-regulated genes and 1203 up-regulated genes in STOSE compared to M0505 cells, many associated with aberrant Wnt/β-catenin and Nf-κB signaling. Upregulation of Ccnd1 and loss of Cdkn2a in STOSE tumors is consistent with changes identified in human ovarian cancers by The Cancer Genome Atlas. Intraperitoneal injection of STOSE cells into severe combined immunodeficient and syngeneic FVB/N mice produced cytokeratin+, WT1+, inhibin-, and PAX8+ tumors, a histotype resembling human HGSC. Based on evidence that a SCA1+ stem cell-like population exists in M0505 cells, we examined a subpopulation of SCA1+ cells that is present in STOSE cells. Compared to SCA1- cells, SCA1+ STOSE cells have increased colony-forming capacity and form palpable tumors 8 days faster after intrabursal injection into FVB/N mice. This study has identified the STOSE cells as the first spontaneous murine model of HGSC and provides evidence for the OSE as a possible origin of HGSC. Furthermore, this model provides a novel opportunity to study how normal stem-like OSE cells may transform into tumor-initiating cells.

Indexed as

high-grade serous cancermouse model of ovarian cancerovarian cancerovarian surface epitheliumstem cellsyngeneictumor-initiating cell

Identifiers

PMID24672774
PMCPMC3957277
OpenAlexW2108852607

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.