Evidence map›Paper›PMID 21761359›Full record

ReviewHormones & cancer2010

Microenvironment and pathogenesis of epithelial ovarian cancer.

Antonio F Saad, Wei Hu, Anil K Sood

Open access · bronzeAbstract readReview
In one paragraph

Review in Hormones & cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.2field-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

47 citing papers in PubMed, 72 citations in OpenAlex.

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  17. Anti-tumour effects of all-trans retinoid acid on serous ovarian cancer.Journal of experimental & clinical cancer research : CR · 2019
    Article
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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

3 authors at 2 institutions in 1 country.

Antonio F SaadDepartment of Obstetrics and Gynecology, U.T.M.B. Galveston Branch, 301 University Blvd, Galveston, TX 77555, USA.
Wei Hu
Anil K Sood
Center for Clinical Studies · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS MD ANDERSON SPORE IN OVARIAN CANCERP50CA083639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BAST, ROBERT C · 1999 to 2015
$33.0M
Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
Texas Center for Cancer NanomedicineU54CA151668 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI CRISTINI, VITTORIO, FERRARI, MAURO · 2010 to 2014
$12.4M
Ovarian Cancer: Mechanisms of Neuroendocrine RegulationR01CA109298 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SOOD, ANIL K · 2005 to 2017
$4.5M
Subcellular localization of nanoparticlesRC2GM092599 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI CHIU, WAH, DECUZZI, PAOLO · 2009 to 2010
$3.0M
Tumor metastasis: Biobehavioral mechanismsR01CA110793 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SOOD, ANIL K · 2004 to 2009
$2.1M
Nanovectors for Characterization and Destruction of Breast Tumor VasculatureR01CA128797 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI FERRARI, MAURO · 2007 to 2010
$1.7M
NCI NIH HHS CA 109298NCI NIH HHS CA 110793NCI NIH HHS CA128797NCI NIH HHS P50 CA083639NCI NIH HHS P50 CA098258NCI NIH HHS R01 CA109298NCI NIH HHS R01 CA110793NCI NIH HHS R01 CA128797NCI NIH HHS U54 CA151668NIGMS NIH HHS RC2 GM092599NIGMS NIH HHS RC2GM092599
6 · The paper itself

Abstract

Multiple genetic alterations play a role in the pathogenesis of ovarian cancer. Although many key proteins and pathways involved in ovarian carcinogenesis and metastasis have been discovered, knowledge of the early steps leading to malignancy remains poorly understood. This poor understanding stems from lack of data from early-stage cancers and absence of a well-established premalignant state universal to all ovarian cancer subtypes. Existing evidence suggests that ovarian cancers develop either through a stepwise mutation process (low-grade pathway), through genetic instability resulting in hastened metastasis (high-grade pathway), or more recently through what has been described as the "'fimbrial-ovarian' serous neoplasia theory." In this latter model, ovarian serous cancers evolve from premalignant lesions in the distal fallopian tube called tubal intraepithelial carcinoma. In this manuscript, we review key genetic and molecular changes that occur in cancer cell progression and suggest a model of ovarian cancer pathogenesis involving both tumor cell mutations and microenvironmental factors.

Indexed as

Carcinoma in SituCell Transformation, NeoplasticNeoplasms, Glandular and EpithelialOvarian NeoplasmsPrecancerous ConditionsTumor MicroenvironmentAnimalsCarcinoma, Ovarian EpithelialDisease ProgressionFemaleHumans

Identifiers

PMID21761359
PMCPMC3199131
OpenAlexW1983194513

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.