Evidence map›Paper›PMID 19383821›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2009

Estrous cycle modulates ovarian carcinoma growth.

Guillermo N Armaiz-Pena, Lingegowda S Mangala, Whitney A Spannuth, Yvonne G Lin, Nicholas B Jennings, Alpa M Nick, Robert R Langley, Rosemarie Schmandt, Susan K Lutgendorf, Steven W Cole and 1 more

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

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  6. Regulation of semaphorin 4D expression and cell proliferation of ovarian cancer by ERalpha and ERbeta.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
    Article
  7. Article
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  9. Estrogen signaling crosstalk: Implications for endocrine resistance in ovarian cancer.The Journal of steroid biochemistry and molecular biology · 2014
    Review
  10. Article
  11. Article
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  15. Review
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  18. Src Inhibition with saracatinib reverses fulvestrant resistance in ER-positive ovarian cancer models in vitro and in vivo.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
    Article
  19. 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

11 authors at 4 institutions in 1 country.

Guillermo N Armaiz-PenaDepartment of Gynecologic Oncology and Cancer Biology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA.
Lingegowda S Mangala
Whitney A Spannuth
Yvonne G Lin
Nicholas B Jennings
Alpa M Nick
Robert R Langley
Rosemarie Schmandt
Susan K Lutgendorf
Steven W Cole
Anil K Sood
Gynecologic Oncology Group · USThe University of Texas MD Anderson Cancer Center · USUniversity of California, Los Angeles · USUniversity of Iowa · US

Funding

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
Ovarian Cancer: Mechanisms of Neuroendocrine RegulationR01CA109298 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SOOD, ANIL K · 2005 to 2017
$4.5M
Biobehavioral Influences and the Ovarian Tumor MicroenvironmentR01CA140933 · NCI · UNIVERSITY OF IOWA · PI LUTGENDORF, SUSAN K · 2009 to 2013
$2.8M
Tumor metastasis: Biobehavioral mechanismsR01CA110793 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SOOD, ANIL K · 2004 to 2009
$2.1M
Combinatorial Genomics in CancerR01CA116778 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI COLE, STEVE W · 2006 to 2010
$1.5M
Role of Src in Stress-Mediated Progression of Ovarian CancerF31CA126474 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ARMAIZ-PENA, GUILLEROMO N · 2006 to 2009
$108k
NCI NIH HHS CA109298NCI NIH HHS CA110793NCI NIH HHS F31 CA126474NCI NIH HHS F31CA126474NCI NIH HHS P50 CA083639NCI NIH HHS P50CA083639NCI NIH HHS R01 CA109298NCI NIH HHS R01 CA110793NCI NIH HHS R01 CA116778NCI NIH HHS R01 CA140933PHS HHS NCI T32
6 · The paper itself

Abstract

purposeThe effects of reproductive hormones on ovarian cancer growth are not well understood. Here, we examined the effects of estrous cycle variation and specific reproductive hormones on ovarian cancer growth. EXPERIMENTAL

designWe investigated the role of reproductive hormones in ovarian cancer growth using both in vivo and in vitro models of tumor growth.

resultsIn vivo experiments using the HeyA8 and SKOV3ip1 ovarian cancer models showed that tumor cell inoculation during proestrus significantly increased tumor burden (251-273%) compared with injection during the estrus phase. Treatment of ovariectomized mice with 17beta-estradiol resulted in a 404% to 483% increase in tumor growth compared with controls. Progestins had no significant effect, but did block estrogen-stimulated tumor growth. Tumors collected from mice sacrificed during proestrus showed increased levels of vascular endothelial growth factor (VEGF) and microvessel density compared with mice injected during estrus. HeyA8, SKOV3ip1, and mouse endothelial (MOEC) cells expressed estrogen receptor alpha and beta and progesterone receptor at the protein and mRNA levels, whereas 2774 ovarian cancer cells were estrogen receptor-negative. In vitro assays showed that 17beta-estradiol significantly increased ovarian cancer cell adhesion to collagen in estrogen receptor-positive, but not in estrogen receptor-negative cells. Additionally, 17beta-estradiol increased the migratory potential of MOEC cells, which was abrogated by the mitogen-activated protein kinase (MAPK) inhibitor, PD 09859. Treatment with 17beta-estradiol activated MAPK in MOEC cells, but not in HeyA8 or SKOV3ip1 cells.

conclusionOur data suggest that estrogen may promote in vivo ovarian cancer growth, both directly and indirectly, by making the tumor microenvironment more conducive for cancer growth.

Indexed as

AnimalsBlotting, WesternCell AdhesionCell MovementCell ProliferationEstradiolEstrogen Receptor alphaEstrogensEstrous CycleFemaleHormone Replacement TherapyHumansImmunoenzyme TechniquesImmunoprecipitationMiceMice, NudeEstradiolEstrogen Receptor alphaEstrogensMitogen-Activated Protein KinasesReceptors, ProgesteroneRNA, MessengerVascular Endothelial Growth Factor A

Identifiers

PMID19383821
PMCPMC2743312
OpenAlexW2171325859

What OpenQuestion holds

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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.