Evidence map›Paper›PMID 26797759›Full record

ArticleOncotarget2016

Multiple direct and indirect mechanisms drive estrogen-induced tumor growth in high grade serous ovarian cancers.

Alessandra Ciucci, Gian Franco Zannoni, Marianna Buttarelli, Lucia Lisi, Daniele Travaglia, Enrica Martinelli, Giovanni Scambia, Daniela Gallo

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
7.9field-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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.

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  16. Regulation of aromatase in cancer.Molecular and cellular biochemistry · 2021
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  17. Article
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  20. The Role of the Estrogen Pathway in the Tumor Microenvironment.International journal of molecular sciences · 2018
    Review
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 at 1 institution in 1 country.

Alessandra CiucciDepartment of Obstetrics and Gynecology, Catholic University of The Sacred Heart, 00168 Rome, Italy.
Gian Franco ZannoniDepartment of Histopathology, Catholic University of The Sacred Heart, 00168 Rome, Italy.
Marianna ButtarelliDepartment of Obstetrics and Gynecology, Catholic University of The Sacred Heart, 00168 Rome, Italy.
Lucia LisiInstitute of Pharmacology, Catholic University of The Sacred Heart, 00168 Rome, Italy.
Daniele TravagliaDepartment of Obstetrics and Gynecology, Catholic University of The Sacred Heart, 00168 Rome, Italy.
Enrica MartinelliDepartment of Obstetrics and Gynecology, Catholic University of The Sacred Heart, 00168 Rome, Italy.
Giovanni ScambiaDepartment of Obstetrics and Gynecology, Catholic University of The Sacred Heart, 00168 Rome, Italy.
Daniela GalloDepartment of Obstetrics and Gynecology, Catholic University of The Sacred Heart, 00168 Rome, Italy.
Università Cattolica del Sacro Cuore · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The notion that menopausal estrogen replacement therapy increases ovarian cancer risk, but only for the two more common types (i.e. serous and endometrioid), while possibly decreasing risk for clear cell tumors, is strongly suggestive of causality. However, whether estradiol (E2) is tumorigenic or promotes development of occult preexisting disease is unknown. The present study investigated molecular and cellular mechanisms by which E2 modulates the growth of high grade serous ovarian cancer (HGSOC). Results showed that ERα expression was necessary and sufficient to induce the growth of HGSOC cells in in vitro models. Conversely, in vivo experimental studies demonstrated that increasing the levels of circulating estrogens resulted in a significant growth acceleration of ERα-negative HGSOC xenografts, as well. Tumors from E2-treated mice had significantly higher proliferation rate, angiogenesis, and density of tumor-associated macrophage (TAM) compared to ovariectomized females. Accordingly, immunohistochemical analysis of ERα-negative tissue specimens from HGSOC patients showed a significantly greater TAM infiltration in premenopausal compared to postmenopausal women. This study describes novel insights into the impact of E2 on tumor microenvironment, independently of its direct effect on tumor cell growth, thus supporting the idea that multiple direct and indirect mechanisms drive estrogen-induced tumor growth in HGSOC.

Indexed as

Cell ProliferationAdolescentAdultAgedAnimalsBlotting, WesternCase-Control StudiesCystadenocarcinoma, SerousEstradiolEstrogensFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansImmunoenzyme TechniquesMiceEstradiolEstrogensReceptors, EstrogenRNA, MessengerERestradiolovarytumor-associated macrophagestumor microenvironment

Identifiers

PMID26797759
PMCPMC4884983
OpenAlexW2279734137

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.