Evidence map›Paper›PMID 30956772›Full record

ArticleOncotarget2019

Estrogen stimulates female cancer progression by inducing myeloid-derived suppressive cells: investigations on pregnant and non-pregnant experimental models.

Katsumi Kozasa, Seiji Mabuchi, Yuri Matsumoto, Hiromasa Kuroda, Eriko Yokoi, Naoko Komura, Mahiru Kawano, Ryoko Takahashi, Tomoyuki Sasano, Kotaro Shimura and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 29 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

15 authors at 2 institutions in 1 country.

Katsumi KozasaDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Seiji MabuchiDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Yuri MatsumotoDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Hiromasa KurodaDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Eriko YokoiDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Naoko KomuraDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Mahiru KawanoDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Ryoko TakahashiDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Tomoyuki SasanoDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Kotaro ShimuraDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Michiko KodamaDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Kae HashimotoDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Kenjiro SawadaDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Kazunori NagasakaDepartment of Obstetrics and Gynecology, Teikyo University School of Medicine, Tokyo, Japan.
Tadashi KimuraDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka, Japan.
Osaka University · JPTeikyo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the clinical implications of 17β-estradiol (E2) in estrogen receptor α (ERα)-negative female cancer progression as well as the underlying biological mechanisms.

methodsClinical data from 306 locally-advanced cervical cancer (stage IIB-IVA) patients were analyzed in order to investigate the relationships between age, serum E2 levels, and treatment outcomes. Clinical samples, ERα-negative cervical and breast cancer cell lines, and mouse xenograft models of cervical and breast cancers were employed in order to elucidate the mechanisms responsible for the E2- and pregnancy-mediated progression of cervical and breast cancers, with a focus on the role of myeloid-derived suppressor cells (MDSC).

resultsYounger patients with elevated E2 levels showed significantly shorter progression-free survival (

conclusionsE2 facilitates the progression of ERα-negative cervical or breast cancer under non-pregnant and pregnant conditions by inducing MDSC. MDSC inhibition therapy may have therapeutic efficacy in premenopausal or pregnant female cancer patients.

Indexed as

brest cancercervical cancerestrogenMDSCpregnancy

Identifiers

PMID30956772
PMCPMC6443012
OpenAlexW2921913306

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.