Evidence map›Paper›PMID 30610551›Full record

ArticleBreast cancer (Tokyo, Japan)2019

Cancer stem-like properties of hormonal therapy-resistant breast cancer cells.

Kanami Uchiumi, Kouki Tsuboi, Nozomi Sato, Takako Ito, Hisashi Hirakawa, Toshifumi Niwa, Yuri Yamaguchi, Shin-Ichi Hayashi

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Article in Breast cancer (Tokyo, Japan), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 13 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

8 authors at 4 institutions in 1 country.

Kanami UchiumiDepartment of Molecular and Functional Dynamics, Graduate School of Medicine, Tohoku University, 2-1 Seiryo-machi, Aoba-ku, Sendai, 980-8575, Japan.
Kouki TsuboiDepartment of Molecular and Functional Dynamics, Graduate School of Medicine, Tohoku University, 2-1 Seiryo-machi, Aoba-ku, Sendai, 980-8575, Japan.
Nozomi SatoDepartment of Molecular and Functional Dynamics, Graduate School of Medicine, Tohoku University, 2-1 Seiryo-machi, Aoba-ku, Sendai, 980-8575, Japan.
Takako ItoDepartment of Blood and Cell Treatment, Tohoku University Hospital, Sendai, 980-8574, Japan.
Hisashi HirakawaDepartment of Surgery, Tohoku Kosai Hospital, Sendai, 980-0803, Japan.
Toshifumi NiwaDepartment of Molecular and Functional Dynamics, Graduate School of Medicine, Tohoku University, 2-1 Seiryo-machi, Aoba-ku, Sendai, 980-8575, Japan.
Yuri YamaguchiResearch Institute for Clinical Oncology, Saitama Cancer Center, Saitama, 362-0806, Japan.
Shin-Ichi HayashiDepartment of Molecular and Functional Dynamics, Graduate School of Medicine, Tohoku University, 2-1 Seiryo-machi, Aoba-ku, Sendai, 980-8575, Japan. shin@med.tohoku.ac.jp.
Tohoku University · JPKKR Tohoku Kosai Hospital · JPSaitama Cancer Center · JPTohoku University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPresently, hormonal therapy targeting estrogen receptors is the most effective treatment available for luminal breast cancer. However, many patients relapse after the therapy. It has been suggested that cancer stem-like cells are involved with hormonal therapy resistance; in the present study, we evaluated this hypothesis.

methodsIn the present study, we used our previously established hormonal therapy-resistant cell lines, including aromatase inhibitor (AI)-resistant cells (Type 1 and Type 2) and fulvestrant-resistant cells (MFR).

resultsAI-resistant cell lines expressing ER (Type 1 V1 and V2) showed high cancer stemness in terms of their CD44/CD24 expression and side populations, which were stimulated by the addition of estrogen and inhibited by fulvestrant. However, ALDH activity was lower than in the ER-negative resistant cells, suggesting that the stemness of luminal cells is distinct from that of basal-like breast cancer cells. The migration and invasion activity of the ER-positive Type 1 V1 and V2 cells were higher than in the ER-negative cell lines, Type 2 and MFR.

conclusionsFractionation of parental cells based on CD44/CD24 expression and colony formation assay indicated that CD44+/CD24+ cells might be the origin of hormonal therapy-resistant cells. This population reconstituted various other subpopulations under estrogen deprivation. These results indicate that hormonal therapy resistance is closely related to the cancer stem cell-like properties of luminal breast cancer.

Indexed as

Antineoplastic Agents, HormonalAromatase InhibitorsBreast NeoplasmsCD24 AntigenCell Line, TumorDrug Resistance, NeoplasmEstradiolEstrogen Receptor AntagonistsFemaleFulvestrantGene Expression Regulation, NeoplasticHumansHyaluronan ReceptorsMCF-7 CellsNeoplastic Stem CellsReceptors, EstrogenAntineoplastic Agents, HormonalAromatase InhibitorsCD24 AntigenCD24 protein, humanCD44 protein, humanEstradiolEstrogen Receptor AntagonistsFulvestrantHyaluronan ReceptorsReceptors, EstrogenBreast cancerCancer stem-like cellsEstrogen receptorHormonal therapy resistance

Identifiers

PMID30610551
OpenAlexW2908448029

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Registered trials

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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.