Evidence map›Paper›PMID 37634223›Full record

ArticleHuman cell2023

De-differentiation in cultures of organoids from luminal-type breast cancer is restored by inhibition of NOTCH signaling.

Hiroyuki Uematsu, Chieko Saito, Jumpei Kondo, Kunishige Onuma, Roberto Coppo, Yukiko Mori, Manabu Muto, Yuichiro Kikawa, Manami Tada, Tomoharu Sugie and 1 more

Abstract read
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Article in Human cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.4field-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

11 citing papers in PubMed, 19 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

11 authors at 2 institutions in 1 country.

Hiroyuki UematsuDepartment of Clinical Bio-Resource Research and Development, Graduate School of Medicine, Kyoto University, 46-29, Shimoadachi-cho, Sakyo-ku, Kyoto, 606-8304, Japan.
Chieko SaitoDepartment of Clinical Bio-Resource Research and Development, Graduate School of Medicine, Kyoto University, 46-29, Shimoadachi-cho, Sakyo-ku, Kyoto, 606-8304, Japan.
Jumpei KondoDepartment of Clinical Bio-Resource Research and Development, Graduate School of Medicine, Kyoto University, 46-29, Shimoadachi-cho, Sakyo-ku, Kyoto, 606-8304, Japan.
Kunishige OnumaDepartment of Clinical Bio-Resource Research and Development, Graduate School of Medicine, Kyoto University, 46-29, Shimoadachi-cho, Sakyo-ku, Kyoto, 606-8304, Japan.
Roberto CoppoDepartment of Clinical Bio-Resource Research and Development, Graduate School of Medicine, Kyoto University, 46-29, Shimoadachi-cho, Sakyo-ku, Kyoto, 606-8304, Japan.
Yukiko MoriDepartment of Therapeutic Oncology, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Manabu MutoDepartment of Therapeutic Oncology, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Yuichiro KikawaDepartment of Breast Surgery, Kansai Medical University, Hirakata, Osaka, 573-1191, Japan.
Manami TadaDepartment of Breast Surgery, Kansai Medical University, Hirakata, Osaka, 573-1191, Japan.
Tomoharu SugieDepartment of Breast Surgery, Kansai Medical University, Hirakata, Osaka, 573-1191, Japan.
Masahiro InoueDepartment of Clinical Bio-Resource Research and Development, Graduate School of Medicine, Kyoto University, 46-29, Shimoadachi-cho, Sakyo-ku, Kyoto, 606-8304, Japan. masa_inoue@kuhp.kyoto-u.ac.jp.ORCID http://orcid.org/0000-0001-7315-026X
Kyoto University · JPKansai Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Estrogen receptor (ER) expression in breast cancer can change during progression and the treatment, but the mechanism has not been well studied. In this study, we successfully prepared organoids from samples obtained from 33 luminal-type breast cancer patients and studied their ER expression. The expression status was well maintained in primary organoids, whereas it decreased after passaging in most of the cases. In fact, the studied organoid lines were classified into those that retained a high level of ER expression (9%), those that completely lost it (9%), and those that repressed it to varying degrees (82%). In some cases, the ER expression was suddenly and drastically decreased after passaging. Marker protein immunohistochemistry revealed that after passaging, the differentiation status shifted from a luminal- to a basal-like status. Differentially expressed genes suggested the activation of NOTCH signaling in the passaged organoids, wherein a NOTCH inhibitor was able to substantially rescue the decreased ER expression and alter the differentiation status. Our findings suggest that the differentiation status of luminal-type cancer cells is quite flexible, and that by inhibiting the NOTCH signaling we can preserve the differentiation status of luminal-type breast cancer organoids.

Indexed as

Breast NeoplasmsCell DedifferentiationCell DifferentiationOrganoidsReceptors, NotchSignal TransductionFemaleGene ExpressionHumansReceptors, EstrogenReceptors, EstrogenReceptors, NotchBreast cancerDifferentiationEstrogen receptorNotchOrganoid

Identifiers

PMID37634223
OpenAlexW4386203537

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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.