Evidence map›Paper›PMID 35611554›Full record

ArticleDisease models & mechanisms2022

Identification of two cancer stem cell-like populations in triple-negative breast cancer xenografts.

Jun Nakayama, Hiroko Matsunaga, Koji Arikawa, Takuya Yoda, Masahito Hosokawa, Haruko Takeyama, Yusuke Yamamoto, Kentaro Semba

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2022. 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
1.2field-weighted citation impact, top 20% 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, 12 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 2 institutions in 1 country.

Jun NakayamaLaboratory of Integrative Oncology, National Cancer Center Research Institute, Tokyo 104-0045, Japan.ORCID 0000-0001-8844-4295
Hiroko MatsunagaResearch Organization for Nano & Life Innovation, Waseda University, Tokyo 169-8555, Japan.
Koji ArikawaComputational Bio-Big Data Open Innovation Laboratory (CBBD-OIL), National Institute of Advanced Industrial Science and Technology (AIST), Tokyo 169-8555, Japan.
Takuya YodaDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering, Waseda University, Tokyo 162-8480, Japan.
Masahito HosokawaDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering, Waseda University, Tokyo 162-8480, Japan.ORCID 0000-0002-7070-4690
Haruko TakeyamaDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering, Waseda University, Tokyo 162-8480, Japan.
Yusuke YamamotoLaboratory of Integrative Oncology, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Kentaro SembaDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering, Waseda University, Tokyo 162-8480, Japan.ORCID 0000-0001-7507-8214
Waseda University · JPFukushima Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene expression analysis at the single-cell level by next-generation sequencing has revealed the existence of clonal dissemination and microheterogeneity in cancer metastasis. The current spatial analysis technologies can elucidate the heterogeneity of cell-cell interactions in situ. To reveal the regional and expressional heterogeneity in primary tumors and metastases, we performed transcriptomic analysis of microtissues dissected from a triple-negative breast cancer (TNBC) cell line MDA-MB-231 xenograft model with our automated tissue microdissection punching technology. This multiple-microtissue transcriptome analysis revealed three cancer cell-type clusters in the primary tumor and axillary lymph node metastasis, two of which were cancer stem cell (CSC)-like clusters (CD44/MYC-high, HMGA1-high). Reanalysis of public single-cell RNA-sequencing datasets confirmed that the two CSC-like populations existed in TNBC xenograft models and in TNBC patients. The diversity of these multiple CSC-like populations could cause differential anticancer drug resistance, increasing the difficulty of curing this cancer.

Indexed as

Antineoplastic AgentsTriple Negative Breast NeoplasmsCell Line, TumorHeterograftsHumansNeoplastic Stem CellsAntineoplastic AgentsBreast cancerCancerCancer stem cellscRNA-seqSpatial transcriptomeXenograft model

Identifiers

PMID35611554
PMCPMC9235877
OpenAlexW4281481145

What OpenQuestion holds

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LicenceCC BY
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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.