Evidence map›Paper›PMID 29472726›Full record

ArticleScientific reports2018

Combinatory use of distinct single-cell RNA-seq analytical platforms reveals the heterogeneous transcriptome response.

Yukie Kashima, Ayako Suzuki, Ying Liu, Masahito Hosokawa, Hiroko Matsunaga, Masataka Shirai, Kohji Arikawa, Sumio Sugano, Takashi Kohno, Haruko Takeyama and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. LncRNA MAFG-AS1 is involved in human cancer progression.European journal of medical research · 2023
    Review
  4. Article
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  11. Review
  12. Article
  13. SMARTer single cell total RNA sequencing.Nucleic acids research · 2019
    Article
  14. 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

12 authors at 5 institutions in 1 country.

Yukie KashimaDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba, 277-8562, Japan.
Ayako SuzukiDivision of Translational Genomics, The Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Chiba, 277-8577, Japan.
Ying LiuDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba, 277-8562, Japan.
Masahito HosokawaDepartment of Life Science and Medical Bioscience, Waseda University, Shinjuku-ku, Tokyo, 162-8480, Japan.ORCID 0000-0002-7070-4690
Hiroko MatsunagaHitachi Ltd., Research & Development Group, Kokubunji-shi, Tokyo, 185-8601, Japan.
Masataka ShiraiHitachi Ltd., Research & Development Group, Kokubunji-shi, Tokyo, 185-8601, Japan.
Kohji ArikawaHitachi Ltd., Research & Development Group, Kokubunji-shi, Tokyo, 185-8601, Japan.
Sumio SuganoDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba, 277-8562, Japan.
Takashi KohnoDivision of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, 104-0045, Japan.
Haruko TakeyamaDepartment of Life Science and Medical Bioscience, Waseda University, Shinjuku-ku, Tokyo, 162-8480, Japan.
Katsuya TsuchiharaDivision of Translational Genomics, The Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Chiba, 277-8577, Japan.
Yutaka SuzukiDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba, 277-8562, Japan. ysuzuki@hgc.jp.
The University of Tokyo · JPHitachi (Japan) · JPChiba Cancer Center · JPWaseda University · JPNational Cancer Centre Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Single-cell RNA-seq is a powerful tool for revealing heterogeneity in cancer cells. However, each of the current single-cell RNA-seq platforms has inherent advantages and disadvantages. Here, we show that combining the different single-cell RNA-seq platforms can be an effective approach to obtaining complete information about expression differences and a sufficient cellular population to understand transcriptional heterogeneity in cancers. We demonstrate that it is possible to estimate missing expression information. We further demonstrate that even in the cases where precise information for an individual gene cannot be inferred, the activity of given transcriptional modules can be analyzed. Interestingly, we found that two distinct transcriptional modules, one associated with the Aurora kinase gene and the other with the DUSP gene, are aberrantly regulated in a minor population of cells and may thus contribute to the possible emergence of dormancy or eventual drug resistance within the population.

Indexed as

Aurora Kinase ACell Line, TumorDual Specificity Phosphatase 1Gene Expression Regulation, NeoplasticHigh-Throughput Nucleotide SequencingHumansNeoplasmsSingle-Cell AnalysisTranscriptomeAURKA protein, humanAurora Kinase ADual Specificity Phosphatase 1DUSP1 protein, human

Identifiers

PMID29472726
PMCPMC5823859
OpenAlexW2807244581

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.