Evidence map›Paper›PMID 27941887›Full record

ArticleOncogene2017

Evolution and heterogeneity of non-hereditary colorectal cancer revealed by single-cell exome sequencing.

H Wu, X-Y Zhang, Z Hu, Q Hou, H Zhang, Y Li, S Li, J Yue, Z Jiang, S M Weissman and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

48 citing papers in PubMed, 83 citations in OpenAlex.

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  13. Advances in SEMA3F regulation of clinically high-incidence cancers.Cancer biomarkers : section A of Disease markers · 2023
    Article
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  17. Article
  18. High-throughput single-сell sequencing in cancer research.Signal transduction and targeted therapy · 2022
    Review
  19. Article
  20. Article
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

13 authors at 3 institutions in 3 countries.

H WuCancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, China.
X-Y ZhangCancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, China.
Z HuCancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, China.
Q HouCancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, China.
H ZhangCancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, China.
Y LiCancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, China.
S LiCancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, China.
J YueCancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, China.
Z JiangCancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, China.
S M WeissmanDepartment of Genetics, Yale School of Medicine, New Haven, CT, USA.
X PanDepartment of Genetics, Yale School of Medicine, New Haven, CT, USA.
B-G JuDepartment of Life Science, Sogang University, Seoul, South Korea.
S WuCancer Research Institute, Hangzhou Cancer Hospital, Hangzhou, China.
Hangzhou Cancer Hospital · CNYale University · USSogang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently single-cell whole-exome sequencing (scWES) has deeply expanded and sharpened our knowledge of cancer evolution and subclonality. Herein, with scWES and matched bulk whole-exome sequencing (bulk WES) on two colorectal cancer (CRC) patients with normal or adenomatous polyps, we found that both the adenoma and cancer were of monoclonal origin, and both shared partial mutations in the same signaling pathways, but each showed a specific spectrum of heterogeneous somatic mutations. In addition, the adenoma and cancer further developed intratumor heterogeneity with the accumulation of nonrandom somatic mutations specifically in GPCR, PI3K-Akt and FGFR signaling pathways. We identified novel driver mutations that developed during adenoma and cancer evolution, particularly in OR1B1 (GPCR signaling pathway) for adenoma evolution, and LAMA1 (PI3K-Akt signaling pathway) and ADCY3 (FGFR signaling pathway) for CRC evolution. In summary, we demonstrated that both colorectal adenoma and CRC are monoclonal in origin, and the CRCs further diversified into different subclones with heterogeneous mutation profiles accumulating in GPCR, PI3K-Akt and FGFR signaling pathways. ScWES provides evidence for the importance of mutations in certain pathways that would not be as apparent from bulk sequencing of tumors, and can potentially establish whether specific mutations are mutually exclusive or occur sequentially in the same subclone of cells.

Indexed as

ExomeGenetic Predisposition to DiseaseHigh-Throughput Nucleotide SequencingAgedAged, 80 and overBiomarkersCell Transformation, NeoplasticColonic PolypsColorectal NeoplasmsFemaleHumansMaleMiddle AgedMutationPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktBiomarkersPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID27941887
OpenAlexW2561021019

What OpenQuestion holds

Textmetadata
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.