Evidence map›Paper›PMID 29118272›Full record

ArticleOpen biology2017

Beyond cancer genes: colorectal cancer as robust intrinsic states formed by molecular interactions.

Ruoshi Yuan, Suzhan Zhang, Jiekai Yu, Yanqin Huang, Demin Lu, Runtan Cheng, Sui Huang, Ping Ao, Shu Zheng, Leroy Hood and 1 more

Abstract read
In one paragraph

Article in Open biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

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  8. Oncogenic and tumor suppressor function of MEIS and associated factors.Turkish journal of biology = Turk biyoloji dergisi · 2020
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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.

Ruoshi YuanKey Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, People's Republic of China.ORCID 0000-0002-9508-7326
Suzhan ZhangKey Laboratory of Cancer Prevention and Intervention, Chinese Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, Hangzhou, Zhejiang Province 310009, People's Republic of China.
Jiekai YuKey Laboratory of Cancer Prevention and Intervention, Chinese Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, Hangzhou, Zhejiang Province 310009, People's Republic of China.
Yanqin HuangKey Laboratory of Cancer Prevention and Intervention, Chinese Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, Hangzhou, Zhejiang Province 310009, People's Republic of China.
Demin LuKey Laboratory of Cancer Prevention and Intervention, Chinese Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, Hangzhou, Zhejiang Province 310009, People's Republic of China.
Runtan ChengKey Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, People's Republic of China.
Sui HuangInstitute for Systems Biology, 401 Terry Ave. N., Seattle, WA 98109-5234, USA.
Ping AoKey Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, People's Republic of China aoping@sjtu.edu.cn.ORCID 0000-0001-7109-628X
Shu ZhengKey Laboratory of Cancer Prevention and Intervention, Chinese Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, Hangzhou, Zhejiang Province 310009, People's Republic of China.
Leroy HoodInstitute for Systems Biology, 401 Terry Ave. N., Seattle, WA 98109-5234, USA.
Xiaomei ZhuKey Laboratory of Systems Biomedicine, Ministry of Education, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai 200240, People's Republic of China xiaomeizhu@yahoo.com.ORCID 0000-0002-3674-3565

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) has complex pathological features that defy the linear-additive reasoning prevailing in current biomedicine studies. In pursuing a mechanistic understanding behind such complexity, we constructed a core molecular-cellular interaction network underlying CRC and investigated its nonlinear dynamical properties. The hypothesis and modelling method has been developed previously and tested in various cancer studies. The network dynamics reveal a landscape of several attractive basins corresponding to both normal intestinal phenotype and robust tumour subtypes, identified by their different molecular signatures. Comparison between the modelling results and gene expression profiles from patients collected at the second affiliated hospital of Zhejiang University is presented as validation. The numerical 'driving' experiment suggests that CRC pathogenesis may depend on pathways involved in gastrointestinal track development and molecules associated with mesenchymal lineage differentiation, such as Stat5, BMP, retinoic acid signalling pathways, Runx and Hox transcription families. We show that the multi-faceted response to immune stimulation and therapies, as well as different carcinogenesis and metastasis routes, can be straightforwardly understood and analysed under such a framework.

Indexed as

Models, TheoreticalSystems BiologyCase-Control StudiesColorectal NeoplasmsHumansNonlinear DynamicsStochastic Processescolorectal cancerendogenous molecular–cellular networkrobust dynamical statesstochastic nonlinear dynamicssystems biology

Identifiers

PMID29118272
PMCPMC5717345

What OpenQuestion holds

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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.