How the interplay among the tumor microenvironment and the gut microbiota influences the stemness of colorectal cancer cells

doi:10.4252/wjsc.v15.i5.281

Advanced Search

BPG is committed to discovery and dissemination of knowledge

Home / Archive / Volume 15, Issue 5

This Article

Academic Content and Language Evaluation of This Article

CrossCheck and Google Search of This Article

Academic Rules and Norms of This Article

Citation of this article

Corresponding Author of This Article

Research Domain of This Article

Article-Type of This Article

Open-Access Policy of This Article

Times Cited Counts in Google of This Article

Number of Hits and Downloads for This Article

Total Article Views (3032)

All Articles published online

The chart showing PDF series, WORD series, HTML series, Figures (1-2) series, Tables (1-3) series.

Item

Count

PDF

130

WORD

HTML

1863

Figures (1-2)

129

Tables (1-3)

133

Sum=2292

Publishing Process of This Article

The chart showing Browse series, Download series.

Item

Count

Browse

187

Download

553

Sum=740

May 26, 2023 (publication date) through Jul 29, 2024

Times Cited of This Article

Times Cited (2)

Journal Information of This Article

Publication Name

World Journal of Stem Cells

ISSN

1948-0210

Publisher of This Article

Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Review

World J Stem Cells. May 26, 2023; 15(5): 281-301
Published online May 26, 2023. doi: 10.4252/wjsc.v15.i5.281

Table 2 Consensus molecular subtypes of colorectal cancer

	CMS1-immune (14%)	CMS2-canonical (37%)	CMS3-metabolic (13%)	CMS4-mesenchymal (23%)	Unclassified (13%)
General features	Hypermutated	Epithelial	Epithelial	TGF-β activation. Angiogenesis	Mixed phenotype of multiple CMS
General features	Microsatellite unstable	WNT and MYC signaling activation	Metabolic dysregulation	Upregulation of EMT	Mixed phenotype of multiple CMS
Mutations	BRAF, MSH6, RNF43, ATM, TGFBr2, PTEN	APC, KRAS, TP53, PIK3CA	APC, KRAS, TP53, PIK3CA	APC, KRAS, TP53, PIK3CA
TME	Decrease of CAFs	Decrease of CAFs	Decrease of CAFs	Increase of CAFs; Immunosuppressive signature
TME	High immune and inflammatory signature	Low immune and inflammatory signature	Low immune and inflammatory signature	Increase of CAFs; Immunosuppressive signature

This Table is based on Islas et al[1], 2022; Fidelle et al[79], 2020; Trinh et al[169], 2018; Becht et al[78], 2016; Guinney et al[77], 2015. APC: Adenomatous polyposis coli gene; ATM: Ataxia telangiectasia mutated gene; BRAF: Serine/threonine-protein kinase B-raf gene; CAFs: Cancer associated fibroblasts; CMS: Consensus molecular subtype; EMT, Epithelial to mesenchymal transition; KRAS: Ki-ras2 kirsten rat sarcoma viral oncogene homolog gene; MSH6: MutS homolog 6 gene; PIK3CA: Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha gene; PTEN: Phosphatase and tensin homolog gene; RNF43: Ring finger protein 43 gene; TGF-β: Transforming growth factor beta; TGFBr2: Transforming growth factor beta receptor 2 gene; TME: Tumor microenvironment; TP53: Transformation-related protein 53 gene.

Citation: Novoa Díaz MB, Carriere P, Gentili C. How the interplay among the tumor microenvironment and the gut microbiota influences the stemness of colorectal cancer cells. World J Stem Cells 2023; 15(5): 281-301
URL: https://www.wjgnet.com/1948-0210/full/v15/i5/281.htm
DOI: https://dx.doi.org/10.4252/wjsc.v15.i5.281