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suck abstract from ncbi


10.1038/ncomms15107

http://scihub22266oqcxt.onion/10.1038/ncomms15107
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suck abstract from ncbi


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pmid28561063
      Nat+Commun 2017 ; 8 (ä): 15107
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  • Selective analysis of cancer-cell intrinsic transcriptional traits defines novel clinically relevant subtypes of colorectal cancer #MMPMID28561063
  • Isella C ; Brundu F ; Bellomo SE ; Galimi F ; Zanella E ; Porporato R ; Petti C ; Fiori A ; Orzan F ; Senetta R ; Boccaccio C ; Ficarra E ; Marchionni L ; Trusolino L ; Medico E ; Bertotti A
  • Nat Commun 2017[May]; 8 (ä): 15107 PMID28561063 show ga
  • Stromal content heavily impacts the transcriptional classification of colorectal cancer (CRC), with clinical and biological implications. Lineage-dependent stromal transcriptional components could therefore dominate over more subtle expression traits inherent to cancer cells. Since in patient-derived xenografts (PDXs) stromal cells of the human tumour are substituted by murine counterparts, here we deploy human-specific expression profiling of CRC PDXs to assess cancer-cell intrinsic transcriptional features. Through this approach, we identify five CRC intrinsic subtypes (CRIS) endowed with distinctive molecular, functional and phenotypic peculiarities: (i) CRIS-A: mucinous, glycolytic, enriched for microsatellite instability or KRAS mutations; (ii) CRIS-B: TGF-? pathway activity, epithelial-mesenchymal transition, poor prognosis; (iii) CRIS-C: elevated EGFR signalling, sensitivity to EGFR inhibitors; (iv) CRIS-D: WNT activation, IGF2 gene overexpression and amplification; and (v) CRIS-E: Paneth cell-like phenotype, TP53 mutations. CRIS subtypes successfully categorize independent sets of primary and metastatic CRCs, with limited overlap on existing transcriptional classes and unprecedented predictive and prognostic performances.
  • |*Transcriptome [MESH]
  • |Animals [MESH]
  • |Antineoplastic Agents, Immunological/pharmacology [MESH]
  • |Cell Lineage [MESH]
  • |Cetuximab/pharmacology [MESH]
  • |Colorectal Neoplasms/*classification/*genetics/pathology [MESH]
  • |Epithelial-Mesenchymal Transition [MESH]
  • |ErbB Receptors/antagonists & inhibitors/immunology/metabolism [MESH]
  • |Female [MESH]
  • |Gene Expression Profiling [MESH]
  • |Genes, p53 [MESH]
  • |Glycolysis [MESH]
  • |Heterografts [MESH]
  • |Humans [MESH]
  • |Insulin-Like Growth Factor II/genetics [MESH]
  • |Male [MESH]
  • |Mice [MESH]
  • |Microsatellite Instability [MESH]
  • |Mutation [MESH]
  • |Prognosis [MESH]
  • |Signal Transduction [MESH]
  • |Stromal Cells/*metabolism/pathology [MESH]


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  • suck abstract from ncbi

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