Gastrointestinal cancer articles within Nature

Featured

  • Article |

    LGR5+ cells in human colorectal cancer tissue xenografted into mice act as cancer stem cells, and differentiated cancer cells can revert to cancer stem cells and express LGR5 after ablation of existing LGR5+ cells.

    • Mariko Shimokawa
    • , Yuki Ohta
    •  & Toshiro Sato

  • Article
    | Open Access

    The Cancer Genome Atlas Research Network report integrated genomic and molecular analyses of 164 squamous cell carcinomas and adenocarcinomas of the oesophagus; they find genomic and molecular features that differentiate squamous and adenocarcinomas of the oesophagus, and strong similarities between oesophageal adenocarcinomas and the chromosomally unstable variant of gastric adenocarcinoma, suggesting that gastroesophageal adenocarcinoma is a single disease entity.

    • Jihun Kim
    • , Reanne Bowlby
    •  & Jiashan Zhang

  • Article |

    A high-fat diet increases the number of intestinal stem cells in mammals, both in vivo and in intestinal organoids; a pathway that involves PPAR-δ confers organoid-initiating capacity to non-stem cells and induces them to form in vivo tumours after loss of the Apc tumour suppressor.

    • Semir Beyaz
    • , Miyeko D. Mana
    •  & Ömer H. Yilmaz

  • Article |

    An integrated genomic analysis of 456 human pancreatic ductal adenocarcinomas identifies four subtypes defined by transcriptional expression profiles and show that these are associated with distinct histopathological characteristics and differential prognosis.

    • Peter Bailey
    • , David K. Chang
    •  & Sean M. Grimmond

  • Article |

    Glypican-1 identifies cancer exosomes and serves as a biomarker for detection of early pancreatic cancer in patients and mouse models of the disease; the findings may enable early and non-invasive identification, and prevention of malignant cancer.

    • Sonia A. Melo
    • , Linda B. Luecke
    •  & Raghu Kalluri

  • Letter |

    Examination of allele-specific expression identifies 71 genes with excess somatic cis-regulatory effects in colorectal cancer (CRC), and 1,693 and 948 expression quantitative trait loci (eQTLs) in normal samples and tumours, respectively (with 36% of tumour eQTLs exclusive to CRC); tumour-specific eQTLs are more enriched for low CRC genome-wide association study P values and accumulate more somatic mutations than shared eQTLs, suggesting a role as germline-derived cancer regulatory drivers.

    • Halit Ongen
    • , Claus L. Andersen
    •  & Emmanouil T. Dermitzakis

  • Article
    | Open Access

    The Cancer Genome Atlas reports on molecular evaluation of 295 primary gastric adenocarcinomas and proposes a new classification of gastric cancers into 4 subtypes, which should help with clinical assessment and trials of targeted therapies.

    • Adam J. Bass
    • , Vesteinn Thorsson
    •  & Jia Liu

  • Article |

    Proteome analysis of The Cancer Genome Atlas (TCGA) colorectal cancer specimens reveals that DNA- or RNA-level measurements cannot reliably predict protein abundance, colorectal tumours can be separated into distinct proteotypes, and that copy number alterations drive mRNA abundance changes but few extend to protein-level changes.

    • Bing Zhang
    • , Jing Wang
    •  & R. Reid Townsend

  • Letter |

    Gain-of-function mutations in isocitrate dehydrogenase (IDH) are among the most common genetic alterations in intrahepatic cholangiocarcinoma (IHCC), a deadly cancer of the liver bile ducts; now mutant IDH is shown to block liver cell differentiation through the suppression of HNF-4α, a master regulator of hepatocyte identity and quiescence, leading to expansion of liver progenitor cells primed for progression to IHCC.

    • Supriya K. Saha
    • , Christine A. Parachoniak
    •  & Nabeel Bardeesy

  • Letter |

    A mechanism to explain chromosomal instability (CIN) in colorectal cancer is demonstrated; three new CIN-suppressor genes (PIGN, MEX3C and ZNF516) encoded on chromosome 18q are identified, the loss of which leads to DNA replication stress, resulting in structural and numerical chromosome segregation errors, which are shown to be identical to phenotypes seen in CIN cells.

    • Rebecca A. Burrell
    • , Sarah E. McClelland
    •  & Charles Swanton

  • Article |

    Exome sequencing and copy number analysis are used to define genomic aberrations in early sporadic pancreatic ductal adenocarcinoma; among the findings are mutations in genes involved in chromatin modification and DNA damage repair, and frequent and diverse somatic aberrations in genes known as embryonic regulators of axon guidance.

    • Andrew V. Biankin
    • , Nicola Waddell
    •  & Sean M. Grimmond

  • Letter |

    IL-22 is one of the factors that, although important for wound healing, also promote tumorigenesis; the regulation of IL-22BP, the IL-22 binding protein, via the NLRP3 and NLRP6 inflammasomes provides an unanticipated mechanism, controlling IL-22 and thereby the development of colon cancer.

    • Samuel Huber
    • , Nicola Gagliani
    •  & Richard A. Flavell

  • Letter
    | Open Access

    Exomes, transcriptomes and copy-number alterations in a sample of more than 70 primary human colonic tumours were analysed in an attempt to characterize the genomic landscape; in addition to finding alterations in genes associated with commonly mutated signalling pathways, recurrent gene fusions involving R-spondin family members were also found to occur in approximately 10% of colonic tumours, revealing a potential new therapeutic target.

    • Somasekar Seshagiri
    • , Eric W. Stawiski
    •  & Frederic J. de Sauvage

  • Article
    | Open Access

    The Cancer Genome Atlas consortium reports on their genome-wide characterization of somatic alterations in colorectal cancer; in addition to revealing a remarkably consistent pattern of genomic alteration, with 24 genes being significantly mutated, the study identifies new targets for therapeutic intervention and suggests an important role for MYC-directed transcriptional activation and repression.

    • Donna M. Muzny
    • , Matthew N. Bainbridge
    •  & Elizabeth Thomson.

  • Letter |

    This work on colorectal cancer shows that secondary mutations in KRAS that confer resistance to panitumumab, an anti-EGFR monoclonal antibody, are already present when antibody treatment begins; the apparent inevitability of resistance suggests that combinations of drugs targeting at least two different oncogenic pathway will be needed for treatment.

    • Luis A. Diaz Jr
    • , Richard T. Williams
    •  & Bert Vogelstein

  • Letter |

    An in vivo transposon screen in a pancreatic cancer model identifies frequent inactivation of Usp9x; deletion of Usp9x cooperates with KrasG12D to accelerate rapidly pancreatic tumorigenesis in mice, validating their genetic interaction.

    • Pedro A. Pérez-Mancera
    • , Alistair G. Rust
    •  & David A. Tuveson

  • News & Views |

    A drug for treating melanoma is ineffective in colorectal cancers that have the same causative mutation. Studies of how cells adapt to the drug reveal why this is so, and suggest combination therapies that may be more effective. See Letter p.100

    • David B. Solit
    •  & Pasi A. Jänne

  • Letter |

    A mouse model is developed in which the pro-apoptotic activity of DCC is silenced and the mice are more prone to intestinal tumour progression, giving insight into the role of DCC in human colorectal cancer.

    • Marie Castets
    • , Laura Broutier
    •  & Patrick Mehlen

  • News & Views |

    Damaged cells can initiate cancer. To avert this, faulty cells disable their own propagation by undergoing senescence. But for full protection against liver cancer, the senescent cells must be cleared by the immune system. See Letter p.547

    • Manuel Serrano

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