Colorectal cancer articles within Nature

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  • Article
    | Open Access

    A study reveals that Fusobacterium nucleatum subspecies animalis is bifurcated into two distinct clades, and shows that only one of these dominates the colorectal cancer niche, probably through increased colonization of the human gastrointestinal tract.

    • Martha Zepeda-Rivera
    • , Samuel S. Minot
    •  & Christopher D. Johnston

  • Article |

    Transcriptomic and chromatin accessibility analyses of naive and transplanted colon cancer organoids in a mouse model reveal a key role for the transcription factor SOX17 in establishing a permissive immune environment for tumour cells.

    • Norihiro Goto
    • , Peter M. K. Westcott
    •  & Ömer H. Yilmaz

  • Article |

    A murine colorectal cancer (CRC) model shows that mutant KRAS-STAT4-mediated upregulation of Y chromosome KDM5D contributes to the sex differences in KRAS-mutant CRC, providing an actionable therapeutic strategy for metastasis risk reduction for men afflicted with KRAS-mutant CRC.

    • Jiexi Li
    • , Zhengdao Lan
    •  & Ronald A. DePinho

  • Article
    | Open Access

    A study maps genetic and epigenetic heterogeneity of primary colorectal adenomas and cancers at single-clone resolution through spatial multi-omic profiling of individual glands and adjacent normal tissue.

    • Timon Heide
    • , Jacob Househam
    •  & Andrea Sottoriva

  • Article
    | Open Access

    Intratumour genetic ancestry only infrequently affects gene expression traits and subclonal evolution in colorectal cancer, with most genetic intratumour variation having no detected phenotypic consequence and transcriptional plasticity being widespread within a tumour.

    • Jacob Househam
    • , Timon Heide
    •  & Trevor A. Graham

  • Article
    | Open Access

    Membrane-bound E3 ubiquitin ligases RNF43 and ZNRF3 are overexpressed in colorectal cancer, and can be repurposed using proteolysis-targeting antibodies (PROTABs) to selectively degrade cell-surface receptors in tumours.

    • Hadir Marei
    • , Wen-Ting K. Tsai
    •  & Felipe de Sousa e Melo

  • Article |

    A genetic lineage-tracing system in human colorectal organoids identifies a population of dormant cancer cells that persists during chemotherapy and enables cancer regrowth, and the cell-adhesion molecule COL17A1 has a key role in the process of breaking dormancy.

    • Yuki Ohta
    • , Masayuki Fujii
    •  & Toshiro Sato

  • Article |

    The growth of colorectal cancer is reduced by ketogenic diet consumption, the properties of which are mediated by the ketone body β-hydroxybutyrate.

    • Oxana Dmitrieva-Posocco
    • , Andrea C. Wong
    •  & Maayan Levy

  • Article
    | Open Access

    A survey of potency and efficacy of 2,025 clinically relevant two-drug combinations against 125 molecularly characterized breast, colorectal and pancreatic cancer cell lines identifies rare synergistic effects of anticancer drugs, informing rational combination treatments for specific cancer subtypes.

    • Patricia Jaaks
    • , Elizabeth A. Coker
    •  & Mathew J. Garnett

  • Review Article |

    This Review describes the interplay between host genetics, host immunity and the gut microbiome in the modulation of colorectal cancer, and discusses the role of specific bacterial species and metabolites alongside technological advances that will facilitate more in-depth investigation of the microbiome in disease.

    • Alina Janney
    • , Fiona Powrie
    •  & Elizabeth H. Mann

  • Article |

    In patients with ulcerative colitis, chronic inflammation can lead to remodelling of the colorectal epithelium through positive selection of clones with mutations in genes related to IL-17 signalling, which, however, might be negatively selected during colitis-associated carcinogenesis.

    • Nobuyuki Kakiuchi
    • , Kenichi Yoshida
    •  & Seishi Ogawa

  • Letter |

    Sporadic inactivation of the interleukin-22 receptor in the intestinal epithelium of the mouse shows that IL-22 is required for effective activation of the DNA damage response following DNA damage.

    • Konrad Gronke
    • , Pedro P. Hernández
    •  & Andreas Diefenbach

  • 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 |

    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

  • 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 |

    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 |

    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

  • 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.

  • News & Views |

    Rare tumour cells with mutations that confer drug resistance can go undetected by standard testing procedures, according to two studies, which show that such mutations can be detected in patients' blood. See Letters p.532 and p.537

    • Eduardo Vilar
    •  & Josep Tabernero

  • 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

  • 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

  • Letter |

    This study shows, via a mouse model of intestinal cancer, that in the absence of CKIα, the loss of p53 dramatically enhances tumour progression and metastasis. p53 is shown to normally limit cancer cell invasion via the regulation of p21 and a set of invasion genes that include Prox1. This study adds important insights to the emerging picture that during tumour development the p53 tumour suppressor gene not only controls cell death and proliferation but also metastasis.

    • Ela Elyada
    • , Ariel Pribluda
    •  & Yinon Ben-Neriah

  • Letter |

    Cancer 'chemoprevention' uses substances to reverse, suppress or prevent the initial phase of carcinogenesis or the progression of neoplastic cells to cancer cells. Here it is shown that treatment with TRAIL proteins and all-trans-retinyl acetate can cause the death, in vitro and in vivo, of premalignant cells deficient in the adenomatous polyposis coli gene. Normal cells are unaffected. Selectively eliminating premalignant tumour cells in this way is thus an effective method for chemoprevention.

    • Ling Zhang
    • , Xiaoyang Ren
    •  & Xiangwei Wu

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