Cancer models

Cancer models are naturally existing or artificially induced systems that share features with human cancers. Experimental systems for studying human cancer include cell lines and organisms such as fruit flies and genetically modified mice to investigate cancer biochemical or genetic pathways and pathology.

Latest Research and Reviews

  • Research |

    Genome-wide CRISPR screens in mouse cancer cell lines are used to identify a core, conserved set of genes and pathways that govern how cancer cells evade killing by cytotoxic T lymphocytes.

    • Keith A. Lawson
    • , Cristovão M. Sousa
    • , Xiaoyu Zhang
    • , Eiru Kim
    • , Rummy Akthar
    • , Joseph J. Caumanns
    • , Yuxi Yao
    • , Nicholas Mikolajewicz
    • , Catherine Ross
    • , Kevin R. Brown
    • , Abdelrahman Abou Zid
    • , Zi Peng Fan
    • , Shirley Hui
    • , Jordan A. Krall
    • , Donald M. Simons
    • , Chloe J. Slater
    • , Victor De Jesus
    • , Lujia Tang
    • , Richa Singh
    • , Joshua E. Goldford
    • , Sarah Martin
    • , Qian Huang
    • , Elizabeth A. Francis
    • , Andrea Habsid
    • , Ryan Climie
    • , David Tieu
    • , Jiarun Wei
    • , Ren Li
    • , Amy Hin Yan Tong
    • , Michael Aregger
    • , Katherine S. Chan
    • , Hong Han
    • , Xiaowei Wang
    • , Patricia Mero
    • , John H. Brumell
    • , Antonio Finelli
    • , Laurie Ailles
    • , Gary Bader
    • , Gromoslaw A. Smolen
    • , Gillian A. Kingsbury
    • , Traver Hart
    • , Charles Kung
    •  & Jason Moffat
    Nature, 1-7
  • Research
    | Open Access

    The Rho signalling pathway is frequently activated in squamous carcinomas. Here, the authors find that the Rho GEF VAV2 is over expressed in both cutaneous and head and neck squamous cell carcinomas and that at the molecular level VAV2 promotes a pro-tumorigenic stem cell-like signalling programme.

    • L. Francisco Lorenzo-Martín
    • , Natalia Fernández-Parejo
    • , Mauricio Menacho-Márquez
    • , Sonia Rodríguez-Fdez
    • , Javier Robles-Valero
    • , Sonia Zumalave
    • , Salvatore Fabbiano
    • , Gloria Pascual
    • , Juana M. García-Pedrero
    • , Antonio Abad
    • , María C. García-Macías
    • , Nazareno González
    • , Pablo Lorenzano-Menna
    • , Miguel A. Pavón
    • , Rogelio González-Sarmiento
    • , Carmen Segrelles
    • , Jesús M. Paramio
    • , José M. C. Tubío
    • , Juan P. Rodrigo
    • , Salvador A. Benitah
    • , Myriam Cuadrado
    •  & Xosé R. Bustelo
  • Research
    | Open Access

    Intratumoural spatial heterogeneity is crucial to enhance therapeutic resistance in glioblastoma. Here, the authors show a paracrine signaling mechanism where glioblastoma-initiating cells located in the tumour edge elevate their malignancy by interaction with core-located tumour cells.

    • Soniya Bastola
    • , Marat S. Pavlyukov
    • , Daisuke Yamashita
    • , Sadashib Ghosh
    • , Heejin Cho
    • , Noritaka Kagaya
    • , Zhuo Zhang
    • , Mutsuko Minata
    • , Yeri Lee
    • , Hirokazu Sadahiro
    • , Shinobu Yamaguchi
    • , Svetlana Komarova
    • , Eddy Yang
    • , James Markert
    • , Louis B. Nabors
    • , Krishna Bhat
    • , James Lee
    • , Qin Chen
    • , David K. Crossman
    • , Kazuo Shin-Ya
    • , Do-Hyun Nam
    •  & Ichiro Nakano
  • Research
    | Open Access

    RNF43 is frequently mutated in cancers and negatively regulates Wnt signalling. Here, the authors report that RNF43 phosphorylation at a serine triplet is required for the negative regulation of Wnt signalling and that the phosphorylation of RNF43 suppresses cancer-associated oncogenic RNF43 mutants.

    • Tadasuke Tsukiyama
    • , Juqi Zou
    • , Jihoon Kim
    • , Shohei Ogamino
    • , Yuki Shino
    • , Takamasa Masuda
    • , Alessandra Merenda
    • , Masaki Matsumoto
    • , Yoichiro Fujioka
    • , Tomonori Hirose
    • , Sayuri Terai
    • , Hidehisa Takahashi
    • , Tohru Ishitani
    • , Keiichi I. Nakayama
    • , Yusuke Ohba
    • , Bon-Kyoung Koo
    •  & Shigetsugu Hatakeyama

News and Comment

  • Research Highlights |

    Aitken et al. have used mutagen-induced liver tumours to trace individual strands of the DNA double helix to which damage occurred and correlate this with mutational patterns to inform upon tumour evolution.

    • Anna Dart
  • News and Views |

    Reprogramming normal cells into tumour precursors involves complex reconditioning of the tissue microenvironment. Cumulative integration of genetic drivers with extrinsic mechanical inputs is now shown to engage YAP/TAZ to rewire cell mechanics and initiate tumorigenic reprogramming.

    • Sayan Chakraborty
    •  & Wanjin Hong
    Nature Materials 19, 707-709
  • News and Views |

    KEAP1 is a tumor suppressor encoded by a gene commonly mutated in lung cancer. A systematic search for Keap1-mutant cancer vulnerabilities now reveals that Slc33a1 is a context-specific essential gene that represents a promising new anti-cancer target.

    • Luke A. Gilbert
    Nature Cancer 1, 575-576
  • News and Views |

    Small-cell lung cancer rapidly develops resistance to standard-of-care therapy. Two papers now establish xenograft models derived from patient-derived circulating tumor cells and show that initially homogeneous, chemoresponsive tumors rapidly recur as heterogeneous drug-refractory disease.

    • Anton Berns
    Nature Cancer 1, 374-375
  • News and Views |

    Human cancer is a disease of cooperating genetic events that is complex to model in vivo. A new study combines somatic base editing with a mouse model of breast cancer, demonstrating the potential to rapidly investigate the function of disease-specific point mutations.

    • Kirsteen J. Campbell
    •  & Karen Blyth
    Lab Animal 49, 115-116