Cancer stem cells articles within Nature

Featured

  • 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 |

    Experiments in mice show that expression of the oncogene SmoM2 induces basal cell carcinoma in the ear epidermis but not in the back skin, and that this difference in susceptibility is regulated by the extracellular matrix.

    • Nordin Bansaccal
    • , Pauline Vieugue
    •  & Cédric Blanpain

  • Article |

    Glioblastoma stem cells co-opt lysine uptake and degradation to shunt the production of crotonyl-CoA, remodelling the chromatin landscape to evade interferon-induced intrinsic effects on glioblastoma stem cell maintenance and extrinsic effects on immune response.

    • Huairui Yuan
    • , Xujia Wu
    •  & Jeremy N. Rich

  • Article |

    Integrated single-cell atlases of human fetal cerebella and MBs show potential cell populations predisposed to transformation and regulatory circuitries underlying tumour cell states and oncogenesis, highlighting hitherto unrecognized transitional progenitor intermediates predictive of disease prognosis.

    • Zaili Luo
    • , Mingyang Xia
    •  & Q. Richard Lu

  • Article
    | Open Access

    Aberrant crosstalk between cancer stem cells and their microenvironment triggers angiogenesis and TGFβ signalling, creating conditions that are conducive for hijacking leptin and leptin receptor signalling, which in turn launches downstream PI3K–AKT–mTOR signalling during the benign-to-malignant transition.

    • Shaopeng Yuan
    • , Katherine S. Stewart
    •  & Elaine Fuchs

  • Article |

    A hierarchical model of melanoma tumour growth mirrors the cellular and molecular logic of cell-fate specification and differentiation of the underlying embryonic neural crest, and suggests that the ability to support growth and metastasis are limited to distinct pools of cells.

    • Panagiotis Karras
    • , Ignacio Bordeu
    •  & Jean-Christophe Marine

  • 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 |

    In mouse and human squamous cell carcinoma, loss of function of FAT1 promotes tumour initiation, malignant progression and metastasis through the activation of a hybrid epithelial-to-mesenchymal transition phenotype.

    • Ievgenia Pastushenko
    • , Federico Mauri
    •  & Cédric Blanpain

  • Letter |

    Cellular senescence induced by chemotherapy leads to the acquisition of stemness in cancer cells, which results in enhanced tumour-promoting capacity after forced release or spontaneous escape from the senescent cell-cycle arrest.

    • Maja Milanovic
    • , Dorothy N. Y. Fan
    •  & Clemens A. Schmitt

  • 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 |

    During emergency myelopoiesis in mice, clusters of self-renewing granulocyte/macrophage progenitors (GMP) are transiently formed in the bone marrow cavity to produce a burst of myeloid cells; in leukaemia, GMP clusters persist and constantly generate myeloid leukaemia cells.

    • Aurélie Hérault
    • , Mikhail Binnewies
    •  & Emmanuelle Passegué

  • Article |

    The translation of upstream open reading frames in skin tumour models protects some cancer-related mRNAs from global reductions in protein synthesis during the early stages of tumour initiation, suggesting that unconventional translation has a crucial role in tumorigenesis.

    • Ataman Sendoel
    • , Joshua G. Dunn
    •  & Elaine Fuchs

  • Letter |

    A rapid gene signature test (LSC17) that captures stem cell expression programs in acute myeloid leukaemia patients at diagnosis is associated with therapy response and survival, facilitating initial treatment stratification.

    • Stanley W. K. Ng
    • , Amanda Mitchell
    •  & Jean C. Y. Wang

  • Article |

    Skin stem cells, but not their progenitors, are able to form tumours owing to the ability of oncogene-targeted stem cells to increase symmetric self-renewing division and a higher p53-dependent resistance to apoptosis.

    • Adriana Sánchez-Danés
    • , Edouard Hannezo
    •  & Cédric Blanpain

  • Article |

    Leukaemic stem cells (LSCs) are responsible for BCR–ABL-driven chronic myeloid leukaemia relapse; here, p53 and MYC signalling networks are shown to regulate LSCs concurrently, and targeting both these pathways has a synergistic effect in managing the disease.

    • Sheela A. Abraham
    • , Lisa E. M. Hopcroft
    •  & Tessa L. Holyoake

  • Letter |

    This study finds that the epithelial-to-mesenchymal (EMT) transition program, which is common to both mammary gland reconstituting stem cells and mammary tumour-initiating cells, is differentially regulated by two distinct EMT factors, Slug and Snail; the findings illustrate that although they appear similar, normal tissue stem cells and tumour-initiating cells are controlled by distinct regulatory processes.

    • Xin Ye
    • , Wai Leong Tam
    •  & Robert A. Weinberg

  • Letter |

    Although imatinib gives good clinical results in chronic myeloid leukaemia (CML), residual disease attributed to quiescent CML stem cells remains in many patients; here glitazones are shown to reduce the pool of CML stem cells and achieve lasting disease eradication in CML patients in combination with imatinib.

    • Stéphane Prost
    • , Francis Relouzat
    •  & Philippe Leboulch

  • Letter |

    Using human bladder cancer xenograft models, a new mechanism involving an active proliferative response of cancer stem cells to chemotherapy-induced damage is shown, driven by prostaglandin E2 (PGE2) release in a manner similar to PGE2-induced wound repair; pharmacological inhibition of the PGE2/COX2 axis by celecoxib attenuates chemoresistance, suggesting a possible adjunctive therapy for bladder carcinomas.

    • Antonina V. Kurtova
    • , Jing Xiao
    •  & Keith Syson Chan

  • Letter |

    KRAS mutations are a driver event of pancreatic ductal adenocarcinoma; here, a subpopulation of dormant tumour cells, relying on oxidative phosphorylation for survival, is shown to be responsible for tumour relapse after treatment targeting the KRAS pathway.

    • Andrea Viale
    • , Piergiorgio Pettazzoni
    •  & Giulio F. Draetta

  • Outlook |

    A subterranean species that seems to be cancer-proof is providing promising clues on how we might prevent the disease in humans.

    • Sarah Deweerdt

  • Outlook |

    Even as cancer therapies improve, basic questions about drug resistance, tumour spread and the role of normal tissue remain unanswered.

    • Katherine Bourzac

  • Article |

    The authors identify pre-leukaemic haematopoietic stem cells (HSCs) in patients with acute myeloid leukaemia; these pre-leukaemic HSCs have the capacity of normal multi-lineage haematopoietic differentiation with a competitive growth advantage over wild-type HSCs, and owing to their persistence may serve as a reservoir for therapeutic resistance and relapse.

    • Liran I. Shlush
    • , Sasan Zandi
    •  & John E. Dick

  • Outlook |

    Leukaemia treatments must eliminate the versatile cells that can bring the cancer back to life years later.

    • Cassandra Willyard

  • Outlook |

    Stem cells from the umbilical cord are among the latest weapons in the fight against leukaemia.

    • Melinda Wenner Moyer

  • News & Views Forum |

    New research backs the contentious idea that solid tumours are not masses of equivalent cells, but instead contain cancer stem cells that support tumour maintenance. Here, two experts provide complementary views on the findings and on the implications for potential therapies. See Letters p.522 & p.527

    • Richard J. Gilbertson
    •  & Trevor A. Graham

  • News |

    The master builders that underlie tumour growth may inform treatment strategies.

    • Monya Baker

  • Letter |

    Using genetic lineage tracing, tumour cells are traced in vivo in an unperturbed solid tumour; in a carcinogen-induced papilloma mouse model, cells in these benign lesions are found to mirror the clonal hierarchy organization of normal tissue.

    • Gregory Driessens
    • , Benjamin Beck
    •  & Cédric Blanpain

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