Cancer therapy articles within Nature

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  • Letter |

    Tumour cells respond to an effective, targeted drug treatment with BRAF, ALK or EGFR kinase inhibitors by inducing a complex network of secreted signals that promote tumour growth, dissemination and metastasis of drug-resistant cancer cell clones, and increase the survival of drug-sensitive tumour cells, potentially contributing to incomplete tumour regression.

    • Anna C. Obenauf
    • , Yilong Zou
    •  & Joan Massagué

  • Letter |

    Loss of REV7 is shown to regulate end resection of double-stranded DNA breaks in BRCA1-deficient cells, leading to PARP inhibitor resistance and restoration of homologous recombination; REV7 dictates pathway choice in BRCA1-deficient cells and during immunoglobulin class switching.

    • Guotai Xu
    • , J. Ross Chapman
    •  & Sven Rottenberg

  • Letter |

    In studies in mammalian cells, polymerase theta (Polθ, also known as POLQ) is identified as the polymerase responsible for non-homologous end joining DNA repair; this DNA repair pathway acts in many tumours when homologous recombination is inactivated and the identification of the polymerase responsible may aid the development of new therapeutic approaches.

    • Raphael Ceccaldi
    • , Jessica C. Liu
    •  & Alan D. D’Andrea

  • Letter |

    A novel anti-microRNA delivery platform that targets the acidic tumour microenvironment, in which a chosen anti-miRNA is coupled to a peptide that can transport the anti-miRNA across cell membranes specifically in an acidic environment.

    • Christopher J. Cheng
    • , Raman Bahal
    •  & Frank J. Slack

  • Letter |

    The mTORC1 complex has been implicated in tumorigenesis owing partially to its ability to increase protein translation; now, mTORC1 activity in the mouse intestine is shown not to be required for normal homeostasis but to be necessary for the triggering of tumorigenesis by APC mutations, suggesting that it could be a good target for the prevention of colorectal cancer in high-risk patients.

    • William J. Faller
    • , Thomas J. Jackson
    •  & Owen J. Sansom

  • Letter |

    Using a structure-based approach, small molecule inhibitors that selectively target the GTPase Ral are identified and characterized; these first-generation inhibitors will be valuable tools for elucidating the Ral signalling pathway and constitute a step towards developing Ral-specific agents for cancer therapy.

    • Chao Yan
    • , Degang Liu
    •  & Dan Theodorescu

  • Article |

    The translation of many messenger RNAs that encode important oncogenes and transcription factors depends on the eIF4A RNA helicase to resolve G-quadruplex structures, implying eIF4A inhibition as an effective cancer therapy.

    • Andrew L. Wolfe
    • , Kamini Singh
    •  & Hans-Guido Wendel

  • Article |

    Mutations that dysregulate Notch1 and Ras/PI3K signalling are common in T-cell acute lymphoblastic leukaemia; here, treatment with a PI3K inhibitor is shown to induce drug resistance that is associated with downregulation of activated Notch1 signalling, suggesting that inhibition of both Notch1 and PI3K could promote drug resistance.

    • Monique Dail
    • , Jason Wong
    •  & Kevin Shannon

  • Outlook |

    • Herb Brody

  • Outlook |

    Tailoring cancer treatment to individual and evolving tumours is the way of the future, but scientists are still hashing out the details.

    • Lauren Gravitz

  • Outlook |

    Much of the world is ill-equipped to cope with its rising cancer burden and are pushing prevention and screening.

    • Eric Bender

  • Outlook |

    Genomics can provide powerful tools against cancer — but only once clinical information can be made broadly available, says John Quackenbush.

    • John Quackenbush

  • Outlook |

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

    • Katherine Bourzac

  • Letter |

    A new mechanism by which acute myeloid leukaemia patients become resistant to Ara-C and a newer treatment, ribavirin, is uncovered; these drugs can be glucuronidated and thereby inactivated by members of the UDP glucuronosyltransferase family of enzymes activated through GLI1 signalling.

    • Hiba Ahmad Zahreddine
    • , Biljana Culjkovic-Kraljacic
    •  & Katherine L. B. Borden

  • Outlook |

    Researchers have made good progress with animal tests for cognition. The next step is to devise a rodent model for drug development.

    • Alla Katsnelson

  • Outlook |

    Schizophrenia debilitates not just by psychosis but by depriving people of the ability to feel pleasure.

    • Elie Dolgin

  • Article |

    In order to find a general treatment for cancer, this study found that MTH1 activity is essential for the survival of transformed cells, and isolated two small-molecule inhibitors of MTH1, TH287 and TH588 — in the presence of these inhibitors, damaged nucleotides are incorporated into DNA only in cancer cells, causing cytotoxicity and eliciting a beneficial response in patient-derived mouse xenograft models.

    • Helge Gad
    • , Tobias Koolmeister
    •  & Thomas Helleday

  • Article |

    A chemoproteomic screen is used here to identify MTH1 as the target of SCH51344, an experimental RAS-dependent cancer drug; a further search for inhibitors revealed (S)-crizotinib as a potent MTH1 antagonist, which suppresses tumour growth in animal models of colon cancer, and could be part of a new class of anticancer drugs.

    • Kilian V. M. Huber
    • , Eidarus Salah
    •  & Giulio Superti-Furga

  • Outlook |

    Increased understanding of immune- and tumour-cell biology has led to an explosion of research into potential ways to harness the immune system to kill cancer. By Emily Elert.

    • Emily Elert

  • Outlook |

    Tumours can put a brake on the immune system, but new therapies work by removing these brakes. Now, researchers have to figure out how to use them most effectively.

    • Karen Weintraub

  • Outlook |

    William Coley found a way to prompt the immune system to fight cancer over a century ago. After years of neglect, scientists are now seeking to replicate his success.

    • Sarah DeWeerdt

  • Outlook |

    An experimental vaccine implanted beneath the skin could usher in biomaterial-based immunotherapies for cancer.

    • Elie Dolgin

  • Outlook |

    Immunologist Karolina Palucka, at the Baylor Institute for Immunology Research in Dallas, Texas, helped treat Nobel prizewinner Ralph Steinman's pancreatic cancer with dendritic cells — the cells he co-discovered. Here she explains the use of dendritic cells in cancer immunotherapy.

    • Karolina Palucka

  • Outlook |

    Using a variety of creative imaging techniques, researchers are tracking the dynamic interactions of immune and cancer cells. Their results will guide drug development.

    • Katherine Bourzac

  • Letter |

    Small molecules are developed that irreversibly bind to the common G12C mutant of K-Ras but not the wild-type protein; crystallographic studies reveal the formation of an allosteric pocket that is not apparent in previous Ras studies, and the small molecules shift the affinity of K-Ras to favour GDP over GTP.

    • Jonathan M. Ostrem
    • , Ulf Peters
    •  & Kevan M. Shokat

  • Outlook |

    Drugs to protect vulnerable neurons and encourage neural circuits to reform could one day improve the outlook for patients with acute spinal cord trauma.

    • Megan Cully

  • Letter |

    Expression of more than 15,500 genes individually in a melanoma cell line treated with RAF, MEK, ERK or combined RAF–MEK inhibitors reveals a cyclic-AMP-dependent melanocytic signalling network associated with drug resistance; this may represent a novel therapeutic target for melanoma treatment.

    • Cory M. Johannessen
    • , Laura A. Johnson
    •  & Levi A. Garraway

  • Outlook |

    Real-time imaging of a patient's body is guiding surgeons and radiologists past healthy tissue to the diseased cells.

    • Jessica Wright

  • Letter |

    In mice with Eµ-myc transgenic lymphomas in which therapy-induced senescence (TIS) depends on the H3K9 histone methyltransferase Suv39h1, TIS-competent lymphomas but not TIS-incompetent Suv39h1– lymphomas show increased glucose utilization and ATP production after senescence-inducing chemotherapy to cope with proteotoxic stress elicited by factors of the senescence-associated secretory phenotype (SASP); senescent cancers are selectively vulnerable to drugs that block glucose utilization or autophagy.

    • Jan R. Dörr
    • , Yong Yu
    •  & Clemens A. Schmitt

  • Letter |

    The mechanism of action of three different allosteric MEK inhibitors that target the MAP kinase pathway is investigated, and their efficacy is shown to be explained by the distinct mechanisms regulating MEK activation in KRAS- versus BRAF-driven tumours; this work provides a rationale for designing more effective cancer therapies for these common genetic subtypes of cancer.

    • Georgia Hatzivassiliou
    • , Jacob R. Haling
    •  & Marcia Belvin

  • Outlook |

    Bruce L. Levine and Carl H. June explore how to make engineered immune cells that can eradicate cancer widely available.

    • Bruce L. Levine
    •  & Carl H. June

  • Outlook |

    Better designs for clinical trials and the use of combination therapies may improve leukaemia treatment.

    • Alla Katsnelson

  • Outlook |

    Enzymes that modify gene expression without changing the DNA sequence are now viewed as central to the development of leukaemia — and may lead to new drugs.

    • Jessica Wright

  • Outlook |

    Leukaemia in children is highly curable, but many survivors suffer severe, even life-threatening, long-term effects. Scientists are seeking ways to deliver a safer cure.

    • Mary Carmichael

  • Outlook |

    Beginning treatment with a combination of drugs should help to stop drug resistance developing, says Charles L. Sawyers.

    • Charles L. Sawyers

  • Letter |

    T-helper-1-cell cytokines tumour necrosis factor and interferon-γ are shown to drive tumour cells into senescence in a mouse model of β-cell carcinoma and human carcinoma cells.

    • Heidi Braumüller
    • , Thomas Wieder
    •  & Martin Röcken

  • Outlook |

    The latest drugs hold fantastic promise for people with severe psoriasis. But where are the treatment options for the far larger number with less serious cases?

    • James Mitchell Crow

  • News & Views |

    It is increasingly accepted that metabolic changes in cancer cells can drive tumour formation. The finding that the SIRT6 protein suppresses tumour formation by regulating metabolism adds weight to this view.

    • Luisa Tasselli
    •  & Katrin F. Chua

  • Outlook |

    Software models of complex tissues and disease are yielding a better understanding of cancer and suggesting potential treatments.

    • Neil Savage

  • Outlook |

    Complex mathematical models are helping researchers understand cancer's evolution and providing clues on how to thwart drug resistance.

    • Katharine Gammon

  • News & Views |

    Tumour cells can respond to targeted immune-cell therapies by losing proteins that mark them as being cancerous. Subverting this resistance mechanism may lead to more durable cancer-treatment strategies. See Letter p.412

    • Antoni Ribas
    •  & Paul C. Tumeh

  • Letter |

    A genetically engineered mouse model is used to determine the mechanism of acquired resistance to adoptive therapy with cytotoxic T cells specific for a melanocytic differentiation antigen; tumour necrosis factor (TNF)-α is identified as a crucial factor that causes reversible dedifferentiation of mouse and human melanoma cells.

    • Jennifer Landsberg
    • , Judith Kohlmeyer
    •  & Thomas Tüting

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