Melanoma articles within Nature

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  • Article |

    Remote tumours cause liver dysfunction by releasing extracellular vesicles and particles containing palmitic acid, which induces TNF signalling in Kupffer cells, resulting in inflammation, fatty deposits and metabolic dysregulation, thus both reducing the efficacy and increasing the toxicity of chemotherapies.

    • Gang Wang
    • , Jianlong Li
    •  & David Lyden

  • Article
    | Open Access

    Patients with resectable clinical stage III or oligometastatic stage IV melanoma were given neoadjuvant relatlimab and nivolumab combination immunotherapy, which induced a high pathologic complete response rate, indicating the efficacy and safety of this regimen.

    • Rodabe N. Amaria
    • , Michael Postow
    •  & Hussein A. Tawbi

  • 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 |

    Changes in the microenvironment of the aged lung relative to younger lung tissue can lead to the reactivation of dormant melanoma cells through a mechanism that involves a decrease in WNT5A and AXL signalling and an increase in MERTK.

    • Mitchell E. Fane
    • , Yash Chhabra
    •  & Ashani T. Weeraratna

  • Article |

    A survey of the CD4+ T cells in human melanomas indicates that immune evasion is mediated through direct stimulation of neoantigen-specific tumour-reactive regulatory T cells by HLA class II-positive melanoma cells.

    • Giacomo Oliveira
    • , Kari Stromhaug
    •  & Catherine J. Wu

  • Article |

    In a zebrafish model of human cutaneous and acral melanomas, CRKL amplification causes tumours to favour a fin location, indicating that tumour location is determined by both the driver oncogenes and the pre-existing positional identity gene program.

    • Joshua M. Weiss
    • , Miranda V. Hunter
    •  & Richard M. White

  • Article |

    KDM5B recruits SETDB1 to repress endogenous retroelements such as MMVL30, suppressing anti-tumour immunity, and the depletion of KDM5B induces a robust adaptive immune response and enhances the response to immune checkpoint blockade.

    • Shang-Min Zhang
    • , Wesley L. Cai
    •  & Qin Yan

  • Article |

    HLA peptidomic analysis identifies recurrent intracellular bacteria-derived peptides presented on HLA-I and HLA-II molecules in melanoma tumours, revealing how bacteria can modulate immune functions and responses to cancer therapies.

    • Shelly Kalaora
    • , Adi Nagler
    •  & Yardena Samuels

  • Article |

    Tryptophan depletion in melanoma cells after prolonged treatment with interferon-γ (IFNγ) results in ribosomal frameshifting and the production of aberrant peptides that can be presented to T cells and induce an immune response.

    • Osnat Bartok
    • , Abhijeet Pataskar
    •  & Reuven Agami

  • Article |

    A combination of clonal expansion and DNA amplification is used to sequence genetic material from individual melanocytes, shedding light on the mutational landscape of these cells and the development of melanomas.

    • Jessica Tang
    • , Eleanor Fewings
    •  & A. Hunter Shain

  • Article |

    Melanoma cells undergo less oxidative stress and less ferroptosis in lymph than in blood, owing to higher levels of oleic acid in lymph, and thus exposure to the lymphatic environment increases subsequent metastasis through blood.

    • Jessalyn M. Ubellacker
    • , Alpaslan Tasdogan
    •  & Sean J. Morrison

  • Article |

    Multiomic profiling of several cohorts of patients treated with immune checkpoint blockade highlights the presence and potential role of B cells and tertiary lymphoid structures in promoting therapy response.

    • Beth A. Helmink
    • , Sangeetha M. Reddy
    •  & Jennifer A. Wargo

  • Letter |

    A range of SF3B1 mutations promote tumorigenesis through the repression of BRD9, a core component of the non-canonical BAF complex, and correcting BRD9 mis-splicing in these SF3B1-mutant cells suppresses tumour growth.

    • Daichi Inoue
    • , Guo-Liang Chew
    •  & Robert K. Bradley

  • Letter |

    A transplantable mouse model of persistent cutaneous melanoma shows that immune-mediated tumour suppression can result in a state of melanoma–immune equilibrium, and that tissue-resident memory T cells are essential drivers of this equilibrium state.

    • Simone L. Park
    • , Anthony Buzzai
    •  & Thomas Gebhardt

  • Letter |

    The identification of an ERK2–JUNB–FRA1 signalling pathway that drives addiction to therapeutic drugs in cancer cells, and an ERK2-dependent phenotype switch that precedes cell death after drug withdrawal, may help to guide therapies that exploit the addiction phenotype.

    • Xiangjun Kong
    • , Thomas Kuilman
    •  & Daniel S. Peeper

  • Letter |

    Analyses of tumour samples and tumour-infiltrating lymphocytes from two patients with melanoma who were treated with adoptive T-cell therapy provide evidence for tumour escape by loss and downregulation of immunogenic antigens.

    • Els M. E. Verdegaal
    • , Noel F. C. C. de Miranda
    •  & Sjoerd H. van der Burg

  • Letter |

    An analysis of cancer genomic data reveals an increased rate of somatic mutations at active transcription factor binding sites located both within promoter regions and distal from genes; the increased mutation rate at these genomic regions can be explained by reduced accessibility of the protein-bound DNA to nucleotide excision repair machinery.

    • Radhakrishnan Sabarinathan
    • , Loris Mularoni
    •  & Núria López-Bigas

  • Letter |

    A known oncogene, MITF, resides in a region of chromosome 3 that is amplified in melanomas and associated with poor prognosis; now, a long non-coding RNA gene, SAMMSON, is shown to also lie in this region, to also act as a melanoma-specific survival oncogene, and to be a promising therapeutic target for anti-melanoma therapy.

    • Eleonora Leucci
    • , Roberto Vendramin
    •  & Jean-Christophe Marine

  • Article |

    Human melanoma cells grown in mice experience high levels of oxidative stress in the bloodstream such that few metastasizing cells survive to form tumours; the rare melanoma cells that successfully metastasize undergo metabolic changes that increase their capacity to withstand this stress, and antioxidant treatments increase metastasis formation by human melanoma cells, while inhibiting antioxidant pathways had the reverse effect.

    • Elena Piskounova
    • , Michalis Agathocleous
    •  & Sean J. Morrison

  • Letter |

    A novel ALK transcript expressed in a subset of human cancers, arising from a de novo alternative transcription initiation site within the ALK gene, is described; the ALK transcript encodes three protein isoforms that stimulate tumorigenesis in vivo in mouse models; resultant tumours are sensitive to treatments with ALK inhibitors, indicating a possible therapeutic avenue for patients expressing these isoforms.

    • Thomas Wiesner
    • , William Lee
    •  & Ping Chi

  • Letter |

    BRAF mutations occur frequently in melanomas, but patients generally develop resistance to agents targeting mutant BRAF; now, the persistent formation of the translation initiation complex eIF4F has been described as an indicator of multiple mechanisms of resistance that arise in BRAF-mutated tumours and as a promising therapeutic target.

    • Lise Boussemart
    • , Hélène Malka-Mahieu
    •  & Stéphan Vagner

  • Letter |

    Exposing mice with the BRAF (V600E) mutation to levels of ultraviolet radiation that mimic mild sunburn in humans is shown to induce mutations in the tumour suppressor Trp53 (TP53 in humans), accelerating the development of melanoma; these results support the use of sunscreen in individuals at risk of this cancer.

    • Amaya Viros
    • , Berta Sanchez-Laorden
    •  & Richard Marais

  • Letter |

    Patients with melanomas carrying an activating BRAF mutation respond to treatment with BRAF inhibitors although resistance to the inhibitor usually emerges; this resistance is shown to arise through increased expression of receptor tyrosine kinases such as EGFR; however, these changes decrease cell fitness and during a break from inhibitor treatment these cells are selected against, revealing that some patients who acquire EGFR expression may benefit from inhibitor re-treatment after a drug holiday.

    • Chong Sun
    • , Liqin Wang
    •  & Rene Bernards

  • 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

  • Letter |

    BRAF inhibitors such as vemurafenib have shown promising effects in patients with BRAF-mutant melanomas, but the tumours generally develop resistance; vemurafenib-resistant melanomas are now shown to be drug dependent, and an intermittent dosing schedule can help prevent drug resistance.

    • Meghna Das Thakur
    • , Fernando Salangsang
    •  & Darrin D. Stuart

  • News & Views |

    Sun exposure indisputably increases the risk of skin cancer. Mouse studies suggest that, in red-haired individuals, genetic factors also contribute through a mechanism that acts independently of exposure to sunlight. See Letter p.449

    • Mizuho Fukunaga-Kalabis
    •  & Meenhard Herlyn

  • Letter |

    Individuals with the red hair/fair skin phenotype usually carry a polymorphism in the gene encoding the melanocortin 1 receptor (Mc1r) that results in the production of pigment containing a high pheomelanin-to-eumelanin ratio; here it is shown in a mouse model that inactivation of Mc1r promotes melanoma formation in the presence of the Braf oncogene, thus suggesting that pheomelanin synthesis is carcinogenic by an ultraviolet-radiation-independent mechanism.

    • Devarati Mitra
    • , Xi Luo
    •  & David E. Fisher

  • 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

  • Letter
    | Open Access

    Whole-genome sequencing of 25 metastatic melanomas and matched germline DNA in humans reveals that the highest mutation load is associated with chronic sun exposure, and that the PREX2 gene is mutated in approximately 14 per cent of cases

    • Michael F. Berger
    • , Eran Hodis
    •  & Levi A. Garraway

  • 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

  • News & Views |

    The efficacy of the anticancer drug vemurafenib, which is used to treat metastatic melanoma, is plagued by acquired resistance. A picture of how such resistance develops is emerging. See Letter p.387

    • Hugo Lavoie
    •  & Marc Therrien

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