Skin cancer articles within Nature Communications

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  • Article
    | Open Access

    It is unclear how resident p16-expressing senescent cells affect the propensity of tissues to develop cancer. Here, the authors show that chronic p16 expression in the mouse epidermis causes hyperplasia and dysplasia through Wnt-mediated paracrine stimulation of proliferating keratinocytes, and can contribute to tumour formation.

    • Narmen Azazmeh
    • , Benjamin Assouline
    •  & Ittai Ben-Porath

  • Article
    | Open Access

    A significant proportion of patients develop innate or acquired resistance to immune checkpoint inhibitors. Here, the authors show that resistance to anti-PD-1 blockade is associated with TGF-beta driven major histocompatibility complex I (MHCI) down-regulation and a de-differentiated phenotype in melanoma patients.

    • Jenny H. Lee
    • , Elena Shklovskaya
    •  & Helen Rizos

  • Article
    | Open Access

    Immunotherapies now dominate the treatment landscape for melanoma, but why they only work in a subset of patients remains unclear. Here, the authors perform an immunogenomic analysis on 67 intratumor sub-regions of a PD-1 inhibitor resistant melanoma, and 2 additional metastases from a single patient, mapping the spatial relationships between genomic and immune heterogeneity at high resolution.

    • Akash Mitra
    • , Miles C. Andrews
    •  & P. Andrew Futreal

  • Article
    | Open Access

    It is known that there are sex differences in the incidence and prognosis of certain cancers, including melanoma. In this study, the authors utilize a melanoma model to reveal that castrated mice have a higher metastatic burden associated with androgen dependent impaired neutrophil function.

    • Janet L. Markman
    • , Rebecca A. Porritt
    •  & Moshe Arditi

  • Article
    | Open Access

    The response to immunotherapy of melanoma patients is heterogeneous. Here, the authors demonstrate that a high expression of the two major components of the immunoproteasome, PSMB8 and PSMB9, modulates the production of HLA peptides and it is predictive of better survival and improved response to immune-checkpoint inhibitors of melanoma patients.

    • Shelly Kalaora
    • , Joo Sang Lee
    •  & Yardena Samuels

  • Article
    | Open Access

    Erastin, the ferroptosis activator, binds to voltage gated ion channels CDAC2 and VDCA3 but treatment with erastin can result in the degradation of the channels. Here, the authors show that Nedd4 is induced following erastin treatment, which leads to the ubiquitination and subsequent degradation of the channels.

    • Yongfei Yang
    • , Meiying Luo
    •  & Wei Chen

  • Article
    | Open Access

    There are many patients who do not respond to immune checkpoint inhibitor (ICI) immunotherapy. Here, the authors show a significant negative correlation between sphingosine kinase-1 (SK1) expression and survival for ICI-treated melanoma patients, and further show that targeting SK1 improves response to ICI in mouse cancer models.

    • Caroline Imbert
    • , Anne Montfort
    •  & Céline Colacios

  • Article
    | Open Access

    Metastatic cells can mimic many of the phenotypic behaviors of embryonic cells. Here, the authors generate a melanoblast-specific transcriptome using a genetically engineered mouse model and identify KDELR3 as a pro-metastasis gene in melanoma.

    • Kerrie L. Marie
    • , Antonella Sassano
    •  & Pravin J. Mishra

  • Article
    | Open Access

    The ubiquitin ligase Siah2 has been implicated in immune responses. Here, the authors show that Siah2 null immune cells have an increased inflammatory response to inoculated melanoma cells, along with a reduced number of infiltrating immunosuppressive regulatory T cells, resulting in inhibition of tumour growth.

    • Marzia Scortegagna
    • , Kathryn Hockemeyer
    •  & Ze’ev A. Ronai

  • Article
    | Open Access

    Histology data exists for many cancer samples and the ability to automatically image this data may provide prognostic information. Here, the authors generated an algorithm to measure tumour infiltrating lymphocytes in melanoma histology specimens and show that the ratio of these immune cells to tumour cells has prognostic value.

    • Balazs Acs
    • , Fahad Shabbir Ahmed
    •  & David L. Rimm

  • Article
    | Open Access

    The ERK signalling pathway is activated in many cancers, however ERK1 and ERK2 are difficult to target pharmacologically. Here, the authors identify a small molecule inhibitor that binds covalently to the D-recruitment site of ERK and induces cell death and reduces tumour growth in mice.

    • Tamer S. Kaoud
    • , William H. Johnson
    •  & Kevin N. Dalby

  • Article
    | Open Access

    MAPK-targeted therapies fail to achieve complete remission. Here, the authors show that anti-apoptosis resistance is acquired in these targeted therapies through the mRNA destabilization of NOXA which leads to dependence on MCL-1, and that sequential combination of MCL-1 inhibition with targeted therapies overcomes this resistance.

    • Joan Montero
    • , Cécile Gstalder
    •  & Rizwan Haq

  • Article
    | Open Access

    CYLD cutaneous syndrome (also known as Brooke-Spiegler syndrome) is characterised by germline mutations in the tumor suppressor CYLD. Here, the authors highlight recurrent mutations in DNMT3A and BCOR, indicating a role for epigenetic dysregulation in this rare genetic skin disease.

    • Helen R. Davies
    • , Kirsty Hodgson
    •  & Neil Rajan

  • Article
    | Open Access

    Immunotherapy can induce antigen spreading of antitumor T cell response, which correlates with better outcomes. Here the authors show that tissue-resident memory CD8 T cells promote antigen spreading via lysing tumor cells and promoting their uptake and cross-presentation by dendritic cells, thereby eliciting de novo T cell responses.

    • Evelyn Menares
    • , Felipe Gálvez-Cancino
    •  & Alvaro Lladser

  • Article
    | Open Access

    Conversion of dermal fibroblasts into Cancer Associated Fibroblasts (CAFs) can play an important role in keratinocyte tumour development. Here the authors reveal that CSL plays a role in maintenance of telomeres and genomic integrity in both dermal fibroblasts and CAFs.

    • Giulia Bottoni
    • , Atul Katarkar
    •  & G. Paolo Dotto

  • Article
    | Open Access

    Mucosal melanomas are challenging to treat partly because so little is known about the genetic drivers underpinning them. Here, the authors perform a genomic landscape analysis of samples collected from three continents, revealing a potential role for CDK4/6 or MEK inhibition in the treatment of the disease.

    • Felicity Newell
    • , Yan Kong
    •  & Richard A. Scolyer

  • Article
    | Open Access

    LNK is a tumor suppressor in hematopoietic cancers, but its function in melanoma is unclear. Here, the authors show that the overexpression of LNK in melanomas correlate with hyperactive signaling of the RAS-RAF-MEK pathway and LNK enhances melanoma growth and survival and immune evasion by inhibiting IFN signalling.

    • Ling-Wen Ding
    • , Qiao-Yang Sun
    •  & H. Phillip Koeffler

  • Article
    | Open Access

    Melanocortin-1 receptor is a palmitoylated protein and variants of the receptor are associated with red hair colour and susceptibility to melanoma. Here, the authors describe a method to enhance the palmitoylation of the receptor, which can inhibit melanomagenesis in mice.

    • Shuyang Chen
    • , Changpeng Han
    •  & Rutao Cui

  • Article
    | Open Access

    Mucosal melanoma is a rare melanoma subtype that is poorly characterised. Here, the authors sequenced human, canine, and equine melanoma samples and performed a cross-species analysis, which revealed candidate driver genes, recurrent copy number alterations in regions syntenic between species, extensive intra-tumour heterogeneity and potential germline predisposing alleles

    • Kim Wong
    • , Louise van der Weyden
    •  & David J. Adams

  • Article
    | Open Access

    Most tumours are characterized by increased aerobic glycolytic activity. Here the authors show that elevated  aerobic glycolysis is not essential for cancer initiation by testing the effect of lactate dehydrogenase depletion on the ability of hair follicle stem cells (HFSCs) to form squamous cell carcinoma (SCC) in mouse genetic models.

    • A. Flores
    • , S. Sandoval-Gonzalez
    •  & W. E. Lowry

  • Article
    | Open Access

    Prolyl hydroxylase domain protein 2 (PHD2) regulates cellular response to hypoxia. Here the authors show that PHD2 is downregulated in melanoma and that PHD2 depletion, in a mouse model, promotes the progression of benign melanocytic lesions into melanoma, via activation of the Akt/mTOR signaling cascade.

    • Shujing Liu
    • , Gao Zhang
    •  & Xiaowei Xu

  • Article
    | Open Access

    Bone marrow-derived epithelial cells can be recruited to sites of chronic inflammation. Here, the authors using allogenic bone marrow transplantation in a multistage murine cutaneous carcinogenesis model show that bone marrow-derived epithelial cells and hair follicle stem cells are recruited to cutaneous neoplasms during tumor promotion of carcinogen-exposed skin and bone marrow.

    • Heuijoon Park
    • , Sonali Lad
    •  & Rebecca J. Morris

  • Article
    | Open Access

    Genetic loci linked to susceptibility for the common skin cancer cutaneous squamous cell carcinoma (cSCC) have been identified by genome wide association studies (GWAS). Here, the authors impute gene expression levels from GWAS data to perform a transcriptome wide association study (TWAS), identifying five novel genetic loci linked to cSCC susceptibility.

    • Nilah M. Ioannidis
    • , Wei Wang
    •  & Alice S. Whittemore

  • Article
    | Open Access

    Acquired resistance is a major problem in cancer immunotherapy. Here the authors report a study of two patients with Merkel cell carcinoma under immunotherapy treatment who develop resistance after deep responses for >1 year and identified a novel mechanism of acquired, gene-specific transcriptional suppression of HLAs.

    • K. G. Paulson
    • , V. Voillet
    •  & A. G. Chapuis

  • Article
    | Open Access

    It is known cutaneous squamous cell carcinoma (cSCC) involves a high tumour mutation burden. Here the authors identify common cSCC mutated genes, copy number changes, altered pathways and report the presence of a novel mutation signature associated with chronic exposure to the immunosuppressive drug azathioprine.

    • Gareth J. Inman
    • , Jun Wang
    •  & Irene M. Leigh

  • Article
    | Open Access

    Aberrant glycosylation patterns on cancer cells promote several pro-tumorigenic functions, including enhancing tumor cell proliferation. Here the authors provide data that show melanoma cells downregulate GCNT2 with consequent loss of I-branched glycans; this leads to the formation of extended i-linear glycans and enhances melanoma growth via increases, in part, by IGF-1- and extracellular matrix-induced signaling.

    • Jenna Geddes Sweeney
    • , Jennifer Liang
    •  & Charles J. Dimitroff

  • Article
    | Open Access

    As melanoma progresses, it evolves. Here, in advanced melanoma the authors study genomic evolution, highlighting trunk mutations dominated by the ultraviolet damage signature, common late truncal whole-genome duplication events, as well as selective copy number gain of mutant BRAF.

    • E. Birkeland
    • , S. Zhang
    •  & P. E. Lønning

  • Article
    | Open Access

    In metastatic melanoma, ADAR1 is downregulated, facilitating proliferation. Here, the authors show an ADAR1-dependent and RNA-editing-independent regulation of melanoma invasion mediated by ITGB3 expression, which can be reversed when ITGB3 is blocked.

    • Yael Nemlich
    • , Erez Nissim Baruch
    •  & Gal Markel

  • Article
    | Open Access

    Functional characterisation of single cells is crucial for uncovering the true extent of cellular heterogeneity. Here the authors offer an approach to infer functional identities of cells from their transcriptomes, identify their dominant function, and reconstruct the underlying regulatory networks.

    • Shahin Mohammadi
    • , Vikram Ravindra
    •  & Ananth Grama

  • Article
    | Open Access

    Monitoring the heterogeneity of circulating tumour cells (CTCs) and their phenotypic changes during treatment is a challenge. This study describes and tests a method for detection and quantitative heterogeneity analysis of melanoma CTCs in 10 stage-IV melanoma patients.

    • Simon Chang-Hao Tsao
    • , Jing Wang
    •  & Matt Trau

  • Article
    | Open Access

    Hypoxia-inducible transcription factor HIF-1α promotes glycolysis allowing cell survival under stress. Here the authors show, using both cell lines and animal models, that in cutaneous squamous cell carcinoma HOXA9 acts as a tumor suppressor and inhibits glycolysis by associating with CRIP2 to repress HIF-1α binding to target genes.

    • Liang Zhou
    • , Yinghui Wang
    •  & Zhenhua Ding

  • Article
    | Open Access

    In melanoma, reduced ADAR1 impairs A-to-I microRNA editing. Here, the authors show that miR-378a-3p undergoes this editing in non-metastatic cells and the edited form of miR-378a-3p binds to the PARVA oncogene, inhibiting its expression and preventing melanoma progression and metastasis.

    • Guermarie Velazquez-Torres
    • , Einav Shoshan
    •  & Menashe Bar-Eli

  • Article
    | Open Access

    The interaction of DOT1L with MLL oncogenic fusion proteins has been implicated in leukemogenesis. Here, the authors show a contrasting role for DOT1L in protecting UVR-induced melanomagenesis by facilitating DNA repair through interaction with XPC.

    • Bo Zhu
    • , Shuyang Chen
    •  & Rutao Cui

  • Article
    | Open Access

    Most melanoma patients do not respond to anti-PD1 therapy. Here, the authors show that TNFα blockade synergizes with anti-PD-1 by preventing anti-PD-1-induced CD8+ T cell death and TIM-3 expression on such cells.

    • Florie Bertrand
    • , Anne Montfort
    •  & Bruno Ségui

  • Article
    | Open Access

    Precise orchestration of gene expression regulation upon DNA damage is essential for genome integrity. Here the authors identify a novel widespread stress-triggered defence mechanism that promotes rapid transcription-driven genomic surveillance thus limiting mutagenesis and shaping cancer genomes.

    • Matthieu D. Lavigne
    • , Dimitris Konstantopoulos
    •  & Maria Fousteri

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