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Showing 1–18 of 18 results
Advanced filters: Author: Preethi Gunaratne Clear advanced filters

  • Cutaneous squamous cell of the skin is a common neoplasm that frequently arises from precancerous actinic keratoses. Here, the authors carry out genomic analysis on matched sets of human lesions and compare with those in ultraviolet treated mice and identify conserved drivers of tumour development.

    • Vida Chitsazzadeh
    • Cristian Coarfa
    • Kenneth Y. Tsai
    ResearchOpen Access
    Nature Communications
    Volume: 7, P: 1-17

  • The Cancer Genome Atlas Research Network reports an integrative analysis of more than 400 samples of clear cell renal cell carcinoma based on genomic, DNA methylation, RNA and proteomic characterisation; frequent mutations were identified in the PI(3)K/AKT pathway, suggesting this pathway might be a potential therapeutic target, among the findings is also a demonstration of metabolic remodelling which correlates with tumour stage and severity.

    • Chad J. Creighton
    • Margaret Morgan
    • Heidi J. Sofia.
    ResearchOpen Access
    Nature
    Volume: 499, P: 43-49

  • Perineural invasion and cancer-induced nerve injury of tumour-associated nerves are associated with poor response to anti-PD-1 therapy, which can be reversed by combining anti-PD-1 therapy with anti-inflammatory interventions.

    • Erez N. Baruch
    • Frederico O. Gleber-Netto
    • Moran Amit
    ResearchOpen Access
    Nature
    Volume: 646, P: 462-473

  • IFNγ signaling is important in the pathogenesis and immune response, emphasizing the need for investigation of its role. Here, the authors show that IFNγ plays a key role in shaping immune microenvironment in AML and developing resistance, providing insights for potential therapeutic strategies.

    • Bofei Wang
    • Patrick K. Reville
    • Hussein A. Abbas
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-16

  • Many tumors evade immunosurveillance by down-modulating expression of antigen-processing machinery and MHC molecules. Yang et al. report triple-negative tumor cell expression of the lncRNA LINK-A enhances degradation of antigen peptide-loading complex molecules and intrinsic tumor suppressors, which contribute to tumor persistence.

    • Qingsong Hu
    • Youqiong Ye
    • Liuqing Yang
    Research
    Nature Immunology
    Volume: 20, P: 835-851

  • Mutations in TP53 and hyperactivation of the PI3K/AKT pathway are the two most frequent drivers of cancer progression across multiple human tumour types. Here, the authors identify two TAp63 regulated long non-coding RNAs, TROLL-2 and TROLL-3, that connect these oncogenic pathways, thus promoting tumour and metastasis formation in a wide variety of cancer types.

    • Marco Napoli
    • Xiaobo Li
    • Elsa R. Flores
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-16

  • AGO-CLIP permits the identification of miRNA target genes. Here, Hamilton et al. compile publicly available AGO-CLIP data and combine this information with miRNA analysis from The Cancer Genome Atlas, permitting the identification of an oncogenic miRNA superfamily that targets tumour suppressor genes.

    • Mark P. Hamilton
    • Kimal Rajapakshe
    • Sean E. McGuire
    ResearchOpen Access
    Nature Communications
    Volume: 4, P: 1-13

  • Margaret Goodell and colleagues report genome-wide mapping of 5-methylcytosine and 5-hydroxymethylcytosine in purified mouse hematopoietic stem cells. They identify large regions of low methylation with borders marked by 5-hydroxymethylcytosine. These borders become eroded in the absence of DNA methyltransferase 3a.

    • Mira Jeong
    • Deqiang Sun
    • Margaret A Goodell
    Research
    Nature Genetics
    Volume: 46, P: 17-23

  • An analysis of the finished sequence of human chromosome 12 representing 4.5% of the human genome determines that chromosome 12 hosts a number of genes mutated in specific cancers, as well as movement disorders and potentially Alzheimer's disease.

    • Steven E. Scherer
    • Donna M. Muzny
    • Richard A. Gibbs
    Research
    Nature
    Volume: 440, P: 346-351

  • p53 is often mutated or lost in cancer; here inactivation of ΔNp63 and ΔNp73 in the absence of p53 is shown to result in metabolic reprogramming and tumour regression via activation of IAPP (islet amyloid polypeptide or amylin), and IAPP-based anti-diabetes therapeutic strategies show potential for the treatment of p53-deficient and mutant tumours.

    • Avinashnarayan Venkatanarayan
    • Payal Raulji
    • Elsa R. Flores
    Research
    Nature
    Volume: 517, P: 626-630

  • The genome of the zebra finch — a songbird and a model for studying the vertebrate brain, behaviour and evolution — has been sequenced. Comparison with the chicken genome, the only other bird genome available, shows that genes that have neural function and are implicated in the cognitive processing of song have been evolving rapidly in the finch lineage. Moreover, vocal communication engages much of the transcriptome of the zebra finch brain.

    • Wesley C. Warren
    • David F. Clayton
    • Richard K. Wilson
    ResearchOpen Access
    Nature
    Volume: 464, P: 757-762

  • The Cancer Genome Atlas consortium reports on their genome-wide characterization of somatic alterations in colorectal cancer; in addition to revealing a remarkably consistent pattern of genomic alteration, with 24 genes being significantly mutated, the study identifies new targets for therapeutic intervention and suggests an important role for MYC-directed transcriptional activation and repression.

    • Donna M. Muzny
    • Matthew N. Bainbridge
    • Elizabeth Thomson.
    ResearchOpen Access
    Nature
    Volume: 487, P: 330-337

  • Current clinical practice is organized according to tissue or organ of origin of tumors. Now, The Cancer Genome Atlas (TCGA) Research Network has started to identify genomic and other molecular commonalities among a dozen different types of cancer. Emerging similarities and contrasts will form the basis for targeted therapies of the future and for repurposing existing therapies by molecular rather than histological similarities of the diseases.

    • Kyle Chang
    • Chad J Creighton
    • Joshua M Stuart
    Comments & OpinionOpen Access
    Nature Genetics
    Volume: 45, P: 1113-1120