ArticlePLoS genetics2017
Whole-genome analysis of papillary kidney cancer finds significant noncoding alterations.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 66 citations in OpenAlex.
- Article
- The roles of long non‑coding RNAs in renal cell carcinoma (Review).Molecular and clinical oncology · 2023Review
- NEAT1 can be a diagnostic biomarker in the breast cancer and gastric cancer patients by targeting XIST, hsa-miR-612, and MTRNR2L8: integrated RNA targetome interaction and experimental expression analysis.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2022Article
- Non-coding driver mutations in human cancer.Nature reviews. Cancer · 2021Review
- Whole-genome sequencing of phenotypically distinct inflammatory breast cancers reveals similar genomic alterations to non-inflammatory breast cancers.Genome medicine · 2021Article
- lncRNA NEAT1 ameliorates LPS‑induced inflammation in MG63 cells by activating autophagy and suppressing the NLRP3 inflammasome.International journal of molecular medicine · 2021Article
- c-Met expression in renal cell carcinoma with bone metastases.Journal of bone oncology · 2020Review
- Discovery of driver non-coding splice-site-creating mutations in cancer.Nature communications · 2020Article
- A SNP-mediated lncRNA (LOC146880) and microRNA (miR-539-5p) interaction and its potential impact on the NSCLC risk.Journal of experimental & clinical cancer research : CR · 2020Article
- Genetic Alterations in Renal Cancers: Identification of The Mechanisms Underlying Cancer Initiation and Progression and of Therapeutic Targets.Medicines (Basel, Switzerland) · 2020Review
- Using sigLASSO to optimize cancer mutation signatures jointly with sampling likelihood.Nature communications · 2020Article
- Development of an Autophagy Score Signature for Predicting Overall Survival in Papillary Renal Cell Carcinoma.Disease markers · 2020Article
- A cluster of long non-coding RNAs exhibit diagnostic and prognostic values in renal cell carcinoma.Aging · 2019Article
- Current Concepts of Non-Coding RNAs in the Pathogenesis of Non-Clear Cell Renal Cell Carcinoma.Cancers · 2019Review
- Article
- Glutathione Metabolism in Renal Cell Carcinoma Progression and Implications for Therapies.International journal of molecular sciences · 2019Review
- Challenges and opportunities in the proteomic characterization of clear cell renal cell carcinoma (ccRCC): A critical step towards the personalized care of renal cancers.Seminars in cancer biology · 2019Review
- Pan-cancer analysis of long non-coding RNA NEAT1 in various cancers.Genes & diseases · 2018Review
- lncRNASNP2: an updated database of functional SNPs and mutations in human and mouse lncRNAs.Nucleic acids research · 2018Article
- Long Non-coding RNA NEAT1: A Novel Target for Diagnosis and Therapy in Human Tumors.Frontiers in genetics · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
To date, studies on papillary renal-cell carcinoma (pRCC) have largely focused on coding alterations in traditional drivers, particularly the tyrosine-kinase, Met. However, for a significant fraction of tumors, researchers have been unable to determine a clear molecular etiology. To address this, we perform the first whole-genome analysis of pRCC. Elaborating on previous results on MET, we find a germline SNP (rs11762213) in this gene predicting prognosis. Surprisingly, we detect no enrichment for small structural variants disrupting MET. Next, we scrutinize noncoding mutations, discovering potentially impactful ones associated with MET. Many of these are in an intron connected to a known, oncogenic alternative-splicing event; moreover, we find methylation dysregulation nearby, leading to a cryptic promoter activation. We also notice an elevation of mutations in the long noncoding RNA NEAT1, and these mutations are associated with increased expression and unfavorable outcome. Finally, to address the origin of pRCC heterogeneity, we carry out whole-genome analyses of mutational processes. First, we investigate genome-wide mutational patterns, finding they are governed mostly by methylation-associated C-to-T transitions. We also observe significantly more mutations in open chromatin and early-replicating regions in tumors with chromatin-modifier alterations. Finally, we reconstruct cancer-evolutionary trees, which have markedly different topologies and suggested evolutionary trajectories for the different subtypes of pRCC.
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Registered trials
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