Cancer models articles within Nature Communications

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  • Article
    | Open Access

    The effects of epigenetic regulators on different tumor cell populations can affect their potential as anticancer targets. In this study, the authors demonstrate that the histone methyltransferase G9a is a suppressor of lung tumor-propagating cells and tumor progression, acting through chromatin modification with MMP10 as one of its targets for metastasis regulation.

    • S. P. Rowbotham
    • , F. Li
    •  & C. F. Kim

  • Article
    | Open Access

    Fusions of the gene RET have been described in thyroid and lung cancers. Here, the AUs identify RET gene alterations, including known fusions, novel fusions, and rearrangements in breast cancer (BC) that are involved in the tumorigenic process and show the benefit of RET therapy in a recurrent BC patient carrying the NCOA4-RET fusion.

    • Bhavna S. Paratala
    • , Jon H. Chung
    •  & Kim M. Hirshfield

  • Article
    | Open Access

    Chromothripsis and chromoanasynthesis lead to locally clustered rearrangements affecting one or a few chromosomes, but their impact on cancer development and progression is unclear. Here the authors analyse the role of DNA repair factors in brain tumors by whole-genome sequencing of tumors from mouse models of medulloblastoma or high grade gliomas.

    • Manasi Ratnaparkhe
    • , John K. L. Wong
    •  & Aurélie Ernst

  • Article
    | Open Access

    The lack of appropriate models restricts pre-clinical research for nasopharyngeal carcinoma (NPC). Here the authors report the development and characterization of NPC patient-derived xenografts (PDXs), and EBV positive NPC cell line from patient tumor, and suggest their potential use in future NPC research.

    • Weitao Lin
    • , Yim Ling Yip
    •  & Sai Wah Tsao

  • Article
    | Open Access

    HIV patients have an increased risk of developing non-AIDS-defining cancers but the molecular mechanisms underlying this predisposition are unclear. Here the authors show that exosomes secreted by HIV-infected T cells or isolated from the blood of HIV-positive patients, stimulate oncogenic properties of cancer cells through the activation of ERK1/2 signaling pathway.

    • Lechuang Chen
    • , Zhimin Feng
    •  & Ge Jin

  • Article
    | Open Access

    Chr3q26 rearrangements cause overexpression of EVI1 and associate with myeloid neoplasms, but the mechanism behind this association is unclear. Here, using a novel mouse model they show that EVI1 causes premalignant myeloid expansion with suppression of other lineages through upregulation of Spi1/PU.1.

    • Edward Ayoub
    • , Michael P. Wilson
    •  & Archibald S. Perkins

  • Article
    | Open Access

    Osteosarcoma is a heterogeneous bone tumour with a high mutational rate. Here the authors use an RGB-based single-cell tracking system to track clonal dynamics in a mouse model of osteosarcoma, which their findings indicate follows a neutral evolution model in which different clones simultaneously coexist and propagate.

    • Stefano Gambera
    • , Ander Abarrategi
    •  & Javier García-Castro

  • Article
    | Open Access

    The c-MYC oncoprotein has many targets whose actions are not fully understood including TFAP4/AP4. Here, the authors show in a mouse model of inherited colorectal cancer that deletion of AP4 decreased the frequency of c-MYC-driven intestinal adenomas, and reveal Ap4 as a mediator of adenoma initiation and regulator of colonic and intestinal stem cell and Paneth cell homeostasis.

    • Stephanie Jaeckel
    • , Markus Kaller
    •  & Heiko Hermeking

  • Article
    | Open Access

    Changes in the DNA methylation status are commonly observed in cancer but their impact on cancer development is unclear. Here, combining DNA methylation and expression profiles from a murine model of hepatocellular carcinoma with those from human samples, the authors report an epigenetic reprogramming process ensuring increased dosage of an “oncogene module”.

    • Maria Arechederra
    • , Fabrice Daian
    •  & Flavio Maina

  • Article
    | Open Access

    Amplification of PDGFRα is a common alteration in glioblastoma. In this study, the authors develop a genetically engineered mouse model of GBM based on autocrine, chronic stimulation of overexpressed PDGFR and discover Stathmin1 as an important PDGFRα regulated-protein involved in the response to vinstabline.

    • Hyun Jung Jun
    • , Vicky A. Appleman
    •  & Al Charest

  • Article
    | Open Access

    Esophageal adenocarcinoma (EAC) has a poor 5-year survival rate and lacks robust preclinical models for use in research. Here, the authors show that newly derived organoids recapitulate the transcriptomic, genetic, and morphological landscape of the primary EAC tumors and provide a platform to test drug sensitivity and study tumor clonality.

    • Xiaodun Li
    • , Hayley E. Francies
    •  & Mathew J. Garnett

  • Article
    | Open Access

    Evidence implicating cancer drivers can be sparse when limited to clonal events. Here, the authors present a retrovirus driven in vivo lymphomagenesis time course including hundreds of thousands of subclonal mutations and demonstrate the utility of these in mapping the selective forces affecting cancer gene loci, including negatively selected mutations.

    • Philip Webster
    • , Joanna C. Dawes
    •  & Anthony G. Uren

  • Article
    | Open Access

    There are few available models to study neuroendocrine prostate cancer. Here they develop and characterize patient derived organoids from metastatic lesions, use these models to show the role of EZH2 in driving neuroendocrine phenotype, and perform high throughput organoid screening to identify therapeutic drug combinations.

    • Loredana Puca
    • , Rohan Bareja
    •  & Himisha Beltran

  • Article
    | Open Access

    SETBP1 variants occur as somatic mutations in several malignancies and as de novo germline mutations in developmental disorders. Here the authors provide evidence that SETBP1 binds to gDNA in AT-rich promoter regions to promote target gene upregulation, indicating SETBP1 functions directly to regulate transcription.

    • Rocco Piazza
    • , Vera Magistroni
    •  & Carlo Gambacorti-Passerini

  • Article
    | Open Access

    Cellular reprogramming and cancer development share properties. Here, the authors examine the impact of in vivo reprogramming on Kras-induced cancer and show reprogramming-mediated repression of somatic cell enhancers in conjunction with Kras mutation results in rapid PDAC development.

    • Hirofumi Shibata
    • , Shingo Komura
    •  & Yasuhiro Yamada

  • Article
    | Open Access

    MYB activity is a key factor for the maintenance of acute myeloid leukemias but it is also a difficult target. Here, the authors develop a peptidomimetic (MYBMIM) that prevents the interaction of the trans-activation domain of MYB with the KIX domain of CBP/P300 and inhibits leukaemia growth.

    • Kavitha Ramaswamy
    • , Lauren Forbes
    •  & Alex Kentsis

  • Article
    | Open Access

    Genome editing technologies enable the rapid interrogation of genetic alterations. Here, the authors present a CRISPR/Cas9-based platform to simultaneously investigate multiple activating point mutations in de novo cancers in mice; and generate panels of Kras-variants in different tissues to induce cancer.

    • Ian P. Winters
    • , Shin-Heng Chiou
    •  & Monte M. Winslow

  • Article
    | Open Access

    Mutations in VHL have been linked to clear cell renal cancer, but the molecular mechanisms involved remain unclear. Here the authors generate a mouse model closely mimicking the human disease and show that VHL loss induces DNA replication stress that is rescued by the concomitant loss of PBRM1 permitting transformation.

    • Judit Espana-Agusti
    • , Anne Warren
    •  & Athena Matakidou

  • Article
    | Open Access

    Macroautophagy can regulate cell signalling and tumorigenesis but the molecular mechanisms are unclear. Here the authors show selective degradation of the signalling scaffold TRAF3 by autophagy and consequent activation of the NF-κB family member RELB regulate gene expression via antagonism of SMAD proteins.

    • Alice C. Newman
    • , Alain J. Kemp
    •  & Simon Wilkinson

  • Article
    | Open Access

    The clonal architecture of colon cancer and the relevance of tumor cell subpopulations for clonal outgrowth are poorly understood. Here, the authors describe the clonal architecture and dynamics in human colon cancer by using a multicolor lineage tracing approach in colon cancer xenografts.

    • Sebastian Lamprecht
    • , Eva Marina Schmidt
    •  & David Horst

  • Article
    | Open Access

    Cancer heritability estimates can be obtained via decomposing trait variance into genetic and other factors. Here, the authors obtain the distribution of absolute genetic risk for 15 common cancers, and they use a number of metrics to show that the genetic risk varies considerably across individuals.

    • Mats Julius Stensrud
    •  & Morten Valberg

  • Article
    | Open Access

    Glioblastoma (GBM) cells are often characterized by the presence of the IDH1 R132H mutation and high expression of anti-apoptotic proteins. Here, the authors show that the inhibition of Bcl-xL is synthetically lethal in IDH1-mutated GBM models and that this effect is mediated by the oncometabolite, 2-HG, which reduces Mcl-1 protein levels.

    • Georg Karpel-Massler
    • , Chiaki Tsuge Ishida
    •  & Markus D. Siegelin

  • Article
    | Open Access

    Combining different types of immune therapies might benefit certain patients. Here, the authors develop an autologous immune-humanized melanoma mouse model that allows the preclinical assessment of cancer cell–T cell interactions from each individual patient and the benefits of immunotherapies combinations.

    • Henrik Jespersen
    • , Mattias F. Lindberg
    •  & Jonas A. Nilsson

  • Article
    | Open Access

    Treatment response in patient-derived models may serve as a biomarker for response in the clinic. Here, the authors use paired patient-derived mouse xenografts and patient-derived primary culture models from head and neck squamous cell carcinomas, including metastasis, as models for high-throughput screening of anti-cancer drugs.

    • Shumei Chia
    • , Joo-Leng Low
    •  & Ramanuj DasGupta

  • Article
    | Open Access

    SMARCB1 mutations predispose to rhabdoid tumors and schwannomas but the mechanisms underlying the tumor type specificity are unknown. Here the authors present new mouse models and show that early Smarcb1 loss causes rhabdoid tumors whereas loss at later stages combined with Nf2 gene inactivation causes shwannomas.

    • Jeremie Vitte
    • , Fuying Gao
    •  & Marco Giovannini

  • Review Article
    | Open Access

    A better understanding of the earliest stages of human cancer formation can enable future improvements in early detection, diagnosis and treatment. In this review, the authors summarize the methods enablingde novotumorigenesis protocols to be applied to human cells and the insights derived from them to date, as well as the exciting and relevant technical developments anticipated to extend even further the utility of these strategies.

    • Sneha Balani
    • , Long V. Nguyen
    •  & Connie J. Eaves

  • Article
    | Open Access

    The heterogeneity of colorectal cancer has important clinical and therapeutic implications. Here the authors analysed the responses of a large biobank of organoids and xenografts derived from colorectal patients to a panel of clinically relevant therapeutic agents to identify genes signatures associated with drug response.

    • Moritz Schütte
    • , Thomas Risch
    •  & Marie-Laure Yaspo

  • Article
    | Open Access

    Colorectal cancers carry multiple mutations. Here, the authors use Drosophilaas a model organism and assess multiple combinations of mutations and their response to various drugs, providing further insight into drug resistance mechanisms.

    • Erdem Bangi
    • , Claudio Murgia
    •  & Ross L. Cagan

  • Article
    | Open Access

    Using mosaic analysis with double markers to label genetically-distinct clones in established tumors, the authors studied the effects of p53 loss in lung and pancreatic cancers. They find that loss of p53 enhances progression in both models but only influences initiation in the pancreas.

    • Mandar Deepak Muzumdar
    • , Kimberly Judith Dorans
    •  & Tyler Jacks

  • Article
    | Open Access

    CYLD is a deubiquitinase known to act as a tumour suppressor in different models of carcinogenesis. Here, the authors show that CYLD suppresses carcinogen-induced tumorigenesis by deubiquitinating p53 and promoting its stabilization and activation in response to DNA damage.

    • Vanesa Fernández-Majada
    • , Patrick-Simon Welz
    •  & Manolis Pasparakis

  • Article
    | Open Access

    Oxaliplatin resistance in colorectal cancers is a major clinical problem, and predictive markers are urgently needed. Here, the authors show that miR-625-3pexpression reduces the sensitivity of colorectal cancer cells to oxaliplatin by targeting the kinase MAP2K6, an activator of the MAPK14 pathway.

    • Mads Heilskov Rasmussen
    • , Iben Lyskjær
    •  & Claus Lindbjerg Andersen

  • Article
    | Open Access

    Glioma can originate from the transformation of neural progenitor cells into glioma initiating cells. Here, the authors demonstrate the use of induced pluripotent stem cells as a suitable model for generating neural progenitor cells, which can be subsequently transformed to glioma initiating cells that are able to the generate human glioma-like tumours in mice.

    • Ignacio Sancho-Martinez
    • , Emmanuel Nivet
    •  & Juan Carlos Izpisua Belmonte

  • Article
    | Open Access

    Cell lines are widely used in cancer research to study tumour biology. Here Domcke et al.compare genomic data from ovarian cancer cell lines with those from clinical ovarian tumour samples and identify cell lines that most closely resemble the genomic features of high-grade serous ovarian cancer.

    • Silvia Domcke
    • , Rileen Sinha
    •  & Nikolaus Schultz

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