Cancer articles within Nature Communications

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  • Article
    | Open Access

    The mechano-properties of the Extracellular Matrix (ECM) are important for tumorigenesis. Here, the authors show that the stiffening of the ECM promotes translocation of the focal adhesion protein—Kindlin-2—to the mitochondria, where it interacts with the proline synthesis enzyme PYCR1, stimulating proline synthesis and cell proliferation.

    • Ling Guo
    • , Chunhong Cui
    •  & Chuanyue Wu

  • Article
    | Open Access

    Pancreatic ductal adenocarcinoma must adapt to a nutrient-poor microenvironment. Here, the authors show that miR-135 accumulates in response to glutamine deprivation and inhibits aerobic glycolysis by targeting phosphofructokinase-1, thereby redirecting glucose carbon to the TCA cycle and allowing pancreatic cancer cells survival.

    • Ying Yang
    • , Mari B. Ishak Gabra
    •  & Mei Kong

  • Article
    | Open Access

    Integration of omics data remains a challenge. Here, the authors introduce iCell, a framework to integrate tissue-specific protein–protein interaction, co-expression and genetic interaction data, enabling identification of the most rewired genes in cancer, unidentifiable in individual data layers.

    • Noël Malod-Dognin
    • , Julia Petschnigg
    •  & Nataša Pržulj

  • Article
    | Open Access

    Radiomics—the quantification of features within tumor images—has shown prognostic potential in cancer. Here, the authors use a machine learning approach to develop a radiomic-based small set of descriptors to predict ovarian cancer patient survival based on CT scans acquired pre-operatively in 364 patients.

    • Haonan Lu
    • , Mubarik Arshad
    •  & Eric O. Aboagye

  • Article
    | Open Access

    Triple negative breast cancers (TNBC) disseminate and metastasise, but the clonal relationship of metastases to primary tumours is poorly understood. Here, the authors use cellular barcoding of TNBC patient-derived xenografts and track the fate of barcoded clones in primary tumours and their metastases, including after resection or chemotherapy.

    • D. Merino
    • , T. S. Weber
    •  & S. H. Naik

  • Article
    | Open Access

    Targeting histone acetylation modulators (HAMPs) is a promising avenue of drug discovery in cancer research. Here, the authors integrate multi-dimensional genomic profiles to systematically investigate recurrent genomic alterations in HAMPs, identifying potential therapeutic targets for precision epigenetic treatment.

    • Zhongyi Hu
    • , Junzhi Zhou
    •  & Lin Zhang

  • Article
    | Open Access

    Whether the Wnt enhanceosome’ components BCL9/9l can affect intestinal homeostasis and tumorigenesis is still unclear. Using conditional Bcl9/9l KO mice, the authors of this study show that the BCL9/9l complex is required for intestinal stem cells to drive tissue regeneration and that loss of BCL9/9l suppresses Wnt-driven transformation.

    • David M. Gay
    • , Rachel A. Ridgway
    •  & Owen J. Sansom

  • Article
    | Open Access

    BCL9 and Pygo are components of Wnt enhanceosome, which facilitates β-catenin-dependent transcription. Here, the authors show that deletion of Bcl9 and Pygo suppresses tumorigenesis and extends disease free survival in two different colorectal cancer models, suggesting a strategy for drugging β-catenin signalling in this cancer.

    • Juliusz Mieszczanek
    • , Laurens M. van Tienen
    •  & Mariann Bienz

  • Article
    | Open Access

    Bladder cancer is one of the most common and highly vascularized cancers. Here the authors perform a whole-genome analysis in urothelial bladder carcinomas and identify recurrent genetic alterations in a set of angiogenesis genes, facilitating the understanding of molecular mechanisms underlying pathological angiogenesis in this type of cancer.

    • Song Wu
    • , Tong Ou
    •  & Zhiming Cai

  • Article
    | Open Access

    Cancer cells respond differently to inhibitors of Poly (ADP-ribose) polymerase. Here the authors reveal that ovarian cancer cells with higher cellular NADP+ levels are more sensitive to clinically relevant PARP1 inhibitors and show that NADP+ act as an endogenous inhibitor of PARP enzymes.

    • Chunjing Bian
    • , Chao Zhang
    •  & Xiaochun Yu

  • Article
    | Open Access

    When examining the evolution of treatment resistance in breast cancer, perceived genomic changes may be due to clonal evolution or heterogeneous tumors. Here, the authors show that apparent clonal change can in fact be due to pre-treatment heterogeneity, and samples from at least two regions are necessary to detect treatment-induced clonal shifts

    • Jennifer L. Caswell-Jin
    • , Katherine McNamara
    •  & Christina Curtis

  • Article
    | Open Access

    Capicua (CIC) is a tumour suppressor in oligodendroglioma. Here, the authors show that ERK activation mediates CIC regulation via ubiquitination and degradation by PJA1 and a degradation resistant form of CIC enhances efficacy of ERK inhibition in glioblastoma.

    • Severa Bunda
    • , Pardeep Heir
    •  & Kenneth Aldape

  • Article
    | Open Access

    PTEN is a lipid phosphatase that functions as a dose-dependent tumor suppressor through the PI3K/AKT pathway. Here the authors describe a signaling feedback mechanism where PTEN stability is regulated through transcriptional upregulation of X-linked ubiquitin-specific protease 11 (USP11) via the PI3K/FOXO pathway.

    • Mi Kyung Park
    • , Yixin Yao
    •  & Min Sup Song

  • Article
    | Open Access

    Non-small cell lung cancers with inactivating SMARCA4 mutations are currently undruggable. Here, the authors show that the absence of SMARCA4/2 reduces chromatin accessibility at the CCND1 locus, leading to a subsequent reduction in cyclin D1 expression, which promotes vulnerability of these cancers to CDK4/6 inhibition.

    • Yibo Xue
    • , Brian Meehan
    •  & Sidong Huang

  • Article
    | Open Access

    Small cell carcinoma of the ovary, hypercalcemic type (SCCOHT) is driven by SMARCA4 loss. Here the authors demonstrate that SCCOHT cells are highly sensitive to CDK4/6 inhibition and provide mechanistic insights, whereby this druggable vulnerability is driven by cyclin D1 deficiency induced by SMARCA4 loss.

    • Yibo Xue
    • , Brian Meehan
    •  & Sidong Huang

  • Article
    | Open Access

    The immunosuppressive tumor environment and the lack of functional anti-tumor immunity are major limiting factors in immunotherapy. Here the authors show that human and mouse tumors are infiltrated by virus-specific memory T cells, which can be harnessed by viral peptides to induce local and systemic anti-tumor immunity and synergize with checkpoint blockade.

    • Pamela C. Rosato
    • , Sathi Wijeyesinghe
    •  & David Masopust

  • Article
    | Open Access

    CD47 is a promising new target in cancer immunotherapy and recently the pro-phagocytic signal SLAMF7 has been shown to have a crucial role in phagocytosis induced by CD47-blocking antibody in hematological tumors. In this study, the authors demonstrate that SLAMF7 expressed by cancer cells is not required for phagocytosis suggesting that, in contrast to CD47 expression, SLAMF7 should not be used as selection criterion for CD47-targeted therapy.

    • Yuan He
    • , Renee Bouwstra
    •  & Edwin Bremer

  • Article
    | Open Access

    Fibrinogen-like protein 2 (FGL2) mediates immune suppression in glioblastoma (GBM). Here, the authors show that FGL-2 expressed by GBM cancer cells acts by suppressing the differentiation of CD103+ DC cells required to activate the anti-tumor CD8+ T cell response via blocking GM-CSF signalling at NFKB, STAT1/5 and p38 level.

    • Jun Yan
    • , Qingnan Zhao
    •  & Shulin Li

  • Article
    | Open Access

    The delivery of single therapeutic microRNAs in brain cancers is challenging. Here, the authors engineer three neuronal microRNAs (miR-124, 128 and 137) into a cluster that, targeting oncogenic chromatin repressors, increases survival of GBM-bearing mice when combined with chemotherapy.

    • Vivek Bhaskaran
    • , Michal O. Nowicki
    •  & Pierpaolo Peruzzi

  • Article
    | Open Access

    Adoptive cell therapy (ACT) using neoantigen-specific T cells can lead to tumor regression. Here the authors use an in vitro stimulation approach to isolate tumor specific memory T cells from peripheral blood of metastatic epithelial cancer patients targeting unique as well as shared mutations in the KRAS oncogene.

    • Gal Cafri
    • , Rami Yossef
    •  & Steven A. Rosenberg

  • Article
    | Open Access

    Similarities in cancers can be studied to interrogate their etiology. Here, the authors use genome-wide association study summary statistics from six cancer types based on 296,215 cases and 301,319 controls of European ancestry, showing that solid tumours arising from different tissues share a degree of common germline genetic basis.

    • Xia Jiang
    • , Hilary K. Finucane
    •  & Sara Lindström

  • Article
    | Open Access

    ER stress and UPR are implicated in various cancers. Here, the authors show that one of the canonical UPR pathways, IRE1α-XBP1 regulates c-MYC signaling to promote prostate tumorigenesis, and pharmacological inhibition of IRE1α with MKC8866 inhibits prostate cancer growth and synergizes with clinically used prostate cancer drugs.

    • Xia Sheng
    • , Hatice Zeynep Nenseth
    •  & Fahri Saatcioglu

  • Article
    | Open Access

    The connection between DNA replication timing and changes that occur to the epigenome in cancer are still poorly understood. Here, the authors perform Repli-Seq and integrated epigenome analyses and find that genomic regions that undergo long-range epigenetic deregulation in prostate cancer also show concordant differences in replication timing.

    • Qian Du
    • , Saul A. Bert
    •  & Susan J. Clark

  • Article
    | Open Access

    Focal amplifications are prevalent in many cancer genomes. Here, the authors present AmpliconArchitect (AA), a computational tool for reconstructing their architecture, and reveal an extrachromosomal origin for focal amplifications, including hybrid human-virus elements in HPV-mediated cancers.

    • Viraj Deshpande
    • , Jens Luebeck
    •  & Vineet Bafna

  • Article
    | Open Access

    It is difficult to identify cancer driver genes in cancers, for instance BRCA1 mutated breast cancer, that are characterised by large scale genomic alterations. Here, the authors develop genetically engineered mouse models of BRCA1-deficient breast cancer that allow highthroughput in vivo perturbation of candidate driver genes, validating drivers Myc, Met, Pten and Rb1, and identifying MCL1 as a collaborating driver whose targeting can impact efficacy of PARP inhibition.

    • Stefano Annunziato
    • , Julian R. de Ruiter
    •  & Jos Jonkers

  • Article
    | Open Access

    Obesity is linked to increased cancer risk but the impact of body size versus weight distribution in determining the increased risk is unclear. Here the authors examined body mass index, waist circumference, and waist to hip ratio in relation to all-cancer incidence and incidence of seven individual cancers in a population of approximately 26,000 individual and conclude that central adiposity appears to be a stronger predictor of all-cancer risk than body size.

    • Amanda M. Barberio
    • , Asalah Alareeki
    •  & Darren R. Brenner

  • Article
    | Open Access

    Somatic alterations in the exonuclease domain of DNA polymerase ɛ have been linked to the development of highly mutated cancers. Here, the authors report that a major consequence of the most common cancer-associated Polɛ variant is a dramatically increased DNA polymerase activity.

    • Xuanxuan Xing
    • , Daniel P. Kane
    •  & Polina V. Shcherbakova

  • Article
    | Open Access

    Acinic cell carcinoma (AciCC) is a rare salivary gland carcinoma that is poorly understood. Here the authors perform genomic, transcriptomic and epigenomic profiling of AciCC and find highly recurrent and specific rearrangements [t(4;9)(q13;q31)], which lead to enhancer hijacking that activates oncogenic transcription factor NR4A3.

    • Florian Haller
    • , Matthias Bieg
    •  & Abbas Agaimy

  • 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

    Enhanced Wnt receptor activity is a major cause of cancer development. Here the authors identify camelid single-domain antibody fragments (VHHs) that bind to the Wnt receptor LRP5/6 ectodomain, determine the crystal structures and show that these VHHs selectively inhibit Wnt3- mediated cellular responses and block the growth of mutant Wnt-hypersensitive intestinal tumor organoids.

    • Nicola Fenderico
    • , Revina C. van Scherpenzeel
    •  & Madelon M. Maurice

  • Article
    | Open Access

    Myelodyplastic hematopoietic stem cells (MDS HSC) have eluded in vivo modeling. Here the authors present a highly efficient MDS patient-derived xenotransplantation model in cytokine-humanized mice with replication of the donors’ genetic complexity and myeloid, erythroid, and megakaryocytic lineage dysplasia.

    • Yuanbin Song
    • , Anthony Rongvaux
    •  & Stephanie Halene

  • Article
    | Open Access

    Medulloblastoma is one of the most prevalent malignant brain tumors in children and has very poor prognosis. In this study, the authors show, using a mouse model of medulloblastoma, that Gfi1 promotes tumor growth by recruiting Lsd1, that this interaction inhibits genes involved in neuronal differentiation, and that Lsd1 may be a therapeutic target in Gfi1-activated tumors.

    • Catherine Lee
    • , Vasilisa A. Rudneva
    •  & Robert J. Wechsler-Reya

  • Article
    | Open Access

    There are distinct hypermethylation patterns in gene promoters in hepatocellular carcinomas (HCCs). Here, the authors show that the enhancer of C/EBPβ is recurrently hypomethylated in human HCCs, recapitulating this in a transgenic murine model and linking aberrant enhancer hypomethylation to hepatocarcinogenesis.

    • Lei Xiong
    • , Feng Wu
    •  & Ka-Fai To

  • Article
    | Open Access

    miR-205 is known to have context-dependent tumor suppressive or oncogenic roles. Here, the authors report the host gene of miR-205, MIR205HG as a nuclear lincRNA that maintains the basal identity of prostate cell and prevents luminal cell differentiation via the repression of interferon responsive genes.

    • Valentina Profumo
    • , Barbara Forte
    •  & Paolo Gandellini

  • Article
    | Open Access

    Neuroendocrine prostate cancer (NEPC) is characterized by loss of androgen receptor (AR) signaling during neuroendocrine transdifferentiation, resulting in resistance to AR-targeted therapy. Here they report ONECUT2 to drive NEPC tumorigenesis via regulation of hypoxia signaling and tumor hypoxia, and find hypoxia directed therapy to be effective in NEPC.

    • Haiyang Guo
    • , Xinpei Ci
    •  & Housheng Hansen He

  • Article
    | Open Access

    Overexpression of RAS proteins is frequently observed in patients with hepatocellular carcinoma. Here, the authors identify an HRAS binding protein, the E3 ubiquitin ligase WDR76, which promotes HRAS degradation, thus functioning as a tumour suppressor in liver cancer

    • Woo-Jeong Jeong
    • , Jong-Chan Park
    •  & Kang-Yell Choi

  • Article
    | Open Access

    The humoral immune response role in cancer is unclear. Here the authors perform an in-depth proteomic profiling of immunoglobulin-bound proteins in plasma from pancreatic ductal adenocarcinoma patients and find cancer-cell specific antibodies neutralized by binding to cancer-cell derived exosomes.

    • Michela Capello
    • , Jody V. Vykoukal
    •  & Samir M. Hanash

  • Article
    | Open Access

    Enzymatic reactions caused by neutrophils can cause the elevation of reactive oxygen species (ROS) in tumour tissue, Here, the authors, inspired by the neutrophils, design and test a synthetic cascade reaction which turns ROS into singlet oxygen and demonstrate the application of the designed nanoparticle

    • Qing Wu
    • , Zhigang He
    •  & Qigang Wang

  • Article
    | Open Access

    Resistance to the new generation EGFR-TKI, Osimertinib, can emerge in patients with EGFR-mutated lung cancer. Here, the authors show that AXL, which is activated by osimertinib, can promote the emergence of tolerant lung cancer cell thus conferring resistance to osimertinib and propose the combination of Osimertinib with AXL inhibitor as a potential therapeutic approach in such resistant cancers.

    • Hirokazu Taniguchi
    • , Tadaaki Yamada
    •  & Seiji Yano

  • Article
    | Open Access

    Activation of the PPARγ/RXRα pathway in luminal bladder cancers has mainly been linked to PPARG gene amplifications and activating point mutations in RXRα. Here, the authors identify recurrent PPARγ mutations with similar effects and elucidate the structural basis for this mutational PPARγ activation.

    • Natacha Rochel
    • , Clémentine Krucker
    •  & Isabelle Bernard-Pierrot

  • Article
    | Open Access

    FLT3 is commonly mutated in acute myeloid leukaemia and treatment with FLT3 inhibitors often ends with relapse. Here, the authors perform exome sequencing of samples from patients treated with the FLT3 inhibitor, crenolanib, to show that resistance occurs due to diverse molecular mechanisms, not primarily due to secondary FLT3 mutations.

    • Haijiao Zhang
    • , Samantha Savage
    •  & Jeffrey W. Tyner

  • Article
    | Open Access

    Chronic hepatitis B virus (HBV) infection is a risk factor for hepatocellular carcinoma (HCC) and is associated with immune tolerance to HBV. Here the authors show, in a transgenic mouse model, that rescuing T cells function via inhibition of co-inhibitory receptor TIGIT results in HCC development via supporting inflammation.

    • Lu Zong
    • , Hui Peng
    •  & Zhigang Tian

  • Article
    | Open Access

    Cancer patients are at an increased risk of suicide: elderly, white, unmarried males with localized disease are at highest risk vs other cancer patients. Among those diagnosed at < 50 years of age, the plurality of suicides is from hematologic and testicular tumors; if > 50, from prostate, lung, and colorectal cancer patients.

    • Nicholas G. Zaorsky
    • , Ying Zhang
    •  & Vernon M. Chinchilli

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