Cancer therapy articles within Nature Communications

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  • Article
    | Open Access

    The Wnt/β-catenin signalling pathway contributes to radio resistance in intestinal stem cells but the underlying mechanism is currently unknown. In this study, the authors demonstrate that LIG4, a DNA ligase involved in the DNA repair process, is a direct target of β-catenin and it specifically mediates non-homologous end joining repair in colorectal cancer cells.

    • Sohee Jun
    • , Youn-Sang Jung
    •  & Jae-Il Park

  • Article
    | Open Access

    Signals through VEGF receptor 2 (VEGFR2) increase vascular permeability, promoting cancer progression. Here the authors show that a point mutation in VEGFR2 preventing its auto-phosphorylation leads to reduced metastatic spread and improved response to chemotherapy in tumor-bearing mice, without affecting tumor inflammation.

    • Xiujuan Li
    • , Narendra Padhan
    •  & Lena Claesson-Welsh

  • Article
    | Open Access

    PGRMC1 binds to EGFR and cytochromes P450, and is known to be involved in cancer proliferation and in drug resistance. Here, the authors determine the structure of the cytosolic domain of PGRMC1, which forms a dimer via haem–haem stacking, and propose how this interaction could be involved in its function.

    • Yasuaki Kabe
    • , Takanori Nakane
    •  & Makoto Suematsu

  • Article
    | Open Access

    Radiotherapy can induce fibrosis in cancer patients, limiting its use in clinical settings. Here, the authors identify a differentially methylated enhancer of the lipid kinase DGKA in fibroblasts from breast cancer patients developing fibrosis after radiotherapy and they show that DGKA inhibition affects lipid homeostasis and reduces pro-fibrotic fibroblast activation.

    • Christoph Weigel
    • , Marlon R. Veldwijk
    •  & Odilia Popanda

  • Article
    | Open Access

    The anti-apoptotic protein Bcl-2 is selectively expressed in intestinal stem cells (ISCs). Here, the authors show that, in intestinal stem cells, Bcl-2 alleviates apoptotic priming induced by the loss of the tumour suppressor Apc in ISCs and that the absence of Bcl-2 or pharmacological blockade of Bcl-2 can inhibit the intestinal tumorigenesis driven by the Apc-loss.

    • Maartje van der Heijden
    • , Cheryl D. Zimberlin
    •  & Louis Vermeulen

  • Article
    | Open Access

    Chronic myelomonocytic leukaemia is treated with agents that modify DNA methylation but whether they have direct cytotoxic effects is unclear. Here, the authors show that cells from treated patients show marked methylation changes without altered somatic mutation burden, suggesting that cytotoxicity is not a major factor in therapeutic efficacy.

    • Jane Merlevede
    • , Nathalie Droin
    •  & Eric Solary

  • Article
    | Open Access

    Cancer cells that survive initial drug treatment can persist in the presence of drugs. Here, the authors generate persister cells that are resistant to the EGFR tyrosine kinase inhibitor erlotinib and show by single cell analysis that multiple mechanism give rise to the drug-resistant persister state.

    • Michael Ramirez
    • , Satwik Rajaram
    •  & Steven J. Altschuler

  • Article
    | Open Access

    Intravital microscopy has been used in laboratory animals to visualise the blood vessels in tumours. Here, the authors use this technique in melanoma patients undergoing surgery and show that vessels in situhave a larger diameter than excised tissue

    • Daniel T. Fisher
    • , Jason B. Muhitch
    •  & Joseph J. Skitzki

  • Article
    | Open Access

    Blocking immune checkpoints is a promising strategy to treat lung cancer, but patients often become resistant to the therapy. Here, the authors analyse resistance in mouse models of lung cancer and show in mice and two patients, an increase in the expression of TIM3, which is also involved in the immune response to cancer.

    • Shohei Koyama
    • , Esra A. Akbay
    •  & Peter S. Hammerman

  • Article
    | Open Access

    ER+ breast cancer patients treated with endocrine therapies often acquire resistance and develop metastasis. In this study, the authors demonstrate that endocrine therapies can promote the self-renewal of CD133hi/ERlodrug resistant cells with metastatic potential driven through the IL6-Notch3 axis activation.

    • Pasquale Sansone
    • , Claudio Ceccarelli
    •  & Jacqueline Bromberg

  • Article
    | Open Access

    Amino acid substitutions in K-Ras that constitutively activate the protein are common in cancer. Here, the authors describe mutations in the K-RasSwitch 2 domain and show that the mutant proteins accumulate in the active conformation, exhibit defective binding to PI3 kinase, and are hypersensitive to MEK inhibitors.

    • Yasmine White
    • , Aditi Bagchi
    •  & Ari J. Firestone

  • Article
    | Open Access

    During colorectal inflammation and cancer, myeloid cells accumulate in the spleen and suppress the host immunity response. In this study, the authors use a mouse model of colitis to demonstrate that upon vagus stimulation splenic memory T cells release TFF2, which suppresses the expansion of myeloid cells and cancer progression.

    • Zina Dubeykovskaya
    • , Yiling Si
    •  & Timothy C. Wang

  • Article
    | Open Access

    The potassium channel KCNK9 mediates important biological processes and is often overexpressed in breast and lung cancers. In this study, the authors developed a specific monoclonal antibody against the extracellular domain of KCNK9 and show that it inhibits cancer growth and metastasis in vivothrough both cell autonomous and immune-dependent cellular cytotoxicity.

    • Han Sun
    • , Liqun Luo
    •  & Min Li

  • Article
    | Open Access

    Immunotherapy is used to treat melanoma, however patient responses vary widely highlighting the need for factors that can predict therapeutic success. Here, the authors show that MHC-II molecules expressed by tumour cells are positively correlated with a good response to therapy and overall patient survival.

    • Douglas B. Johnson
    • , Monica V. Estrada
    •  & Justin M. Balko

  • Article
    | Open Access

    Bcl-xL is an anti-apoptotic protein that has also been implicated in metastasis. In this study, the authors show that nuclear Bcl-xL promotes metastasis by regulating TGFβ signaling, which is independent of the anti-apoptotic activity of Bcl-xL.

    • Soyoung Choi
    • , Zhengming Chen
    •  & Yi-Chieh Nancy Du

  • Article
    | Open Access

    c-MYC genomic distribution is dictated by the epigenetic context but the mechanisms are unknown. Here, the authors show that c-MYC requires the chromatin reader BPTF to activate its transcriptional program and promote tumour development in vivo, suggesting that BPTF is a potential target for cancer therapy.

    • Laia Richart
    • , Enrique Carrillo-de Santa Pau
    •  & Francisco X. Real

  • Article
    | Open Access

    Resistance to receptor tyrosine kinase inhibitors is a major obstacle in treatment of lung adenocarcinoma. Yamaguchi et al.identify the orphan receptor ROR1 as a potential target to overcome this resistance, by virtue of its role in promoting cell survival through stabilisation of caveolae.

    • Tomoya Yamaguchi
    • , Can Lu
    •  & Takashi Takahashi

  • Article
    | Open Access

    p53 is a tumour suppressor that is mutated in a large number of cancers and its expression is controlled largely by the ubiquitin ligase MDM2. Here, the authors show that the homeoprotein, Six1, can regulate p53 in an MDM2- independent manner via regulation of miR-27a and the RNA binding protein, RPL26.

    • Christina G. Towers
    • , Anna L. Guarnieri
    •  & Heide L. Ford

  • Article
    | Open Access

    Cancer cells and stromal cells have been shown to pass cellular information between each other via exosomes. Here, the authors demonstrate that cancer cells can communicate with endothelial cells through nanoscale membrane bridges, and demonstrate that microRNAs are passed through these nanobridges, which modulates endothelial cell phenotype.

    • Yamicia Connor
    • , Sarah Tekleab
    •  & Shiladitya Sengupta

  • Article
    | Open Access

    Chemotherapeutic agents elicit ER and oxidative stress as part of their mode of action. Here the authors show that chemotherapy and ER stress trigger MGST2-based biosynthesis of LTC4, whose inhibition abolishes chemotherapy- and ER stress-triggered oxidative stress and DNA damage, resulting in the attenuation of cell death.

    • Efrat Dvash
    • , Michal Har-Tal
    •  & Menachem Rubinstein

  • Article
    | Open Access

    Acquired resistance to anti-angiogenic drugs, including bevacizumab, may occur in cancer patients. In this study the authors identify in the tumour microenvironment, fibrocyte-like cells derived from the bone marrow that mediate the resistance to bevacizumab through the production of FGF2.

    • Atsushi Mitsuhashi
    • , Hisatsugu Goto
    •  & Yasuhiko Nishioka

  • Article
    | Open Access

    Current endoscopes are limited to detection or treatment of colon cancers and growths, or resolution is too low for clinical application. Here the authors present a multimodal endoscope with theranostic nanoparticles that integrates fluorescence-based mapping, electrical impedance, pH and temperature monitoring, RF ablation and localized phototherapy or chemotherapy.

    • Hyunjae Lee
    • , Youngsik Lee
    •  & Dae-Hyeong Kim

  • Article
    | Open Access

    Aberrant Ras signalling resulting in downstream Mek/Erk pathway activation is found in many cancers. Here, the authors show that the phosphatase SHP2 dephosphorylates Ras resulting in increased Ras activity, and that increased SHP2 activity is found in glioblastomas.

    • Severa Bunda
    • , Kelly Burrell
    •  & Michael Ohh

  • Article
    | Open Access

    The high expression of the DNA repair enzyme O6-methylguanine DNA methyltransferase (MGMT) often confers resistance to chemotherapy in several cancers. In this study, the authors propose the inhibition of the Wnt signalling pathway as an alternative strategy to modulate MGMT expression and sensitize tumours to chemotherapy.

    • Malin Wickström
    • , Cecilia Dyberg
    •  & John Inge Johnsen

  • Article |

    Transgenic diatom algae can incorporate proteins in their silica shells. Here the authors design diatoms that can be decorated with tumour-specific antibody of choice and use them as natural nanoparticles for targeted delivery of a chemotherapeutic drug, impeding mouse xenograft tumour growth.

    • Bahman Delalat
    • , Vonda C. Sheppard
    •  & Nicolas H. Voelcker

  • Article
    | Open Access

    Synthetic biology can be used to regulate target genes and uncover gene function in physiologically relevant settings. Here Robles-Oteiza et al. describe a new recombinase-based system for conditional inactivation and inducible restoration of gene function and develop new mouse models to study p53 and Rb.

    • Camila Robles-Oteiza
    • , Sarah Taylor
    •  & David M. Feldser

  • Article
    | Open Access

    Cancer genome analysis has demonstrated that some breast and ovarian tumours show reduced homologous recombination, a feature that can be therapeutically exploited. Here, Alexandrov et al.search for this mutational signature in 36 different cancer types and find that some gastric tumours also harbour this mutational spectrum.

    • Ludmil B. Alexandrov
    • , Serena Nik-Zainal
    •  & Michael R Stratton

  • Article
    | Open Access

    Drug-loaded nanoparticles allow controlled release and enhanced delivery, yet understanding in vivobehavior has been difficult. Here, the authors develop a platinum prodrug coupled to a polymer platform, and use intravital imaging to show that the nanoparticle accumulates in macrophages, from the which drug redistributes to neighboring tumour cells.

    • Miles A. Miller
    • , Yao-Rong Zheng
    •  & Ralph Weissleder

  • Article
    | Open Access

    With no cell lines available, investigating the aetiology of human fibrolamellar hepatocellular carcinomas (hFL-HCCs) has proved problematic. Here, Oikawa et al. establish a model of hFL-HCCs as a transplantable tumour line maintained in immune-compromised mice, which proves rich in cancer stem cells.

    • Tsunekazu Oikawa
    • , Eliane Wauthier
    •  & Lola M. Reid

  • Article
    | Open Access

    Centrosome amplification is common in cancer, but the mechanism is not clear. Here the authors uncover a role for Kruppel-like factor 14 (KLF14) as a transcriptional repressor of polo-like kinase 4 (PLK4); KLF14 depletion correlates with increased PLK4 in human samples and leads to centrosome amplification and tumorigenesis in mice.

    • Guangjian Fan
    • , Lianhui Sun
    •  & Chuangui Wang

  • Article
    | Open Access

    Cohesion is associated with many forms of cancer. De Lange et al. show that such cohesion defects can sensitise cells to apoptosis in response to a new APC/C ubiquitin ligase inhibitor, by prolonging mitotic arrest and checkpoint activation due to cohesion fatigue.

    • Job de Lange
    • , Atiq Faramarz
    •  & Rob M. F. Wolthuis

  • Article
    | Open Access

    Chemokines and their receptors have key roles in tumorigenesis. Here, the authors demonstrate that CXRC4 is overexpressed in hepatocellular carcinoma and is associated with poor prognosis and, mechanistically CXCR4 is increased in expression via EZH2 repression of microRNA-622.

    • Haiou Liu
    • , Yidong Liu
    •  & Jiejie Xu

  • Article
    | Open Access

    Cancer patients often respond well to primary treatment but then develop resistance. Here, Misale et al. show that dual treatment with EGFR and MEK inhibitors block resistance in mice containing patient-derived xenografts and provide a mathematical model that describes the temporal development of resistant tumour clones.

    • Sandra Misale
    • , Ivana Bozic
    •  & Alberto Bardelli

  • Article
    | Open Access

    Glucocorticoids are widely used as coadjuvants in the treatment of solid tumours. Here, Chen et al. show that genes regulated by dexamethasone- but not Compound A-liganded glucocorticoid receptor are associated with therapy resistance and unfavourable clinical outcomes in triple-negative breast cancer.

    • Zhong Chen
    • , Xun Lan
    •  & Qianben Wang

  • Article
    | Open Access

    Tumors hijack cellular pathways to evade the effects of cancer therapy. Here, Advaniet al. show that DNA damage-induced phosphorylation of CRAF Serine 338 triggers DNA repair by recruiting CHK2, highlighting a role for CRAF independent from its canonical function as a kinase.

    • Sunil J. Advani
    • , Maria Fernanda Camargo
    •  & David A. Cheresh

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