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HDAC Inhibitors Finally Open Up: Chromatin Accessibility Signatures of CTCL
10.1016/j.ccell.2017.06.008 2017-07-10 In this issue ofCancer Cell, Qu et al. describe the chromatin accessibility profiles of cutaneous T cell lymphoma, with dynamic assessments of response and resistance to histone deacetylase inhibitor therapy. Their “personal regulome” analysis framework revea... |
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Redefining Hormonal Therapy for Advanced Prostate Cancer: Results from the LATITUDE and CHAARTED Studies
10.1016/j.ccell.2017.06.007 2017-07-10 Two papers published recently in theNew England Journal of Medicinedescribe the utility of abiraterone acetate, an androgen biosynthesis inhibitor, in the early treatment of metastatic prostate cancer. In addition to establishing a new standard of care, these... |
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MUC-king with HIF May Rewire Pyrimidine Biosynthesis and Curb Gemcitabine Resistance in Pancreatic Cancer
10.1016/j.ccell.2017.06.006 2017-07-10 In this issue ofCancer Cell, Singh and colleagues report a role for MUC1-induced HIF expression in rewiring ribose synthesis, which drives pyridimine production as a possible resistance mechanism to gemcitabine, adding to complexity and multiple paths to resi... |
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Choose and Use Your Chemical Probe Wisely to Explore Cancer Biology
10.1016/j.ccell.2017.06.005 2017-07-10 Small-molecule chemical probes or tools have become progressively more important in recent years as valuable reagents to investigate fundamental biological mechanisms and processes causing disease, including cancer. Chemical probes have also achieved greater ... |
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MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer
10.1016/j.ccell.2017.06.004 2017-07-10 Poor response to cancer therapy due to resistance remains a clinical challenge. The present study establishes a widely prevalent mechanism of resistance to gemcitabine in pancreatic cancer, whereby increased glycolytic flux leads to glucose addiction in cance... |
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Tumor Evolution of Glioma-Intrinsic Gene Expression Subtypes Associates with Immunological Changes in the Microenvironment
10.1016/j.ccell.2017.06.003 2017-07-10 We leveragedIDHwild-type glioblastomas, derivative neurospheres, and single-cell gene expression profiles to define three tumor-intrinsic transcriptional subtypes designated as proneural, mesenchymal, and classical. Transcriptomic subtype multiplicity correla... |
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Oncogenic Activation of the RNA Binding Protein NELFE and MYC Signaling in Hepatocellular Carcinoma
10.1016/j.ccell.2017.06.002 2017-07-10 Global transcriptomic imbalance is a ubiquitous feature associated with cancer, including hepatocellular carcinoma (HCC). Analyses of 1,225 clinical HCC samples revealed that a large numbers of RNA binding proteins (RBPs) are dysregulated and that RBP dysregu... |
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Stabilization of the c-Myc Protein by CAMKIIγ Promotes T Cell Lymphoma
10.1016/j.ccell.2017.06.001 2017-07-10 Although high c-Myc protein expression is observed alongsideMYCamplification in some cancers, in most cases protein overexpression occurs in the absence of gene amplification, e.g., T cell lymphoma (TCL). Here, Ca2+/calmodulin-dependent protein kinase II γ (C... |
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ILF2 Is a Regulator of RNA Splicing and DNA Damage Response in 1q21-Amplified Multiple Myeloma
10.1016/j.ccell.2017.05.011 2017-06-29 Amplification of 1q21 occurs in approximately 30% of de novo and 70% of relapsed multiple myeloma (MM) and is correlated with disease progression and drug resistance. Here, we provide evidence that the 1q21 amplification-driven overexpression of ILF2 in MM pr... |
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Common Molecular Subtypes Among Asian Hepatocellular Carcinoma and Cholangiocarcinoma
10.1016/j.ccell.2017.05.009 2017-06-22 Intrahepatic cholangiocarcinoma (ICC) and hepatocellular carcinoma (HCC) are clinically disparate primary liver cancers with etiological and biological heterogeneity. We identified common molecular subtypes linked to similar prognosis among 199 Thai ICC and H... |