51,461 results match your criteria Cancer research[Journal]


Methylation of C/EBPα by PRMT1 inhibits its tumor suppressive function in breast cancer.

Cancer Res 2019 Apr 23. Epub 2019 Apr 23.

Biochemistry and Molecular Biology, Peking Union Medical College & Chinese Academy of Medical Sciences

C/EBPα is an essential transcription factor involved in regulating the expression or function of certain cell cycle regulators, including in breast cancer cells. Although protein arginine methyltransferases have been shown to play oncogenic roles in a variety of cancers, little is known about the role of arginine methylation in regulating the antiproliferation activity of C/EBPα. Here we report that the protein arginine methyltransferase 1 (PRMT1) is overexpressed in human breast cancer and that elevated PRMT1 correlates with cancer malignancy. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3211DOI Listing

The Cancer Editome Atlas: A Resource for Exploratory Analysis of the Adenosine-to-Inosine RNA Editome in Cancer.

Cancer Res 2019 Apr 23. Epub 2019 Apr 23.

Graduate Institute of Biomedical Informatics, Taipei Medical University

Increasing evidence has suggested a role for adenosine-to-inosine RNA editing in carcinogenesis. However, the clinical utility of RNA editing remains limited because functions of the vast majority of editing events remain largely unexplored. To help the cancer research community investigate functional consequences of individual editing events, we have developed a user-friendly bioinformatic resource, The Cancer Editome Atlas (TCEA; http://tcea. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3501DOI Listing

Positron Emission Tomography Detects In Vivo Expression of Disialoganglioside GD2 in Mouse Models of Primary and Metastatic Osteosarcoma.

Cancer Res 2019 Apr 23. Epub 2019 Apr 23.

Diagnostic Imaging, St. Jude Children's Research Hospital

The cell membrane glycolipid GD2 is expressed by multiple solid tumors, including 88% of osteosarcomas and 98% of neuroblastomas. However, osteosarcomas are highly heterogeneous with many tumors exhibiting GD2 expression on <50% of the individual cells while some tumors are essentially GD2-negative. Anti-GD2 immunotherapy is the current standard of care for high-risk neuroblastoma, but its application to recurrent osteosarcomas, for which no effective therapies exist, has been extremely limited. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3340DOI Listing

MicroRNA-92 expression in CD133+ melanoma stem cells regulates immunosuppression in the tumor microenvironment via integrin-dependent activation of TGF-β.

Cancer Res 2019 Apr 23. Epub 2019 Apr 23.

Pathology, University of South Carolina

In addition to being refractory to treatment, melanoma cancer stem cells (CSC) are known to suppress host anti-tumor immunity, the underlying mechanisms of which need further elucidation. In this study, we established a novel role for microRNA-92 (miR-92) and its associated gene networks in immunosuppression. CSCs were isolated from the B16-F10 murine melanoma cell line based on expression of the putative CSC marker CD133 (Prominin-1). Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-2659DOI Listing

MDM4 is targeted by 1q gain and drives disease in Burkitt lymphoma.

Cancer Res 2019 Apr 18. Epub 2019 Apr 18.

University Hospital and University of Zurich

Oncogenic MYC activation promotes proliferation in Burkitt lymphoma (BL), but also induces cell cycle arrest and apoptosis mediated by p53, a tumor suppressor that is mutated in 40% of BL cases. To identify molecular dependencies in BL, we performed RNAi-based, loss-of-function screening in eight BL cell lines and integrated non-BL RNAi screens and genetic data. We identified 76 genes essential to BL, including genes associated with hematopoietic cell differentiation (FLI1, BCL11A) or B cell development and activation (PAX5, CDKN1B, JAK2, CARD11) and found a number of context-specific dependencies including oncogene addiction in cell lines with TCF3/ID3 or MYD88 mutation. Read More

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http://cancerres.aacrjournals.org/lookup/doi/10.1158/0008-54
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http://dx.doi.org/10.1158/0008-5472.CAN-18-3438DOI Listing
April 2019
2 Reads

tRNA Fragments Show Intertwining with mRNAs of Specific Repeat Content and Have Links to Disparities.

Cancer Res 2019 Apr 17. Epub 2019 Apr 17.

Computational Medicine Center, Thomas Jefferson University

tRNA-derived fragments (tRFs) are a class of potent regulatory RNAs. We mined the datasets from The Cancer Genome Atlas representing 32 cancer types with a deterministic and exhaustive pipeline for tRNA fragments. We found that mitochondrial tRNAs contribute disproportionally more tRFs than the nuclear ones. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-19-0789DOI Listing

Activation of the unfolded protein response via inhibition of protein disulfide isomerase decreases the capacity for DNA repair to sensitize glioblastoma to radiotherapy.

Cancer Res 2019 Apr 17. Epub 2019 Apr 17.

Department of Radiation Oncology, University of Michigan Medical School

Patients with glioblastoma multiforme (GBM) survive on average 12-14 months after diagnosis despite surgical resection followed by radiation and temozolomide therapy. Intrinsic or acquired resistance to chemo- and radiation-therapy is common and contributes to a high rate of recurrence. To investigate the therapeutic potential of protein disulfide isomerase (PDI) as a target to overcome resistance to chemoradiation, we developed a GBM tumor model wherein conditional genetic ablation of prolyl 4-hydroxylase subunit beta (P4HB), the gene that encodes PDI, can be accomplished. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-2540DOI Listing
April 2019
1 Read

BRCA1-No Matter How You Splice It.

Cancer Res 2019 Apr 16. Epub 2019 Apr 16.

The University of Kansas Cancer Center, Kansas City, Kansas.

(breast cancer 1, early onset), a well-known breast cancer susceptibility gene, is a highly alternatively spliced gene. alternative splicing may serve as an alternative regulatory mechanism for the inactivation of the gene in both hereditary and sporadic breast cancers, and other -associated cancers. The alternative transcripts of can mimic known functions, possess unique functions compared with the full-length transcript, and in some cases, appear to function in opposition to full-length In this review, we will summarize the functional "naturally occurring" alternative splicing transcripts of and then discuss the latest next-generation sequencing-based detection methods and techniques to detect alternative splicing patterns and their potential use in cancer diagnosis, prognosis, and therapy. Read More

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http://cancerres.aacrjournals.org/lookup/doi/10.1158/0008-54
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http://dx.doi.org/10.1158/0008-5472.CAN-18-3190DOI Listing
April 2019
1 Read

ROCK Inhibition Induces Terminal Adipocyte Differentiation and Suppresses Tumorigenesis in Chemoresistant Osteosarcoma Cells.

Cancer Res 2019 Apr 16. Epub 2019 Apr 16.

Division of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine

Tumors comprise heterogeneous cell types including cancer stem cells (CSC), progenitor cells, and differentiated cells. Chemoresistance is a potential cause of relapse and a key characteristic of CSC, but the development of novel therapeutic approaches for targeting these cells has been limited. We previously established osteosarcoma-initiating (OSi) cells by introducing the gene for c-Myc into bone marrow stromal cells of Ink4a/Arf knockout mice. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-2693DOI Listing

A human organotypic microfluidic tumor model permits investigation of the interplay between patient-derived fibroblasts and breast cancer cells.

Cancer Res 2019 Apr 16. Epub 2019 Apr 16.

School of Biological and Health Systems Engineering, Arizona State University

Tumor-stroma interactions significantly influence cancer cell metastasis and disease progression. These interactions partly comprise crosstalk between tumor and stromal fibroblasts, but the key molecular mechanisms within the crosstalk that govern cancer invasion are still unclear. Here we adapted our previously developed microfluidic device as a 3D in vitro organotypic model to mechanistically study tumor-stroma interactions by mimicking the spatial organization of the tumor microenvironment on a chip. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-2293DOI Listing

HDAC8 regulates a stress response pathway in melanoma to mediate escape from BRAF inhibitor therapy.

Cancer Res 2019 Apr 15. Epub 2019 Apr 15.

Tumor Biology, H. Lee Moffitt Cancer Center and Research Institute

Melanoma cells have the ability to switch to a dedifferentiated, invasive phenotype in response to multiple stimuli. Here we show that exposure of melanomas to multiple stresses including BRAF-MEK inhibitor therapy, hypoxia, and UV irradiation leads to an increase in histone deacetylase 8 (HDAC8) activity and the adoption of a drug-resistant phenotype. Mass spectrometry-based phosphoproteomics implicated HDAC8 in the regulation of MAPK and AP-1 signaling. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-19-0040DOI Listing
April 2019
1 Read

Inhibition of Ataxia-Telangiectasia Mutated and RAD3-related (ATR) overcomes oxaliplatin resistance and promotes anti-tumor immunity in colorectal cancer.

Cancer Res 2019 Apr 15. Epub 2019 Apr 15.

CRLC Val D'Aurelle, IRCM INSERM U1194

Although many colorectal cancer (CRC) patients initially respond to the chemotherapeutic agent oxaliplatin, acquired resistance to this treatment remains a major challenge to the long-term management of this disease. To identify molecular targets of oxaliplatin resistance in colorectal cancer (CRC), we performed an shRNA-based loss-of-function genetic screen using a kinome library. We found that silencing of ataxia-telangiectasia mutated and RAD3-related (ATR), a serine/threonine protein kinase involved in the response to DNA stress, restored oxaliplatin sensitivity in a cellular model of oxaliplatin resistance. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-2807DOI Listing

Cholesterol induces epithelial-to-mesenchymal transition of prostate cancer cells by suppressing degradation of EGFR through APMAP.

Cancer Res 2019 Apr 15. Epub 2019 Apr 15.

Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences

Cholesterol increases the risk of aggressive prostate cancer (PCa), and has emerged as a potential therapeutic target for PCa. The functional roles of cholesterol in PCa metastasis are not fully understood. Here we found that cholesterol induces the epithelial-to-mesenchymal transition (EMT) through extracellular regulated protein kinases 1/2 pathway activation, which is mediated by epidermal growth factor receptor (EGFR) and adipocyte plasma membrane-associated protein (APMAP) accumulation in cholesterol-induced lipid rafts. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3295DOI Listing

DR4-Ser424 O-GlcNAcylation promotes sensitization of TRAIL-tolerant persisters and TRAIL-resistant cancer cells to death.

Cancer Res 2019 Apr 15. Epub 2019 Apr 15.

School of Biological Science/Bio-Max Institute, Seoul National University

TRAIL resistance, including non-genetically acquired tolerance in cancer persister cells, is a major obstacle to translating TRAIL therapy into cancer patients. However, the underlying mechanisms remain to be elucidated. Here, we show that DR4/TRAILR1 is O-GlcNAcylated at Ser424 in its death domain to mediate both apoptosis and necrosis upon TRAIL ligation. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-1991DOI Listing
April 2019
9.329 Impact Factor

Concurrent Targeting of Glutaminolysis and Metabotropic Glutamate Receptor 1 (GRM1) Reduces Glutamate Bioavailability in GRM1 Melanoma.

Cancer Res 2019 Apr 15;79(8):1799-1809. Epub 2019 Apr 15.

Susan Lehman Cullman Laboratory for Cancer Research, Ernest Mario School of Pharmacy, Department of Chemical Biology, Rutgers University, Piscataway, New Jersey.

Aberrant glutamatergic signaling has been implicated in altered metabolic activity in many cancer types, including malignant melanoma. Previously, we have illustrated the role of metabotropic glutamate receptor 1 (GRM1) in neoplastic transformation of melanocytes and spontaneous metastatic melanoma . In this study, we showed that autocrine stimulation constitutively activates the GRM1 receptor and its downstream mitogenic signaling. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-1500DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6469683PMC
April 2019
1 Read

Lulling the Cancer Cell into an Eternal Sleep.

Cancer Res 2019 Apr;79(8):1756-1757

Division of Genetic Medicine, Department of Medicine, University of Michigan, Ann Arbor, Michigan.

A hallmark of metastasis is the ability of cancer cells to undergo the epithelial-to-mesenchymal transition to invade and disseminate to distal sites. More recently, the case has been made that the critical last step in metastasis is dependent on the ability to undergo reversion to an epithelial phenotype in a process known as the mesenchymal-to-epithelial transition (MET). It is this transition in the metastatic cascade that researchers are focusing on clinically to treat disseminated disease. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-19-0853DOI Listing

When Failure Is Worse Than Giving Up: The Case of CTL.

Cancer Res 2019 Apr;79(8):1753-1755

Molecular Immunology Unit, Department of Research, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.

Although much emphasis is given to the use of immune checkpoint inhibitors to restore the functionality of exhausted lymphocytes, very little is known about the fate of cancer cells that escape from the cytotoxic activity of T cells. In a previous issue of , Stein and colleagues investigated the response of cancer cells to CD8 T cells disarmed of their killing activity. Spared cancer cells acquired stem cell-like features and displayed an enhanced capacity to form tumors and metastasize. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-19-0690DOI Listing
April 2019
2 Reads

Genome-Epigenome-Senescence: Is TET1 a Caretaker of p53-Injured Lung Cancer Cells?

Authors:
Yutaka Kondo

Cancer Res 2019 Apr;79(8):1751-1752

Division of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

The study by Filipczak and colleagues identified the interplay between mutant p53 proteins and methylcytosine dioxygenase ten-eleven translocation 1 (TET1) in lung cancers. p53 transversion mutations were closely associated with high TET1 expression, which prevented genomic instability-associated cellular senescence. Depletion of TET1 was synergistic with classical antitumor drugs, such as cisplatin or doxorubicin, providing an attractive rationale for targeted therapies against TET1 combined with antitumor drugs in patients with p53-mutant lung cancer. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-19-0645DOI Listing

DUBbing Ferroptosis in Cancer Cells.

Authors:
Boyi Gan

Cancer Res 2019 Apr;79(8):1749-1750

Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Ferroptosis, a form of iron-dependent, nonapoptotic cell death that is induced by excessive lipid peroxidation, has been recently identified as a new tumor suppression mechanism. In this issue of , Liu and colleagues demonstrate that the deubiquitinase (DUB) OTUB1 is frequently overexpressed in human cancers, and functions to "dub" (trim) the ferroptosis process in cancer cells and promotes tumor development by stabilizing the cystine transporter, SLC7A11. This study not only reveals a hitherto unappreciated regulatory mechanism of ferroptosis but also identifies potential therapeutic targets for cancer treatment. Read More

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http://cancerres.aacrjournals.org/lookup/doi/10.1158/0008-54
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http://dx.doi.org/10.1158/0008-5472.CAN-19-0487DOI Listing
April 2019
5 Reads

Quest for Tangible Biomarkers for Triple-Negative Breast Cancer.

Authors:
Dipali Sharma

Cancer Res 2019 Apr;79(8):1746-1748

Department of Oncology, Johns Hopkins University School of Medicine and the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland.

Identification of key molecular networks involved in triple-negative breast cancer (TNBC) growth and metastasis will increase our mechanistic understanding of this disease and pave the way for the development of novel therapeutic interventions. The study by Khawaled and colleagues points to a direct antimetastatic function of WW domain-containing oxidoreductase (WWOX) in TNBC and identifies the Myc/miR-146a/fibronectin axis as a molecular mediator of the tumor-suppressive function of WWOX. This information can potentially be used to identify actionable nodes for targeting TNBC, a breast cancer subtype otherwise characterized by the absence of markers. Read More

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http://cancerres.aacrjournals.org/lookup/doi/10.1158/0008-54
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http://dx.doi.org/10.1158/0008-5472.CAN-19-0416DOI Listing
April 2019
1 Read

A Direct Podocalyxin-Dynamin-2 Interaction Regulates Cytoskeletal Dynamics to Promote Migration and Metastasis in Pancreatic Cancer Cells.

Cancer Res 2019 Apr 11. Epub 2019 Apr 11.

Chemical & Biomolecular, Johns Hopkins University

The sialoglycoprotein podocalyxin is absent in normal pancreas but is overexpressed in pancreatic cancer and is associated with poor clinical outcome. Here we investigate the role of podocalyxin in migration and metastasis of pancreatic adenocarcinomas using SW1990 and Pa03c as cell models. Although ezrin is regarded as a cytoplasmic binding partner of podocalyxin that regulates actin polymerization via Rac1 or RhoA, we did not detect podocalyxin-ezrin association in pancreatic cancer cells. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3369DOI Listing
April 2019
9.329 Impact Factor

Exploiting DNA Replication Stress for Cancer Treatment.

Cancer Res 2019 Apr 9;79(8):1730-1739. Epub 2019 Apr 9.

Department of Biochemistry, University of Toronto, 1 King's College Circle, Toronto, Ontario, Canada.

Complete and accurate DNA replication is fundamental to cellular proliferation and genome stability. Obstacles that delay, prevent, or terminate DNA replication cause the phenomena termed DNA replication stress. Cancer cells exhibit chronic replication stress due to the loss of proteins that protect or repair stressed replication forks and due to the continuous proliferative signaling, providing an exploitable therapeutic vulnerability in tumors. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3631DOI Listing
April 2019
1 Read

Analysis of the CDKN2A gene in FAMMM Syndrome families reveals early age of onset for additional syndromic cancers.

Cancer Res 2019 Apr 9. Epub 2019 Apr 9.

Hereditary Cancer Center, Creighton University.

Familial atypical multiple mole melanoma (FAMMM) syndrome is a hereditary cancer syndrome that results from mutations in several genes including the CDKN2A gene. In addition to melanoma, certain other malignancies such as pancreatic cancer are known to occur more frequently in family members who carry the mutation. However, as these families have been followed over time, additional cancers have been observed in both carriers and non-carriers. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-1580DOI Listing
April 2019
1 Read

N6-methylation of adenosine (m6A) of FZD10 mRNA contributes to PARP inhibitor resistance.

Cancer Res 2019 Apr 9. Epub 2019 Apr 9.

Gene Expression and Regulation Program, Wistar Institute

Despite the high initial response rates to PARP inhibitors (PARPi) in BRCA-mutated epithelial ovarian cancers (EOC), PARPi resistance remains a major challenge. Chemical modifications of RNAs have emerged as a new layer of epigenetic gene regulation. N6-methyladenosine (m6A) is the most abundant chemical modification of messenger RNA (mRNA), yet the role of m6A modification in PARPi resistance has not previously been explored. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3592DOI Listing
April 2019
1 Read

Targeting the temporal dynamics of hypoxia-induced tumor-secreted factors halts tumor migration.

Cancer Res 2019 Apr 5. Epub 2019 Apr 5.

Pharmaceutical Sciences, University of Pittsburgh School of Pharmacy

Targeting microenvironmental factors that foster migratory cell phenotypes is a promising strategy for halting tumor migration. However, lack of mechanistic understanding of the emergence of migratory phenotypes impedes pharmaceutical drug development. Using our 3D microtumor model with tight control over tumor size, we recapitulated the tumor size-induced hypoxic microenvironment and emergence of migratory phenotypes in microtumors from epithelial breast cells and patient-derived primary metastatic breast cancer cells, mesothelioma cells, and lung cancer xenograft cells (PDX). Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3151DOI Listing
April 2019
3 Reads

Long noncoding RNA ELIT-1 acts as a Smad3 cofactor to facilitate TGF-β/Smad signaling and promote epithelial-mesenchymal transition.

Cancer Res 2019 Apr 5. Epub 2019 Apr 5.

Department of Molecular Biology, Hamamatsu University School of Medicine

TGF-β is involved in various biological processes, including development, differentiation, growth regulation, and epithelial-mesenchymal transition (EMT). In TGF-β/Smad signaling, receptor-activated Smad complexes activate or repress their target gene promoters. Smad cofactors are a group of Smad-binding proteins that promote recruitment of Smad complexes to these promoters. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3210DOI Listing

Activation of MAPK signaling by CXCR7 leads to enzalutamide resistance in prostate cancer.

Cancer Res 2019 Apr 5. Epub 2019 Apr 5.

Division of Hematology/Oncology, Northwestern University Feinberg School of Medicine

Castration-resistant prostate cancer (CRPC) that has developed resistance to the new-generation androgen receptor (AR) antagonist enzalutamide is a lethal disease. Transcriptome analysis of multiple prostate cancer models identified CXCR7, an atypical chemokine receptor, as one of the most upregulated genes in enzalutamide-resistant cells. AR directly repressed CXCR7 by binding to an enhancer 110kb downstream of the gene and expression was restored upon androgen deprivation. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-2812DOI Listing
April 2019
3 Reads

Estrogen Receptor Covalent Antagonists: The Best Is Yet to Come.

Cancer Res 2019 Apr 5;79(8):1740-1745. Epub 2019 Apr 5.

H3 Biomedicine, Inc., Cambridge, Massachusetts.

The development of tamoxifen and subsequent estrogen receptor alpha (ERα) antagonists represents a tremendous therapeutic breakthrough in the treatment of breast cancer. Despite the ability of ERα antagonists to increase survival rates, resistance to these therapies is an all-too-common occurrence. The majority of resistant tumors, including those with hotspot mutations in the ligand-binding domain of ERα, remain dependent on ERα signaling, indicating that either a more potent or novel class of antagonist could have clinical benefit. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3634DOI Listing
April 2019
2 Reads

Wnt/PCP Signaling Contribution to Carcinoma Collective Cell Migration and Metastasis.

Cancer Res 2019 Apr 5;79(8):1719-1729. Epub 2019 Apr 5.

Department of Biochemistry and Molecular Medicine, UC Davis Comprehensive Cancer Center, UC Davis School of Medicine, Sacramento, California.

Our understanding of the cellular mechanisms governing carcinoma invasiveness and metastasis has evolved dramatically over the last several years. The previous emphasis on the epithelial-mesenchymal transition as a driver of the migratory properties of single cells has expanded with the observation that carcinoma cells often invade and migrate collectively as adherent groups. Moreover, recent analyses suggest that circulating tumor cells within the vasculature often exist as multicellular clusters and that clusters more efficiently seed metastatic lesions than single circulating tumor cells. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-2757DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6467734PMC
April 2019
1 Read

Hemap: An interactive online resource for characterizing molecular phenotypes across hematologic malignancies.

Cancer Res 2019 Apr 2. Epub 2019 Apr 2.

Institute of Biomedicine, School of Medicine, University of Eastern Finland.

Large collections of genome-wide data can facilitate the characterization of disease states and subtypes, permitting pan-cancer analysis of molecular phenotypes and evaluation of disease context for new therapeutic approaches. We analyzed 9,544 transcriptomes from more than 30 hematologic malignancies, normal blood cell types, and cell lines, and showed that disease types could be stratified in a data-driven manner. We then identified cluster-specific pathway activity, new biomarkers and in silico drug target prioritization through interrogation of drug target databases. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-2970DOI Listing
April 2019
1 Read
9.329 Impact Factor

NFAT1-mediated regulation of NDEL1 promotes growth and invasion of glioma stem-like cells.

Cancer Res 2019 Apr 2. Epub 2019 Apr 2.

Department of Neurosurgery, First Hospital of China Medical University

Glioma stem-like cells (GSC) promote tumor generation and progression. However, the mechanism of GSC induction or maintenance is largely unknown. We previously demonstrated that the calcium-responsive transcription factor nuclear factor of activated T cells-1 (NFAT1) is activated in glioblastomas and regulates the invasion of tumor cells. Read More

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http://cancerres.aacrjournals.org/lookup/doi/10.1158/0008-54
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http://dx.doi.org/10.1158/0008-5472.CAN-18-3297DOI Listing
April 2019
4 Reads

Epigenetic regulation of NAMPT by NAMPT-AS drives metastatic progression in triple-negative breast cancer.

Cancer Res 2019 Apr 2. Epub 2019 Apr 2.

Breast surgery, Qilu Hospital of Shandong University

Triple negative breast cancer (TNBC) is highly heterogeneous and has a poor prognosis. It is therefore important to identify the underlying molecular mechanisms in order to develop novel therapeutic strategies. Although emerging research has revealed long noncoding RNAs (lncRNAs) as vital to carcinogenesis and cancer progression, their functional involvement in TNBC has not been well defined. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3418DOI Listing
April 2019
2 Reads

Molecular imaging of deoxycytidine kinase activity using deoxycytidine-enhanced CEST MRI.

Cancer Res 2019 Apr 2. Epub 2019 Apr 2.

F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute

Deoxycytidine kinase (DCK) is a key enzyme for the activation of a broad spectrum of nucleoside-based chemotherapy drugs (e.g., gemcitabine); low DCK activity is one of the most important causes of cancer drug-resistance. Read More

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http://cancerres.aacrjournals.org/lookup/doi/10.1158/0008-54
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http://dx.doi.org/10.1158/0008-5472.CAN-18-3565DOI Listing
April 2019
4 Reads
9.329 Impact Factor

Antagonism between HtrA3 and TGF-β1 Contributes to Metastasis in Non-small-cell Lung Cancer.

Cancer Res 2019 Apr 2. Epub 2019 Apr 2.

Department of Pulmonary and Critical Care Medicine,Institute of Respiratory Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine

High temperature requirement A3 (HtrA3 - long and short isoforms) is a member of the HtrA family and has been implicated as a tumor suppressor in cancer progression in multiple cancer types, yet its molecular functions in non-small cell lung cancer (NSCLC) are not well understood. Here we report that decreased levels of HtrA3 negatively correlate with elevated TGF-β1 in lung tumor tissue with metastasis. Furthermore, high expression of HtrA3 indicated better prognosis independent of TGF-β1 expression. Read More

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http://cancerres.aacrjournals.org/lookup/doi/10.1158/0008-54
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http://dx.doi.org/10.1158/0008-5472.CAN-18-2507DOI Listing
April 2019
2 Reads

Temozolomide treatment induces lncRNA MALAT1 in an NF-кB and p53 co-dependent manner in glioblastoma.

Cancer Res 2019 Apr 2. Epub 2019 Apr 2.

Surgery, University of Chicago

Alkylating chemotherapy is a central component of the management of glioblastoma (GBM). Among the factors that regulate the response to alkylation damage, NF-кB acts to both promote and block cytotoxicity. In this study, we used genome-wide expression analysis in U87 GBM to identify NF-кB-dependent factors altered in response to temozolomide (TMZ) and found the long non-coding RNA (lncRNA) MALAT1 as one of the most significantly upregulated. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-2170DOI Listing
April 2019
2 Reads
9.329 Impact Factor

Solid tumor-induced immune regulation alters the GvHD/GvT paradigm after allogenic bone marrow transplantation.

Cancer Res 2019 Apr 1. Epub 2019 Apr 1.

Microbiology and Immunology and Department of Nephrology, KU Leuven ; UZ Leuven

Growth of solid tumors is often associated with the development of an immunosuppressive tumor microenvironment (TME). It has been suggested that the influence of the TME may extend beyond the local tumor and results in systemic immunosuppression. Here we utilize two murine cancer models to explore the influence of solid tumors on the occurrence of alloreactivity-driven graft-versus-host disease (GvHD) and graft-versus-solid tumor (GvT) effects following MHC-mismatched allogeneic bone marrow transplantation (allogenic BMT). Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3143DOI Listing
April 2019
1 Read

Breast cancer risk and insulin resistance: post genome-wide gene-environment interaction study using a random survival forest.

Cancer Res 2019 Apr 1. Epub 2019 Apr 1.

Department of Epidemiology, Fielding School of Public Health, University of California Los Angeles.

Obesity-insulin connections have been considered potential risk factors for postmenopausal breast cancer, and the association between insulin resistance (IR) genotypes and phenotypes can be modified by obesity-lifestyle factors, affecting breast cancer risk. In this study, we explored the role of IR in those pathways at the genome-wide level. We identified IR-genetic factors and selected lifestyles to generate risk profiles for postmenopausal breast cancer. Read More

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http://cancerres.aacrjournals.org/lookup/doi/10.1158/0008-54
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http://dx.doi.org/10.1158/0008-5472.CAN-18-3688DOI Listing
April 2019
4 Reads

Several Faces of Glutaminase Regulation in Cells.

Cancer Res 2019 Apr;79(7):1302-1304

Brazilian Biosciences National Laboratory (LNBio), Brazilian Center for Research in Energy and Materials (CNPEM), Campinas, Sao Paulo, Brazil.

The cancer target glutaminase (GLS) has proven to be a fascinating protein. Since it was first described to be regulated by the oncogene Myc 10 years ago, several other transcriptional, posttranscriptional, and posttranslational regulatory mechanisms have emerged, and the list is growing. A recent study by Deng and colleagues revealed that an antisense (AS) long noncoding RNA named GLS-AS, which is negatively regulated by Myc, downregulates in pancreatic cancer. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-19-0313DOI Listing
April 2019
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Going Beyond the Sequences: TCR Binding Patterns at the Service of Cancer Detection.

Cancer Res 2019 Apr;79(7):1299-1301

Ludwig Institute for Cancer Research - Lausanne Branch, University of Lausanne, Lausanne, Épalinges, Switzerland.

Deep sequencing of T-cell receptors enables the comprehensive profiling of lymphocyte populations and the characterization of the repertoire of T-cell responses against tumors, which could be applied to diagnose cancers. Ostmeyer and colleagues introduce a novel approach to characterize TCR patterns correlating with antigen recognition. By projecting the large TCR sequence space into a handful of biophysicochemical descriptors for key residues and seeking TCRs with similar antigen-binding capabilities even in the absence of identical amino acids, this approach presents several advantages over current methods. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-19-0225DOI Listing
April 2019
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Remodeling Collapsed DNA Replication Forks for Cancer Development.

Cancer Res 2019 Apr;79(7):1297-1298

Department of Molecular Biology, University of Geneva, Geneva, Switzerland.

DNA replication stress is prevalent in human cancers, but absent in normal cells, suggesting that proteins involved in the cellular response to DNA replication stress could be potential therapeutic targets. SMARCAL1 and ZRANB3 are annealing helicases that mediate the repair of collapsed DNA replication forks. In a study in this issue of , Puccetti and colleagues report that mice lacking either SMARCAL1 or ZRANB3 activity have delayed development of MYC-induced B-cell lymphomas. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-19-0216DOI Listing
April 2019
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Homeostatic Roles of STING in Cell Proliferation and Chromosomal Instability.

Cancer Res 2019 Apr;79(7):1295-1296

Department of Radiation Oncology, Robert Lurie Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

In this issue of , Ranoa and colleagues report on the role of STING (stimulator of IFN genes, ) in regulating critical tumor cell-intrinsic functions including cell-cycle progression, chromosomal stability, and cellular response to therapeutic ionizing radiation. The authors used multiple methods including RNA expression profiling, molecular and biochemical techniques, cell biology, and reagents from genetically modified murine models to test their hypothesis that downregulating the STING pathway in cancer cells promotes cellular transformation through accumulation of chromosomal instability and premature progression of the cell cycle. Their findings demonstrate that STING is a tumor suppressor that inhibits cell proliferation by restricting entry to mitosis as well as protecting cells against aneuploidy. Read More

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http://cancerres.aacrjournals.org/lookup/doi/10.1158/0008-54
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http://dx.doi.org/10.1158/0008-5472.CAN-19-0212DOI Listing
April 2019
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Exosomal miRNA Cargo as Mediator of Immune Escape Mechanisms in Neuroblastoma.

Cancer Res 2019 Apr;79(7):1293-1294

Department of Pharmaceutics, College of Pharmacy, University of Florida, Gainesville, Florida.

Both natural killer (NK) cells and exosomes released from these cells induce tumor cell cytotoxicity by way of the cell killing proteins perforin and granzyme. TGFβ1 protein in the tumor microenvironment generates an immune escape mechanism rendering NK cells inactive. The tumor-suppressive miR-186 that is downregulated in neuroblastoma and in TGFβ-treated NK cells represses oncogenic proteins in neuroblastoma (MYCN and AURKA) and components of the TGFβ pathway. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-19-0021DOI Listing
April 2019
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Anti-CD24 antibody-nitric oxide conjugate (ANC) selectively and potently suppresses hepatic carcinoma.

Cancer Res 2019 Mar 27. Epub 2019 Mar 27.

School of Life Science & Technology, China Pharmaceutical University

Nitric oxide (NO) has a wide range of potential applications in tumor therapy. However, a targeted delivery system for NO donors has remained elusive, creating a bottleneck that limits its druggability. The antibody-drug conjugate (ADC) is a targeted drug delivery system composed of an antibody linked to an active cytotoxic drug. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-2839DOI Listing
March 2019
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Long Noncoding RNA MALAT1 regulates cancer glucose metabolism by enhancing mTOR-mediated translation of TCF7L2.

Cancer Res 2019 Mar 26. Epub 2019 Mar 26.

Biochemistry and Molecular Biology, Institute for Medical Research Israel-Canada, Hebrew University-Hadassah Medical School

Reprogrammed glucose metabolism of enhanced aerobic glycolysis (or the Warburg effect) is known as a hallmark of cancer. The roles of long noncoding RNAs (lncRNA) in regulating cancer metabolism at the level of both glycolysis and gluconeogenesis are mostly unknown. We previously showed that lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) acts as a proto-oncogene in hepatocellular carcinoma (HCC). Read More

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http://cancerres.aacrjournals.org/lookup/doi/10.1158/0008-54
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http://dx.doi.org/10.1158/0008-5472.CAN-18-1432DOI Listing
March 2019
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9.329 Impact Factor

Melanoma-induced reprogramming of Schwann cell signaling aids tumor growth.

Cancer Res 2019 Mar 26. Epub 2019 Mar 26.

Dermatology, University of Pittsburgh Medical Center

The tumor microenvironment has been compared to a non-healing wound involving a complex interaction between multiple cell types. Schwann cells, the key regulators of peripheral nerve repair, have recently been shown to directly affect non-neural wound healing. Their role in cancer progression, however, has been largely limited to neuropathic pain and perineural invasion. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-3872DOI Listing
March 2019
1 Read