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We began analyzing https://www.oncotarget.com/article/23654/text/, but it redirected us to https://www.oncotarget.com/article/23654/text/. The analysis below is for the second page.

Title[redir]:
Distinct histone modifications denote early stress-induced drug tolerance in cancer | Oncotarget
Description:
// Abdullah Al Emran 1,* , Diego M. Marzese 2,* , Dinoop Ravindran Menon 1 , Mitchell S. Stark 1 , Joachim Torrano 1 , Heinz Hammerlindl 1 , Gao Zhang 4 , Patricia Brafford 4 , Matthew P. Salomon 2 , Nellie Nelson 3 , Sabrina Hammerlindl 1 , Deepesh Gupta 1 , Gordon B. Mills 5 , Yiling Lu 5 , Richard A. Sturm 1 , Keith Flaherty 6 , Dave S. B. Hoon 2 , Brian Gabrielli 7 , Meenhard Herlyn 4 and Helmut Schaider 1 1 Dermatology Research Centre, The University of Queensland Diamantina Institute, The University of Queensland, Translational Research Institute, Brisbane, Australia 2 Department of Translational Molecular Medicine, John Wayne Cancer Institute, Santa Monica, CA, USA 3 Sequencing Center, John Wayne Cancer Institute, Santa Monica, CA, USA 4 The Wistar Institute, Philadelphia, PA, USA 5 MD Anderson Centre, Houston, TX, USA 6 Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA 7 Mater Research Institute, Translational Research Institute, The University of Queensland, Woolloongabba, Queensland, Australia * These authors have contributed equally to this study Correspondence to: Helmut Schaider, email: // Keywords : acquired drug resistance; stress-induced resistance; histone modification; DNA methylation; epigenetic reprogramming Received : October 07, 2017 Accepted : November 26, 2017 Published : December 24, 2017 Abstract Besides somatic mutations or drug efflux, epigenetic reprogramming can lead to acquired drug resistance. We recently have identified early stress-induced multi-drug tolerant cancer cells termed induced drug-tolerant cells (IDTCs). Here, IDTCs were generated using different types of cancer cell lines; melanoma, lung, breast and colon cancer. A common loss of the H3K4me3 and H3K27me3 and gain of H3K9me3 mark was observed as a significant response to drug exposure or nutrient starvation in IDTCs. These epigenetic changes were reversible upon drug holidays. Microarray, qRT-PCR and protein expression data confirmed the up-regulation of histone methyltransferases (SETDB1 and SETDB2) which contribute to the accumulation of H3K9me3 concomitantly in the different cancer types. Genome-wide studies suggest that transcriptional repression of genes is due to concordant loss of H3K4me3 and regional increment of H3K9me3. Conversely, genome-wide CpG site-specific DNA methylation showed no common changes at the IDTC state. This suggests that distinct histone methylation patterns rather than DNA methylation are driving the transition from parental to IDTCs. In addition, silencing of SETDB1/2 reversed multi drug tolerance. Alterations of histone marks in early multi-drug tolerance with an increment in H3K9me3 and loss of H3K4me3/H3K27me3 is neither exclusive for any particular stress response nor cancer type specific but rather a generic response.

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Keywords {🔍}

hkme, idtcs, cells, cancer, histone, drug, figure, cell, doi, methylation, resistance, dna, setdb, expression, parental, genes, modifications, melanoma, supplementary, mark, response, idtc, signalling, compared, performed, research, gene, repressive, epigenetic, state, days, control, docetaxel, genomewide, types, loss, significant, early, tolerance, usa, observed, data, transcriptional, stress, drugs, global, exposed, doxorubicin, oncotarget, generated,

Topics {✒️}

induced drug-tolerant cells early multi-drug tolerance multi-drug tolerance promoted genome-wide chromatin accessibility stress-induced drug tolerance thermo fisher scientific substantial global hyper-methylation drug holiday-induced sensitivity genome-wide differential expression significant genome-wide downregulation common stress-induced transition sequence alignment/map format multi-drug resistance potential interferon-related gene signature retinoblastoma tumor-suppressor gene exploring deep-sequencing data genome-wide studies suggest mann-whitney unpaired test raf/ras/mek/erk cancer type-specific program free publication identifying chip-seq enrichment open-access journal dedicated publication alerts subscribe transcriptional enhancer-repressive modification identified cell type-specific slow-cycling melanoma cells supplementary figure 8c-8e paired match-patient expression rna-seq data showed drug-tolerant model induced drug tolerance triple-negative breast cancer chip-seq peaks 20kb stress-induced resistance cell-type specific response genome-wide redistribution genome-wide expression genome-wide levels stat/ifn signalling linked methyl transferase activity global dna methylation early drug tolerance braf-mek-erk1/2 signalling survive early stress inaugural editorial editorial note 5mg/ml glucose media dna methylation patterns acute myeloid leukemia

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Do beta-tubulin mutations have a role in resistance to chemotherapy?

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Article:
      license:https://creativecommons.org/licenses/by/4.0/
      publisher:
         type:Organization
         name:Oncotarget
         logo:
            type:ImageObject
            url:https://www.oncotarget.com/images/oncotarget-logo-square.png
            width:1200
            height:1200
      dateModified:2018-02-02T07:09:00Z
      mainEntityOfPage:
         type:WebPage
         id:https://www.oncotarget.com/article/23654/text/
      headline:Distinct histone modifications denote early stress-induced drug tolerance in cancer
      articleSection:Priority Research Papers
      sameAs:https://doi.org/10.18632/oncotarget.23654
      image:https://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=viewFile&path%5B%5D=23654&path%5B%5D=74469&path%5B%5D=332294
      datePublished:2017-12-24T00:00:00Z
      author:
            type:Person
            name:Al Emran, Abdullah
            type:Person
            name:Marzese, Diego M.
            type:Person
            name:Menon, Dinoop Ravindran
            type:Person
            name:Stark, Mitchell S.
            type:Person
            name:Torrano, Joachim
            type:Person
            name:Hammerlindl, Heinz
            type:Person
            name:Zhang, Gao
            type:Person
            name:Brafford, Patricia
            type:Person
            name:Salomon, Matthew P.
            type:Person
            name:Nelson, Nellie
            type:Person
            name:Hammerlindl, Sabrina
            type:Person
            name:Gupta, Deepesh
            type:Person
            name:Mills, Gordon B.
            type:Person
            name:Lu, Yiling
            type:Person
            name:Sturm, Richard A.
            type:Person
            name:Flaherty, Keith
            type:Person
            name:Hoon, Dave S. B.
            type:Person
            name:Gabrielli, Brian
            type:Person
            name:Herlyn, Meenhard
            type:Person
            name:Schaider, Helmut
Organization:
      name:Oncotarget
      logo:
         type:ImageObject
         url:https://www.oncotarget.com/images/oncotarget-logo-square.png
         width:1200
         height:1200
ImageObject:
      url:https://www.oncotarget.com/images/oncotarget-logo-square.png
      width:1200
      height:1200
WebPage:
      id:https://www.oncotarget.com/article/23654/text/
Person:
      name:Al Emran, Abdullah
      name:Marzese, Diego M.
      name:Menon, Dinoop Ravindran
      name:Stark, Mitchell S.
      name:Torrano, Joachim
      name:Hammerlindl, Heinz
      name:Zhang, Gao
      name:Brafford, Patricia
      name:Salomon, Matthew P.
      name:Nelson, Nellie
      name:Hammerlindl, Sabrina
      name:Gupta, Deepesh
      name:Mills, Gordon B.
      name:Lu, Yiling
      name:Sturm, Richard A.
      name:Flaherty, Keith
      name:Hoon, Dave S. B.
      name:Gabrielli, Brian
      name:Herlyn, Meenhard
      name:Schaider, Helmut

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