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10.1080/21541264.2016.1268245

http://scihub22266oqcxt.onion/10.1080/21541264.2016.1268245
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C5423477!5423477 !28005460
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suck abstract from ncbi


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pmid28005460
      Transcription 2017 ; 8 (2 ): 91-98
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  • The role of alternative splicing in cancer #MMPMID28005460
  • Singh B ; Eyras E
  • Transcription 2017[Mar]; 8 (2 ): 91-98 PMID28005460 show ga
  • The functional capacity of cells is defined by the transcriptome. Many recent studies have identified variations in the transcriptome of tumors due to alternative splicing changes, as well as mutations in splicing factors and regulatory signals in most tumor types. Some of these alterations have been linked to tumor progression, metastasis, therapy resistance, and other oncogenic processes. Here, we describe the different mechanisms that drive splicing changes in tumors and their impact in cancer. Motivated by the current evidence, we propose a model whereby a subset of the splicing patterns contributes to the definition of specific tumor phenotypes, and may hold potential for the development of novel clinical biomarkers and therapeutic approaches.
  • |*Alternative Splicing [MESH]
  • |Antineoplastic Agents/therapeutic use/toxicity [MESH]
  • |Biomarkers/metabolism [MESH]
  • |Chromatin/metabolism [MESH]
  • |DNA Damage/drug effects [MESH]
  • |Drug Resistance, Neoplasm [MESH]
  • |Humans [MESH]
  • |Mutation [MESH]
  • |Neoplasms/genetics/*pathology/therapy [MESH]
  • |Proto-Oncogene Proteins B-raf/genetics/metabolism [MESH]
  • |RNA Polymerase II/metabolism [MESH]
  • |RNA Precursors/genetics/metabolism [MESH]
  • |RNA Splicing Factors/genetics/metabolism [MESH]


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