Systematic Epigenomic Analysis Reveals Chromatin States Associated with Melanoma Progression. Fiziev, P., Akdemir, K. C, Miller, J. P, Keung, E. Z, Samant, N. S, Sharma, S., Natale, C. A, Terranova, C. J, Maitituoheti, M., Amin, S. B, Martinez-Ledesma, E., Dhamdhere, M., Axelrad, J. B, Shah, A., Cheng, C. S, Mahadeshwar, H., Seth, S., Barton, M. C, Protopopov, A., Tsai, K. Y, Davies, M. A, Garcia, B. A, Amit, I., Chin, L., Ernst, J., & Rai, K. Cell Rep., 19(4):875-889, Elsevier, 25~April, 2017.
Systematic Epigenomic Analysis Reveals Chromatin States Associated with Melanoma Progression [link]Paper  doi  abstract   bibtex   
SummaryThe extent and nature of epigenomic changes associated with melanoma progression is poorly understood. Through systematic epigenomic profiling of 35 epigenetic modifications and transcriptomic analysis, we define chromatin state changes associated with melanomagenesis by using a cell phenotypic model of non-tumorigenic and tumorigenic states. Computation of specific chromatin state transitions showed loss of histone acetylations and H3K4me2/3 on regulatory regions proximal to specific cancer-regulatory genes in important melanoma-driving cell signaling pathways. Importantly, such acetylation changes were also observed between benign nevi and malignant melanoma human tissues. Intriguingly, only a small fraction of chromatin state transitions correlated with expected changes in gene expression patterns. Restoration of acetylation levels on deacetylated loci by histone deacetylase (HDAC) inhibitors selectively blocked excessive proliferation in tumorigenic cells and human melanoma cells, suggesting functional roles of observed chromatin state transitions in driving hyperproliferative phenotype. Through these results, we define functionally relevant chromatin states associated with melanoma progression.
@ARTICLE{Fiziev2017-tu,
  title     = "Systematic Epigenomic Analysis Reveals Chromatin States
               Associated with Melanoma Progression",
  author    = "Fiziev, Petko and Akdemir, Kadir C and Miller, John P and Keung,
               Emily Z and Samant, Neha S and Sharma, Sneha and Natale,
               Christopher A and Terranova, Christopher J and Maitituoheti,
               Mayinuer and Amin, Samirkumar B and Martinez-Ledesma, Emmanuel
               and Dhamdhere, Mayura and Axelrad, Jacob B and Shah, Amiksha and
               Cheng, Christine S and Mahadeshwar, Harshad and Seth, Sahil and
               Barton, Michelle C and Protopopov, Alexei and Tsai, Kenneth Y
               and Davies, Michael A and Garcia, Benjamin A and Amit, Ido and
               Chin, Lynda and Ernst, Jason and Rai, Kunal",
  abstract  = "SummaryThe extent and nature of epigenomic changes associated
               with melanoma progression is poorly understood. Through
               systematic epigenomic profiling of 35 epigenetic modifications
               and transcriptomic analysis, we define chromatin state changes
               associated with melanomagenesis by using a cell phenotypic model
               of non-tumorigenic and tumorigenic states. Computation of
               specific chromatin state transitions showed loss of histone
               acetylations and H3K4me2/3 on regulatory regions proximal to
               specific cancer-regulatory genes in important melanoma-driving
               cell signaling pathways. Importantly, such acetylation changes
               were also observed between benign nevi and malignant melanoma
               human tissues. Intriguingly, only a small fraction of chromatin
               state transitions correlated with expected changes in gene
               expression patterns. Restoration of acetylation levels on
               deacetylated loci by histone deacetylase (HDAC) inhibitors
               selectively blocked excessive proliferation in tumorigenic cells
               and human melanoma cells, suggesting functional roles of
               observed chromatin state transitions in driving
               hyperproliferative phenotype. Through these results, we define
               functionally relevant chromatin states associated with melanoma
               progression.",
  journal   = "Cell Rep.",
  publisher = "Elsevier",
  volume    =  19,
  number    =  4,
  pages     = "875-889",
  month     =  "25~" # apr,
  year      =  2017,
  url       = "http://www.cell.com/article/S2211124717304552/abstract",
  language  = "en",
  issn      = "2211-1247",
  doi       = "10.1016/j.celrep.2017.03.078",
  authorclass = {coauthor},
  contribution = {data\_analysis},
  affiliation = {BCM, MDANDERSON}
}

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