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