Results 121 to 130 of about 1,869,696 (352)

Pan-squamous genomic profiling stratified by anatomic tumor site and viral association [PDF]

, 2018
Background: Squamous cell carcinomas (SCC) have diverse anatomic etiologies but may share common genomic biomarkers. We profiled 7,871 unique SCCs across nine anatomic sites to investigate commonality in genomic alterations (GA), tumor mutational burden (
Albacker, L. A., Ali, S. M., Chung, C. H., Frampton, G. M., Johnson, J. M., Kang, H., Khan, S. A., Miller, V. A., Montesion, M., Ross, J. S., Sokol, E. S.   +10 more
core   +1 more source

Pan-urologic cancer genomic subtypes that transcend tissue of origin [PDF]

, 2017
Urologic cancers include cancers of the bladder, kidney, prostate, and testes, with common molecular features spanning different types. Here, we show that 1954 urologic cancers can be classified into nine major genomic subtypes, on the basis of ...
Bossé, Dominick, Chen, Fengju, Choueiri, Toni K, Creighton, Chad J, Gibbons, Don L, Hakimi, A. Ari, Hsieh, James J, Ittmann, Michael, Lalani, Aly-Khan A, Zhang, Yiqun   +9 more
core   +2 more sources

Whole-genome sequencing reveals novel tandem-duplication hotspots and a prognostic mutational signature in gastric cancer

Nature Communications, 2019
Genome-wide analysis of genomic signatures might reveal novel mechanisms for gastric cancer (GC) tumorigenesis. Here, we analysis structural variations (SVs) and mutational signatures via whole-genome sequencing of 168 GCs.
Rui Xing, Yong Zhou, Jun Yu, Yingyan Yu, Y. Nie, Wen Luo, Chao Yang, T. Xiong, W. Wu, Zhongwu Li, Yang Bing, Shuye Lin, Yaping Zhang, Ying Hu, Lin Li, Lijuan Han, Chen Yang, Shaogang Huang, Suiping Huang, R. Zhou, Jing Li, Kaichun Wu, D. Fan, G. Tang, J. Dou, Zhenggang Zhu, J. Ji, X. Fang, Youyong Lu   +28 more
semanticscholar   +1 more source

APOBEC3 signature mutations in chronic lymphocytic leukemia [PDF]

Leukemia, 2014
Cytidine deaminases of the APOBEC family (ApoB mRNA editing catalytic subunit) generate targeted damage in nucleic acids by deaminating cytosins to uracils. The catalytically active family members are APOBEC1, APOBEC3 proteins (which comprise APOBEC3A, APOBEC3B, APOBEC3C, APOBEC3D, APOBEC3F, APOBEC3G, APOBEC3H) and activation-induced deaminase (AID ...
Rebhandl, S, Huemer, M, Gassner, F J, Zaborsky, N, Hebenstreit, D, Catakovic, K, Grössinger, E M, Greil, R, Geisberger, R   +8 more
openaire   +2 more sources

Survivin and Aurora Kinase A control cell fate decisions during mitosis

Molecular Oncology, EarlyView.
Aurora A interacts with survivin during mitosis and regulates its centromeric role. Loss of Aurora A activity mislocalises survivin, the CPC and BubR1, leading to disruption of the spindle checkpoint and triggering premature mitotic exit, which we refer to as ‘mitotic slippage’.
Hana Abdelkabir, Shalitha Wickrama Arachchige, Sally P. Wheatley   +2 more
wiley   +1 more source

Signatures of mutational processes in human cancer [PDF]

Nature, 2013
All cancers are caused by somatic mutations; however, understanding of the biological processes generating these mutations is limited. The catalogue of somatic mutations from a cancer genome bears the signatures of the mutational processes that have been operative.
Alexandrov, L.B., Nik-Zainal, S., Wedge, D.C., Aparicio, S.A., Behjati, S., Biankin, A.V., Bignell, G.R., Bolli, N., Borg, A., Borresen-Dale, A.L., Boyault, S., Burkhardt, B., Butler, A.P., Caldas, C., Davies, H.R., Desmedt, C., Eils, R., Eyfjord, J.E., Foekens, J.A., Greaves, M., Hosoda, F., Hutter, B., Ilicic, T., Imbeaud, S., Imielinsk, M., Jager, N., Jones, D.T., Jones, D., Knappskog, S., Kool, M., Lakhani, S.R., Lopez-Otin, C., Martin, S., Munshi, N.C., Nakamura, H., Northcott, P.A., Pajic, M., Papaemmanuil, E., Paradiso, A., Pearson, J.V., Puente, X.S., Raine, K., Ramakrishna, M., Richardson, A.L., Richter, J., Rosenstiel, P., Schlesner, M., Schumacher, T.N., Span, P.N., Span, P.N., Teague, J.W., Totoki, Y., Tutt, A.N., Valdes-Mas, R., van Buuren, M.M., van 't Veer, L., Vincent-Salomon, A., Waddell, N., Yates, L.R., Zucman-Rossi, J., Futreal, P.A., McDermott, U., Lichter, P., Meyerson, M., Grimmond, S.M., Siebert, R., Campo, E., Shibata, T., Pfister, S.M., Campbell, P.J., Stratton, M.R., Schlooz-Vries, M.S., van Tol, J.J., van Tol, J.J., van Laarhoven, H.W., Sweep, C.G.J., Bult, P., et al, .   +77 more
openaire   +11 more sources

Liquid biopsy epigenetics: establishing a molecular profile based on cell‐free DNA

Molecular Oncology, EarlyView.
Cell‐free DNA (cfDNA) fragments in plasma from cancer patients carry epigenetic signatures reflecting their cells of origin. These epigenetic features include DNA methylation, nucleosome modifications, and variations in fragmentation. This review describes the biological properties of each feature and explores optimal strategies for harnessing cfDNA ...
Christoffer Trier Maansson, Anders Lade Nielsen, Boe Sandahl Sorensen   +2 more
wiley   +1 more source

Identification of multiplicatively acting modulatory mutational signatures in cancer

BMC Bioinformatics, 2022
Background A deep understanding of carcinogenesis at the DNA level underpins many advances in cancer prevention and treatment. Mutational signatures provide a breakthrough conceptualisation, as well as an analysis framework, that can be used to build ...
Dovydas Kičiatovas, Qingli Guo, Miika Kailas, Henri Pesonen, Jukka Corander, Samuel Kaski, Esa Pitkänen, Ville Mustonen   +7 more
doaj   +1 more source

Ultraviolet Radiation Induced Signature Mutations in Photocarcinogenesis

Journal of Investigative Dermatology Symposium Proceedings, 1999
The photons of sunlight begin a series of genetic events in skin leading to cancer. UV signature mutations provide an alternative to inherited mutations as a way of identifying genes that are involved in cancer development. They augment epidemiologic and clinical data by serving as molecular evidence for the role of UV radiation in skin carcinogenesis.
Wikonkal, Norbert M., Brash, Douglas E.
openaire   +2 more sources

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

Molecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto, Nicolò Gualandi, Ylenia Cortolezzis, Raffaella Picco, Monica Colitti, Francesca D'Este, Mariachiara Gani, Wayne W. Hancock, Giovanni Terrosu, Cristina Degrassi, Francesca Agostini, Claudio Brancolini, Luigi E. Xodo, Eros Di Giorgio   +13 more
wiley   +1 more source