Tibor Antal
University of Edinburgh
100 Papers
964 Citations
Tibor Antal is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Population & Mutation (genetic algorithm). The author has an hindex of 38, co-authored 96 publications. Previous affiliations of Tibor Antal include Howard Hughes Medical Institute & Los Alamos National Laboratory.
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Papers
Distant metastasis occurs late during the genetic evolution of pancreatic cancer
Shinichi Yachida,Siân Jones,Ivana Bozic,Tibor Antal,Tibor Antal,Rebecca J. Leary,Baojin Fu,Mihoko Kamiyama,Ralph H. Hruban,James R. Eshleman,Martin A. Nowak,Victor E. Velculescu,Kenneth W. Kinzler,Bert Vogelstein,Christine A. Iacobuzio-Donahue +14 more
TL;DR: In this article, the authors rely on data generated by sequencing the genomes of seven pancreatic cancer metastases to evaluate the clonal relationships among primary and metastatic cancers and find that clonal populations that give rise to distant metastases are represented within the primary carcinoma, but these clones are genetically evolved from the original parental, non-metastatic clone.
Comparative lesion sequencing provides insights into tumor evolution
Siân Jones,Wei Dong Chen,Wei Dong Chen,Giovanni Parmigiani,Frank Diehl,Niko Beerenwinkel,Niko Beerenwinkel,Tibor Antal,Arne Traulsen,Arne Traulsen,Martin A. Nowak,Christopher T. Siegel,Victor E. Velculescu,Kenneth W. Kinzler,Bert Vogelstein,Joseph Willis,Sanford D. Markowitz +16 more
TL;DR: It is shown that the times separating the birth of benign, invasive, and metastatic tumor cells can be determined by analysis of the mutations they have in common, and these results have important implications for understanding human tumor pathogenesis, particularly those associated with metastasis.
Accumulation of driver and passenger mutations during tumor progression
Ivana Bozic,Tibor Antal,Tibor Antal,Hisashi Ohtsuki,Hannah Carter,Dewey Kim,Sining Chen,Rachel Karchin,Kenneth W. Kinzler,Bert Vogelstein,Martin A. Nowak +10 more
TL;DR: A mathematical model is provided that model tumors as a discrete time branching process that starts with a single driver mutation and proceeds as each new driver mutation leads to a slightly increased rate of clonal expansion, providing understanding of the heterogeneity in tumor sizes and development times that have been observed by epidemiologists and clinicians.
Evolutionary dynamics of cancer in response to targeted combination therapy
Ivana Bozic,Johannes G. Reiter,Benjamin L. Allen,Benjamin L. Allen,Tibor Antal,Krishnendu Chatterjee,Preya Shah,Yo Sup Moon,Amin Yaqubie,Nicole Kelly,Dung T. Le,Evan J. Lipson,Paul B. Chapman,Luis A. Diaz,Bert Vogelstein,Martin A. Nowak +15 more
TL;DR: It is found that dual therapy results in long-term disease control for most patients, if there are no single mutations that cause cross-resistance to both drugs; in patients with large disease burden, triple therapy is needed.
Dynamics of social balance on networks
TL;DR: This work studies the evolution of social networks that contain both friendly and unfriendly pairwise links between individual nodes, and finds that an infinite network undergoes a dynamic phase transition from a steady state to "paradise" as the propensity p for friendly links in an update event passes through 1/2.