Zobrazeno 1 - 10
of 23
pro vyhledávání: '"Albert Herms"'
Autor:
Kasumi Murai, Stefan Dentro, Swee Hoe Ong, Roshan Sood, David Fernandez-Antoran, Albert Herms, Vasiliki Kostiou, Irina Abnizova, Benjamin A. Hall, Moritz Gerstung, Philip H. Jones
Publikováno v:
Nature Communications, Vol 13, Iss 1, Pp 1-17 (2022)
Ageing normal oesophagus epithelium contains p53 mutant clones. Here the authors use transgenic mice to show how these clones form and contribute to cancer development.
Externí odkaz:
https://doaj.org/article/1dd89c9fd24a483699e9a724ff044c1c
Autor:
Gabriel Piedrafita, Vasiliki Kostiou, Agnieszka Wabik, Bartomeu Colom, David Fernandez-Antoran, Albert Herms, Kasumi Murai, Benjamin A. Hall, Philip H. Jones
Publikováno v:
Nature Communications, Vol 11, Iss 1, Pp 1-15 (2020)
Understanding how cells maintain tissues is challenging. Here, the authors present a single consistent quantitative approach to analyse cell proliferation and lineage tracing data, which shows a single proliferating cell population that maintains epi
Externí odkaz:
https://doaj.org/article/11e1473f6ed64141ac21fbcd3f57b93b
Autor:
Albert Herms, Philip H. Jones
Publikováno v:
Annual Review of Cancer Biology. 7:189-205
Normal tissues progressively acquire mutations. Some mutations are positively selected, driving clonal expansions that may colonize the majority of a tissue by old age. In several cases mutant clonal expansion is due to biasing stem cell fate toward
Autor:
Emilie Abby, Stefan C. Dentro, Michael W. J. Hall, Joanna C. Fowler, Swee Hoe Ong, Roshan Sood, Albert Herms, Gabriel Piedrafita, Irina Abnizova, Christian W. Siebel, Moritz Gerstung, Benjamin A. Hall, Philip H. Jones
NOTCH1 mutant clones occupy the majority of normal human esophagus by middle age but are comparatively rare in esophageal cancers, suggesting NOTCH1 mutations drive clonal expansion but impede carcinogenesis. Here we test this hypothesis. Sequencing
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5e3995a6ea6c8197c93dc9b47a0c6967
https://www.repository.cam.ac.uk/handle/1810/346529
https://www.repository.cam.ac.uk/handle/1810/346529
Autor:
Albert Herms, David Fernandez-Antoran, Maria P. Alcolea, Argyro Kalogeropoulou, Ujjwal Banerjee, Gabriel Piedrafita, Emilie Abby, Jose Antonio Valverde-Lopez, Inês S. Ferreira, Stefan C. Dentro, Swee Hoe Ong, Bartomeu Colom, Kasumi Murai, Charlotte King, Krishnaa Mahbubani, Kourosh Saeb-Parsy, Alan R Lowe, Moritz Gerstung, Philip H Jones
Studying long-term biological processes such as the colonization of aging epithelia by somatic mutant clones has been slowed by the lack of suitable culture systems. Here we describe epithelioids, a facile, cost-effective method of culturing multiple
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::be52034b8d198820e25cae713558400a
https://doi.org/10.1101/2023.01.03.522589
https://doi.org/10.1101/2023.01.03.522589
Autor:
Albert, Herms, Philip H, Jones
Publikováno v:
Nature cell biology. 24(12)
Autor:
Swee Hoe Ong, Joanna C. Fowler, Charlotte King, Michael W. J. Hall, Moritz Gerstung, Bartomeu Colom, Philip H. Jones, Gabriel Piedrafita, Sood R, Agnieszka Wabik, Stefan C. Dentro, Maria P. Alcolea, Inigo Martincorena, Benjamin A. Hall, Albert Herms
Publikováno v:
Nature Genetics. 52:604-614
During aging, progenitor cells acquire mutations, which may generate clones that colonize the surrounding tissue. By middle age, normal human tissues, including the esophageal epithelium (EE), become a patchwork of mutant clones. Despite their releva
Autor:
Charlotte King, Stefan C. Dentro, Bartomeu Colom, Krishnaa T. Mahbubani, Moritz Gerstung, Maria P. Alcolea, David Fernandez-Antoran, Philip H. Jones, Sood R, Benjamin A. Hall, Albert Herms, Kourosh Saeb-Parsy, Swee Hoe Ong, Joanna C. Fowler
SummaryHuman epithelial tissues accumulate cancer-driver mutations with age1–7, yet tumor formation remains rare. The positive selection of these mutations argues they alter the behavior and fitness of proliferating cells8–10. Hence, normal adult
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::4b35042dc701d74fe8b0b499cea711cc
https://doi.org/10.1101/2021.06.25.449880
https://doi.org/10.1101/2021.06.25.449880
Autor:
David Fernandez-Antoran, Bart Vanhaesebroeck, Kasumi Murai, Christian Frezza, Gabriel Piedrafita, Philip H. Jones, Christopher J. Bryant, Albert Herms, Swee Hoe Ong, Bartomeu Colom
SummaryNormal human tissues progressively accumulate cells carrying mutations. Activating mutations inPIK3CAgenerate large clones in the aging human esophagus, but the underlying cellular mechanisms are unclear. Here, we tracked mutantPIK3CAesophagea
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::f44d9a55c50643b9f4f0a82e52f33ccb
https://doi.org/10.1101/2021.05.28.446104
https://doi.org/10.1101/2021.05.28.446104
Autor:
Stefan C. Dentro, Charlotte King, Joanna C. Fowler, Albert Herms, Bartomeu Colom, Maria P. Alcolea, Krishnaa T. Mahbubani, Kourosh Saeb-Parsy, Benjamin A. Hall, David Fernandez-Antoran, Moritz Gerstung, Sood R, Michael W. J. Hall, Philip H. Jones, Gabriel Piedrafita, Swee Hoe Ong
Publikováno v:
Nature. 598(7881)
Human epithelial tissues accumulate cancer-driver mutations with age1–9, yet tumour formation remains rare. The positive selection of these mutations suggests that they alter the behaviour and fitness of proliferating cells10–12. Thus, normal adu