Author

F. Amary

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cancer Biology· 4

Signature Assays, Organisms & Methods

Click to filter · or open tag

Organism:human· 4 Research Focus:cancer & tumor microenvironment· 3 Approach:experimental assay· 3 Assay:DNA methylation· 2 Research Focus:variant calling· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Assay:ChIP-seq· 1

Frequent Co-Authors

A. M. Flanagan· 4 shared R. Tirabosco· 4 shared A. Giess· 2 shared F. Muyas· 2 shared G. Elgar· 2 shared H. Elrick· 2 shared I. Cortes-Ciriano· 2 shared J. Espejo Valle-Inclan· 2 shared

Activity by Year

2018-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 38 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

4 shared papersCancer Biology

A. M. Flanagan

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

SAVANA: reliable analysis of somatic structural variants and copy number aberrations in clinical samples using long-read sequencing

H. Elrick, C. M. Sauer, J. Espejo Valle-Inclan, K. Trevers, M. Tanguy, S. Zumalave, S. De Noon, F. Muyas, R. Cascao, A. Afonso, F. Amary, R. Tirabosco, A. Giess, T. Freeman, A. Sosinsky, , I. Cortes-Ciriano

SAVANA improves detection of somatic structural variants and copy number aberrations in cancer using long-read sequencing with higher sensitivity and specificity than existing tools.

bioRxiv · Jul 25, 2024 · PreprintCancer Biology

Mechanisms underpinning osteosarcoma genome complexity and evolution

J. Espejo Valle-Inclan, S. De Noon, K. Trevers, H. Elrick, M. Tanguy, T. Butters, F. Muyas, F. Amary, R. Tirabosco, A. Giess, A. Sosinky, G. Elgar, A. M. Flanagan, I. Cortes-Ciriano

This study identifies chromothripsis and a novel LTA chromothripsis mechanism driving genome complexity and evolution in osteosarcoma, with prognostic implications for high-grade tumors.

bioRxiv · Dec 29, 2023 · PreprintCancer Biology

Aberrant paracrine signalling for bone remodelling underlies the mutant histone-driven giant cell tumour of bone.

L. Cottone, L. Ligammari, H. J. Knowles, H.-M. Lee, S. Henderson, S. Bianco, C. Davies, S. Strauss, F. Amary, A. P. Leite, R. Tirabosco, K. Haendler, J. L. Schultze, J. Herrero, P. ODonnell, , A. M. Flanagan

This study identifies aberrant paracrine signaling between osteoprogenitors and osteoclasts driven by H3.3 mutations as a mechanism underlying giant cell tumor of bone and its response to treatment.

bioRxiv · Dec 27, 2021Cancer Biology

Epigenetic inactivation of oncogenic brachyury (TBXT) by H3K27 histone demethylase controls chordoma cell survival

L. Cottone, E. S. Hookway, A. Cribbs, G. Wells, P. Lombard, L. Ligammari, A. Tumber, R. Tirabosco, F. Amary, T. Szommer, C. Johannson, P. E. Brennan, N. Pillay, U. Oppermann, A. M. Flanagan

This study shows that inhibiting H3K27 demethylases reduces TBXT expression and kills chordoma cells by altering epigenetic marks and gene expression.

bioRxiv · Oct 1, 2018 · PreprintCancer Biology