Author

H. Tari

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

Biology Disciplines

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Cancer Biology· 2

Signature Assays, Organisms & Methods

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Organism:human· 2 Assay:ATAC-seq· 1 Approach:Bayesian inference· 1 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell-cell communication· 1 Assay:ChIP-seq· 1 Research Focus:clustering· 1

Frequent Co-Authors

A. Sottoriva· 2 shared C. Jones· 2 shared K. Kessler· 2 shared M. Vinci· 2 shared A. Burford· 1 shared A. Mackay· 1 shared B. Werner· 1 shared D. Castel· 1 shared

Activity by Year

2021-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 40 mutual co-author links

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2 shared papersCancer Biology

A. Sottoriva

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2 papers

Recent·Most cited

Quantification of spatial subclonal interactions enhancing the invasive phenotype of paediatric glioma

H. Tari, K. Kessler, N. Trahearn, B. Werner, M. Vinci, C. Jones, A. Sottoriva

This study quantifies spatial subclonal interactions in paediatric gliomas that enhance invasive phenotype, distinguishing true interactions from spatial confounding factors.

bioRxiv · Jul 19, 2021 · PreprintCancer Biology

Loss of the H4 lysine methyltransferase KMT5B drives tumorigenic phenotypes by depleting H3K27me3 at loci otherwise retained in H3K27M mutant DIPG cells

K. Kessler, A. Mackay, Y. Grabovska, V. Molinari, A. Burford, S. Temelso, H. Tari, E. Yara-Romero, I. Liu, L. Yu, D. Castel, J. Choudhary, A. Sottoriva, M. Filbin, M. Vinci, C. Jones

The paper shows that loss of KMT5B in DIPG cells depletes retained H3K27me3 loci, leading to transcriptional changes that promote tumorigenesis.

bioRxiv · Jul 19, 2021 · PreprintCancer Biology