Author

I. Padioleau

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· 3

Signature Assays, Organisms & Methods

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Research Focus:cancer & tumor microenvironment· 3 Organism:human· 3 Research Focus:chromatin & epigenetic regulation· 2 Approach:experimental assay· 2 Assay:whole-genome sequencing· 2 Research Focus:gene regulatory network inference· 1 Approach:statistical model· 1 Assay:whole-exome sequencing· 1

Frequent Co-Authors

A. A. Yurchenko· 2 shared A. Sarasin· 2 shared S. Nikolaev· 2 shared A. A. Mangaonkar· 1 shared A. Buradkar· 1 shared A. Lehmann· 1 shared A. Vedder· 1 shared A. Yurchenko· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 23 mutual co-author links

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2 shared papersCancer Biology

A. A. Yurchenko

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3 papers

Recent·Most cited

Analysis of Skin Cancers from Xeroderma Pigmentosum Patients Reveals Heterogeneous UV-Induced Mutational Profiles Shaped by DNA Repair

A. A. Yurchenko, F. Rajabi, T. Braz-Petta, H. Fassihi, A. Lehmann, C. Nishigori, I. Padioleau, K. Gunbin, L. Panunzi, F. Morice-Picard, P. Laplante, C. Robert, P. Kannouche, C. F. M. Menck, A. Sarasin, S. I. Nikolaev

The paper analyzes skin cancer genomes from Xeroderma Pigmentosum patients to show how NER activity shapes mutation rates and reveals POLH's role in bypassing UV-induced DNA lesions.

bioRxiv · Oct 14, 2022 · PreprintCancer Biology

XPC deficiency increases risk of hematologic malignancies through mutator phenotype and characteristic mutational signature

A. A. Yurchenko, I. Padioleau, B. T. Matkarimov, J. Soulier, A. Sarasin, S. Nikolaev

This study shows XPC deficiency leads to higher mutation rates and specific mutational signatures in hematologic malignancies, increasing cancer risk through a mutator phenotype.

bioRxiv · Jul 13, 2020Cancer Biology

RAS mutations drive proliferative chronic myelomonocytic leukemia via activation of a novel KMT2A-PLK1 axis

R. M. Carr, D. Vorobyev, T. Lasho, D. L. Marks, E. J. Tolosa, A. Vedder, L. Almada, A. Yurchenko, I. Padioleau, B. Alver, G. Coltro, M. Binder, S. L. Safgren, I. Horn, X. You, , M. M. Patnaik

This study identifies RAS mutations as drivers of proliferative CMML through a novel KMT2A-PLK1 axis, showing PLK1 inhibition can improve disease outcomes in patient-derived xenografts.

bioRxiv · Dec 23, 2019 · PreprintCancer Biology