Author

A. Rio-Machin

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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Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Research Focus:cancer & tumor microenvironment· 2 Organism:human· 2 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

C. Philippe· 2 shared F. Copley· 2 shared J. Fitzgibbon· 2 shared K. Rouault-Pierre· 2 shared P. Casado-Izquierdo· 2 shared P. Cutillas· 2 shared A. Alfonso-Pierola· 1 shared A. Diaz-Mazkiaran· 1 shared

Activity by Year

2020-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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2 shared papersCancer Biology

C. Philippe

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Author profile →

3 papers

Recent·Most cited

SCD inhibition eradicates AML displaying high de novo fatty acid desaturation and synergizes with chemotherapy

V. Dembitz, H. Lawson, R. Burt, C. Philippe, S. C. James, S. Atkinson, J. Durko, L. M. Wang, J. Campos, A. M. Magee, K. Woodley, M. J. Austin, A. Rio-Machin, P. Casado-Izquierdo, F. Bewicke-Copley, , P. Gallipoli

SCD inhibition induces AML cell death and synergizes with chemotherapy to prolong survival in murine AML models.

bioRxiv · Aug 2, 2023Cancer Biology

Transcriptional regulation of HSCs in Aging and MDS reveals DDIT3 as a Potential Driver of Dyserythropoiesis

N. Berastegui, M. Ainciburu, J. P. Romero, A. Alfonso-Pierola, C. Philippe, A. Vilas-Zornoza, P. San Martin, R. Ordonez, D. O. Alignani, S. Sarvide, L. Castro, J. M. Lamo-Espinosa, M. San-Julian, T. Jimenez, F. Lopez Cardenas, , F. Prosper

This study identifies DDIT3 as a driver of dyserythropoiesis in MDS by showing its upregulation in HSCs and its ability to disrupt erythropoiesis when overexpressed.

bioRxiv · Sep 8, 2021 · PreprintCancer Biology

CKS1-dependent proteostatic regulation has dual roles combating acute myeloid leukemia whilst protecting normal hematopoiesis

W. Grey, A. Rio-Machin, P. Casado-Izquierdo, J. Miettinen, F. Copley, A. Parsons, C. Heckman, P. Cutillas, J. Gribben, J. Fitzgibbon, D. Bonnet

This study identifies CKS1-dependent proteostasis as a dual target for combating AML while protecting normal hematopoiesis through inhibition of SCFSKP2-CKS1.

bioRxiv · Dec 27, 2020 · PreprintCancer Biology