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Vashe Chandrakanthan on Muck Rack

Vashe Chandrakanthan

As seen in: Nature, Cell Press
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Articles

Discovery of an embryonically derived bipotent population of endothelial-macrophage progenitor cells in postnatal aorta - Nature Communications

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By Jan Kazenwadel, Natasha Harvey, Antony Vinh, Vashe Chandrakanthan, Luciano G Martelotto, Jose Polo Verified, Alexander R. Pinto
| Nature Verified
Abstract Converging evidence indicates that extra-embryonic yolk sac is the source of both macrophages and endothelial cells in adult mouse tissues. Prevailing views are that these embryonically derived cells are maintained after birth by proliferative self-renewal in their differentiated states.
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Mesoderm-derived PDGFRA+ cells regulate the emergence of hematopoietic stem cells in the dorsal aorta - Nature Cell Biology

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By Vashe Chandrakanthan, Ashwin Unnikrishnan, Simón Méndez-Ferrer, Berthold Göttgens, John E. Pimanda
| Nature Verified
Abstract Mouse haematopoietic stem cells (HSCs) first emerge at embryonic day 10.5 (E10.5), on the ventral surface of the dorsal aorta, by endothelial-to-haematopoietic transition. We investigated whether mesenchymal stem cells, which provide an essential niche for long-term HSCs (LT-HSCs) in the bone marrow, reside in the aorta–gonad–mesonephros and contribute to the development of the dorsal aorta and endothelial-to-haematopoietic transition.
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Integrative Genomics Identifies the Molecular Basis of Resistance to Azacitidine Therapy in Myelodysplastic Syndromes

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By Ashwin Unnikrishnan, Elli Papaemmanuil, Arjun Verma, Laura Richards, Julie A. I. Thoms, Zara Ali, Jake Olivier, Dominik Beck, Nandan P. Deshpande, Ashu Kumari, Petter S. Woll, Kathy Knezevic, Vashe Chandrakanthan, Melinda L. Tursky, Yizhou Huang
| Cell Press Verified
Identification of Pre-treatment Gene Expression Differences between AZA Responders and Non-responders Although AZA is the most efficacious pharmaceutical option for MDS and CMML, only about half of the patients will respond. Given the lack of understanding of the molecular basis of primary resistance and few therapeutic alternatives, the outcome for AZA non-responders is poor (Prébet et al., 2011xOutcome of high-risk myelodysplastic syndrome after azacitidine treatment failure.
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