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Dr Andrew Das

Dr Andrew Das

Details

Role Senior Research Officer
Research area Stem Cell Medicine

Contact

Dr Andrew Das is a Senior Research Officer at MCRI. He works with Professor Melissa Little and Dr Sara Howden, exploring how heterogeneity arises during cell fate decisions.

Andrew completed a combined MBChB/PhD degree at the University of Otago in 2017, gaining expertise in biochemistry and pathology. His thesis explored how various proteins are damaged by metabolic oxidants and how this impacts a rate limiting step in the synthesis of critical nucleotides. His research interests include how metabolism and epigenetics intersect to determine cell phenotype, which he explored during his postdoctoral work.

At the Centre for Redox Biology and Medicine (Christchurch, NZ), he investigated the potential role of ascorbate as an epigenetic therapeutic in specific subtypes of acute myeloid leukaemia. He also explored whether oxidants produced by immune cells can regulate the epigenetic identity of neighbouring cells. He was subsequently awarded a John Gavin Postdoctoral Fellowship to continue his training at the Peter MacCallum Cancer Centre in Melbourne.

Across several different projects, he developed proficiency in stem cell differentiation, single molecule tracking, and the design and analysis of CRISPR screens for probing cell fate decisions. His current work leverages this broad range of expertise to investigate how heterogeneity can arise during cell fate decisions.
Dr Andrew Das is a Senior Research Officer at MCRI. He works with Professor Melissa Little and Dr Sara Howden, exploring how heterogeneity arises during cell fate decisions.

Andrew completed a combined MBChB/PhD degree at the University of Otago in...
Dr Andrew Das is a Senior Research Officer at MCRI. He works with Professor Melissa Little and Dr Sara Howden, exploring how heterogeneity arises during cell fate decisions.

Andrew completed a combined MBChB/PhD degree at the University of Otago in 2017, gaining expertise in biochemistry and pathology. His thesis explored how various proteins are damaged by metabolic oxidants and how this impacts a rate limiting step in the synthesis of critical nucleotides. His research interests include how metabolism and epigenetics intersect to determine cell phenotype, which he explored during his postdoctoral work.

At the Centre for Redox Biology and Medicine (Christchurch, NZ), he investigated the potential role of ascorbate as an epigenetic therapeutic in specific subtypes of acute myeloid leukaemia. He also explored whether oxidants produced by immune cells can regulate the epigenetic identity of neighbouring cells. He was subsequently awarded a John Gavin Postdoctoral Fellowship to continue his training at the Peter MacCallum Cancer Centre in Melbourne.

Across several different projects, he developed proficiency in stem cell differentiation, single molecule tracking, and the design and analysis of CRISPR screens for probing cell fate decisions. His current work leverages this broad range of expertise to investigate how heterogeneity can arise during cell fate decisions.

Top Publications

  • Seddon, AR, Das, AB, Hampton, MB, Stevens, AJ. Site-specific decreases in DNA methylation in replicating cells following exposure to oxidative stress.. Hum Mol Genet 32(4) : 632 -648 2023
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  • Smith-Díaz, CC, Magon, NJ, McKenzie, JL, Hampton, MB, Vissers, MCM, Das, AB. Ascorbate Inhibits Proliferation and Promotes Myeloid Differentiation in TP53-Mutant Leukemia.. Front Oncol 11: 709543 2021
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  • Das, AB, Smith-Díaz, CC, Vissers, MCM. Emerging epigenetic therapeutics for myeloid leukemia: modulating demethylase activity with ascorbate.. Haematologica 106(1) : 14 -25 2021
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  • O'Connor, KM, Das, AB, Winterbourn, CC, Hampton, MB. Inhibition of DNA methylation in proliferating human lymphoma cells by immune cell oxidants.. J Biol Chem 295(23) : 7839 -7848 2020
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  • Das, AB, Kakadia, PM, Wojcik, D, Pemberton, L, Browett, PJ, Bohlander, SK, Vissers, MCM. Clinical remission following ascorbate treatment in a case of acute myeloid leukemia with mutations in TET2 and WT1.. Blood Cancer J 9(10) : 82 2019
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