Mastodawn

Taka Maeda Apr 27, 2023

Very intersting case..."Two-hit" theory of inflammatory disease?

TET2-Driver and NLRC4-Passenger Variants in Adult-Onset Autoinflammation | NEJM https://www.nejm.org/doi/full/10.1056/NEJMc2212928#.ZEm6tH7CuVg.twitter

Taka Maeda Apr 25, 2023

Congrats Iannis! Looking forward to reading the manuscript!
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RT @iannisaifantis1
Excited to share one more 2023 research story from our lab, out today @CD_AACR identifying #Mitochondria and #Mitophagy as a key regulator of Venetoclax and MCL1i resistance in AML. The work was led by @glytsou and @xufeng_chen ...@nyugrossman (1)
https://aacrjournals.org/cancerdiscovery/article/doi/10.1158/2159-8290.CD-22-0601/719030/Mitophagy-pro…
https://twitter.com/iannisaifantis1/status/1650521572937986050

Taka Maeda Apr 13, 2023

Amazing work by @jaiswalmdphd and team. Congratulations, Sidd!
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RT @jaiswalmdphd
Clonal hematopoiesis is an expansion of blood stem cell clones caused by mutations in a recurrent set of genes. Our paper on factors mediating expansion of these mutant clones is published today.
https://www.nature.com/articles/s41586-023-05806-1

Thread below...
https://twitter.com/jaiswalmdphd/status/1646175663756550151

Aberrant activation of TCL1A promotes stem cell expansion in clonal haematopoiesis - Nature

Using data from a single time point, passenger-approximated clonal expansion rate (PACER) estimates the fitness of common driver mutations that lead to clonal haematopoiesis and identifies TCL1A activation as a mediator of clonal expansion.

Nature

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Taka Maeda Apr 6, 2023

I wonder if there is a similar scenario for macrophages harboring a CHIP mutation (IL1β)?

Taka Maeda Apr 6, 2023

Fascinating work revealing cell-autonomous (pre-existing mutations) and non-cell autonomous (inflammatory microenvironment caused by PM2.5-activated macrophages) mechanisms of lung cancers!
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RT @CharlesSwanton
Today our important study on air pollutants in the promotion of lung cancer has been published in @Nature led by @WillHilliam @LimEmilia @DrClareWeeden @SwantonLab ...Thread below🧵https://www.nature.com/articles/s41586-023-…
https://twitter.com/CharlesSwanton/status/1643647031997546497

Taka Maeda Mar 28, 2023

I should also note that Venetoclax can kill Bax/Bak1 double KO and even Bcl2 KO AML cells in a mitochondrial apoptosis-independent manner (Fig. S1g and h). This has been previously proposed by others, such as @MitosRUs.
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RT @TMHemOnc
1/4 Thrilled to announce our latest paper published in @LeukemiaJnl, now accessible here: https://rdcu.be/c8t7q. Our findings reveal that a mitochondrial E3 ubiquitin ligase complex, consisting of MARCH5, …
https://twitter.com/TMHemOnc/status/1640346961420378114

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Taka Maeda Mar 28, 2023

We believe MARCH5 regulates VEN sensitivity by specifically modulating NOXA stability in the context of mitochondrial apoptosis. #apoptosis #mitochondria

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Taka Maeda Mar 27, 2023

4/4 through both NOXA-dependent and -independent mechanisms. This work is spearheaded by Fumihiko and supported by our dedicated co-authors. Congratulations, Fumihiko!

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Taka Maeda Mar 27, 2023

2/4 This regulation occurs by modulating NOXA protein stability. The MARCH5 E3 ligase complex constantly ubiquitinates NOXA, leading to proteasome-mediated degradation, which in turn modulates BAX saturation of anti-apoptotic proteins.

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Taka Maeda Mar 27, 2023

3/4 Our results suggest increased NOXA protein levels primarily account for enhanced VEN sensitivity in MARCH5-depleted AML cells. Our study, along with @KStegmaier_DFCI's recent paper (Lin, S. et al. Cancer Discov. 2022), proposes MARCH5 regulates VEN sensitivity