Sign up to save your podcasts
Or
Share Azacitidine holds promise in VEXAS syndrome; a step forward in precision blood matching; identifying a new vulnerability in TP53-mutated AML
Share to email
Share to Facebook
Share to X
Share to email
Share to Facebook
Share to X
Or
Azacitidine holds promise in VEXAS syndrome; a step forward in precision blood matching; identifying a new vulnerability in TP53-mutated AML
In this week's episode we'll learn about Azacitidine in VEXAS syndrome. Treatment can provide responses in patients with this complex autoinflammatory disorder. But relapse rates were high, so long-term therapy may be required to maintain disease control. After that: A step forward in precision blood matching. High-throughput array genotyping enables extended matching to reduce antibody formation. The results show the potential for reducing harm in regularly transfused patients. Finally, identifying a new vulnerability in TP53-mutated AML. Loss of the tumor suppressor BAP1 defines a unique subtype of TP53-mutated de novo AML. BAP1 loss also confers sensitivity to BCL-xL inhibitors in vivo, opening a new therapeutic avenue.
Featured Articles
- Efficacy and safety of azacitidine for VEXAS syndrome: a large-scale retrospective study from FRENVEX
- Array genotyping of transfusion-relevant blood cell antigens in 6946 ancestrally diverse study participants
- Loss of BAP1 defines a unique subtype of TP53-mutated de novo AML and confers sensitivity to BCL-xL inhibitors
View all episodes
By American Society of Hematology
4.1
4949 ratings
In this week's episode we'll learn about Azacitidine in VEXAS syndrome. Treatment can provide responses in patients with this complex autoinflammatory disorder. But relapse rates were high, so long-term therapy may be required to maintain disease control. After that: A step forward in precision blood matching. High-throughput array genotyping enables extended matching to reduce antibody formation. The results show the potential for reducing harm in regularly transfused patients. Finally, identifying a new vulnerability in TP53-mutated AML. Loss of the tumor suppressor BAP1 defines a unique subtype of TP53-mutated de novo AML. BAP1 loss also confers sensitivity to BCL-xL inhibitors in vivo, opening a new therapeutic avenue.
Featured Articles
- Efficacy and safety of azacitidine for VEXAS syndrome: a large-scale retrospective study from FRENVEX
- Array genotyping of transfusion-relevant blood cell antigens in 6946 ancestrally diverse study participants
- Loss of BAP1 defines a unique subtype of TP53-mutated de novo AML and confers sensitivity to BCL-xL inhibitors
More shows like Blood Podcast
View all
TED Talks Daily
11,147 Listeners
JAMA Editors' Summary
140 Listeners
NEJM This Week
318 Listeners
JAMA Clinical Reviews
499 Listeners
Hematologic Oncology Update
75 Listeners
The Hematologist
26 Listeners
Core IM | Internal Medicine Podcast
1,157 Listeners
VJHemOnc Podcast
2 Listeners
Harrison's PodClass: Internal Medicine Cases and Board Prep
363 Listeners
The Curious Clinicians
373 Listeners
EHA Unplugged
1 Listeners
Blood Cancer Talks
48 Listeners
Two Onc Docs
190 Listeners
WolverHeme Happy Hour
30 Listeners
HemeTalks: Conversations in Hematology Education
4 Listeners