@schunglab.bsky.social
Steve Chung's lab at UT Southwestern. Div. of Heme/Onc, Dept. of Internal Medicine. We study hematopoiesis, stem cells, bone marrow failure, and leukemia.
Honored to contribute to this study by @seanjmorrison.bsky.social and team. In patients undergoing allogeneic transplantation and receiving post-transplant cytoxan, the use of non-selective β-blockers may significantly delay engraftment and worsen survival. aacrjournals.org/cancerdiscov...
Non-selective b adrenergic receptor inhibitors impair hematopoietic regeneration in mice and humans after hematopoietic cell transplants
Abstract. Peripheral nerves promote mouse bone marrow regeneration by activating b2 and b3 adrenergic receptor signaling, raising the possibility that non-selective b blockers could inhibit engraftmen...
aacrjournals.org
December 31, 2024 at 11:21 PM
Honored to contribute to this study by @seanjmorrison.bsky.social and team. In patients undergoing allogeneic transplantation and receiving post-transplant cytoxan, the use of non-selective β-blockers may significantly delay engraftment and worsen survival. aacrjournals.org/cancerdiscov...
Reposted
Now online in Cancer Discovery: Non-selective β-Adrenergic Receptor Inhibitors Impair Hematopoietic Regeneration in Mice and Humans After Hematopoietic Cell Transplants - by Jinsuke Nishino, Wenhuo Hu, Ashwin Kishtagari, Stephen Chung, Sean Morrison and colleagues doi.org/10.1158/2159...
December 30, 2024 at 7:18 PM
Now online in Cancer Discovery: Non-selective β-Adrenergic Receptor Inhibitors Impair Hematopoietic Regeneration in Mice and Humans After Hematopoietic Cell Transplants - by Jinsuke Nishino, Wenhuo Hu, Ashwin Kishtagari, Stephen Chung, Sean Morrison and colleagues doi.org/10.1158/2159...
Reposted
ONLINE NOW in Cancer Discovery: CRI scientists link hematopoietic cell transplant deaths to beta-blocker use. Research from @seanjmorrison.bsky.social & colleagues shows nerve signaling needed for regeneration may be impaired by medication. #relentlessdiscovery 🧪 cri.utsw.edu/cri-scientis...
CRI scientists link hematopoietic cell transplant deaths to beta-blocker use - Children's Medical Center Research Institute (CRI) | Dallas Texas
Morrison Lab research shows nerve signaling needed for bone marrow regeneration may be impaired by medication DALLAS – Dec. 30, 2024 – Patients can die if they take certain previously prescribed beta-...
cri.utsw.edu
December 30, 2024 at 4:09 PM
ONLINE NOW in Cancer Discovery: CRI scientists link hematopoietic cell transplant deaths to beta-blocker use. Research from @seanjmorrison.bsky.social & colleagues shows nerve signaling needed for regeneration may be impaired by medication. #relentlessdiscovery 🧪 cri.utsw.edu/cri-scientis...
Reposted
Congrats to Jinsuke Nishino, @StephenChung16, @AshKishtagari, @huwenhuo for paper out in Cancer Discovery today: use of non-selective b blockers impairs engraftment after allogeneic hematopoietic cell transplants involving post-transplant chemo for GVHD prophylaxis
aacrjournals.org/cancerdiscov...
aacrjournals.org/cancerdiscov...
Non-selective b adrenergic receptor inhibitors impair hematopoietic regeneration in mice and humans after hematopoietic cell transplants
Abstract. Peripheral nerves promote mouse bone marrow regeneration by activating b2 and b3 adrenergic receptor signaling, raising the possibility that non-selective b blockers could inhibit engraftmen...
aacrjournals.org
December 30, 2024 at 4:25 PM
Congrats to Jinsuke Nishino, @StephenChung16, @AshKishtagari, @huwenhuo for paper out in Cancer Discovery today: use of non-selective b blockers impairs engraftment after allogeneic hematopoietic cell transplants involving post-transplant chemo for GVHD prophylaxis
aacrjournals.org/cancerdiscov...
aacrjournals.org/cancerdiscov...
Why do patients with germline mutations in DDX41 who develop MDS or AML have such indolent disease? How do somatic DDX41 mutations cause disease when present at very low levels? What are the role of other cooperating mutations? How does transplant work in these patients?
December 7, 2024 at 3:10 PM
Why do patients with germline mutations in DDX41 who develop MDS or AML have such indolent disease? How do somatic DDX41 mutations cause disease when present at very low levels? What are the role of other cooperating mutations? How does transplant work in these patients?