Zobrazeno 1 - 10
of 15
pro vyhledávání: '"Emily B Casey"'
Autor:
Theresa Okeyo-Owuor, Yanan Li, Riddhi M. Patel, Wei Yang, Emily B. Casey, Andrew S. Cluster, Shaina N. Porter, David Bryder, Jeffrey A. Magee
Publikováno v:
Blood Advances, Vol 3, Iss 15, Pp 2388-2399 (2019)
Abstract: MLL rearrangements are translocation mutations that cause both acute lymphoblastic leukemia and acute myeloid leukemia (AML). These translocations can occur as sole clonal driver mutations in infant leukemias, suggesting that fetal or neona
Externí odkaz:
https://doaj.org/article/7c53817e0774466ab5d2e0cc4eb8a3e9
Autor:
Yanan Li, Wei Yang, Helen C. Wang, Riddhi M. Patel, Emily B. Casey, Elisabeth D Denby, Jeffrey A Magee
Type I interferon (IFN-1) regulates gene expression and hematopoiesis both during development and in response to inflammatory stress. We previously showed that during development, hematopoietic stem cells (HSCs) and multipotent progenitors (MPPs) ind
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9d2c60ef6104a71228eeb1dd4b138d75
https://doi.org/10.1101/2022.07.18.500483
https://doi.org/10.1101/2022.07.18.500483
Publikováno v:
Blood. 140:4485-4486
Publikováno v:
Blood. 140:5887-5888
Autor:
Yanan LI, Wei Yang, Riddhi M Patel, Emily B Casey, Elisabeth Denby, Jonny Mendoza-Castrejon, Priscilla Rodriguez-Lopez, Jeffrey A. Magee
Publikováno v:
Blood. 140:5848-5849
Autor:
Riddhi M Patel, David Bryder, Yanan Li, Wei Yang, Andrew Cluster, Shaina N. Porter, Jeffrey A. Magee, Emily B. Casey, Theresa Okeyo-Owuor
Publikováno v:
Blood Advances. 3:2388-2399
MLL rearrangements are translocation mutations that cause both acute lymphoblastic leukemia and acute myeloid leukemia (AML). These translocations can occur as sole clonal driver mutations in infant leukemias, suggesting that fetal or neonatal hemato
Autor:
Riddhi M Patel, Jeffrey A. Magee, Wei Yang, Andrew Cluster, Emily B. Casey, Theresa Okeyo-Owuor, Ran Chen
Publikováno v:
Cell reports
SUMMARY The myeloid tumor suppressor KMT2C is recurrently deleted in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), particularly therapy-related MDS/AML (t-MDS/t-AML), as part of larger chromosome 7 deletions. Here, we show that KMT
Publikováno v:
Blood. 138:2762-2762
KMT2C is one of several tumor suppressor genes deleted in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) as part of larger chromosome 7q deletions. These deletions are particularly common in therapy-related MDS/AML, raising the quest
Publikováno v:
Blood. 138:3294-3294
Chromosomal translocations involving the MLL1 gene often drive infant acute myeloid leukemia (AML). MLL fusion proteins (e.g., MLL-ENL, MLL-AF9, MLL-AF10) activate self-renewal programs in hematopoietic stem and progenitor cells, ultimately leading t
Autor:
Wei Yang, Yanan Li, Elisabeth Denby, Riddhi M Patel, Emily B. Casey, Priscilla Rodriguez-Lopez, Jeffrey A. Magee
Publikováno v:
Blood. 138:1150-1150
FLT3-Internal Tandem Duplication (FLT3 ITD) mutations occur at similar frequencies in both childhood and adult acute myeloid leukemia (AML) patients, but they cooperate with different initiating mutations at different ages. In childhood AML, FLT3 ITD