Daniel Bottomly
Overview
Explore the profile of Daniel Bottomly including associated specialties, affiliations and a list of published articles.
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48
Citations
2197
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Recent Articles
21.
Joshi S, Sharzehi S, Pittsenbarger J, Bottomly D, Tognon C, McWeeney S, et al.
Am J Hematol
. 2021 Mar;
96(7):E226-E229.
PMID: 33780043
No abstract available.
22.
Damnernsawad A, Bottomly D, Kurtz S, Eide C, McWeeney S, Tyner J, et al.
Haematologica
. 2020 Dec;
107(1):77-85.
PMID: 33375770
Drug resistance impedes the long-term effect of targeted therapies in acute myeloid leukemia (AML), necessitating the identification of mechanisms underlying resistance. Approximately 25% of AML patients carry FLT3 mutations and...
23.
Zhang H, Nakauchi Y, Kohnke T, Stafford M, Bottomly D, Thomas R, et al.
Nat Cancer
. 2020 Oct;
1(8):826-839.
PMID: 33123685
Deregulation of the gene family plays an important role in the pathogenesis of acute myeloid leukemia (AML). The BCL2 inhibitor, venetoclax, has received FDA approval for the treatment of AML....
24.
Joshi S, Keck J, Eide C, Bottomly D, Traer E, Tyner J, et al.
Leukemia
. 2020 May;
34(10):2798-2804.
PMID: 32366937
No abstract available.
25.
Joshi S, Qian K, Bisson W, Watanabe-Smith K, Huang A, Bottomly D, et al.
Blood
. 2020 Apr;
135(24):2159-2170.
PMID: 32315394
Much of what is known about the neurotrophic receptor tyrosine kinase (NTRK) genes in cancer was revealed through identification and characterization of activating Trk fusions across many tumor types. A...
26.
Tyner J, Bottomly D, Wilmot B, McWeeney S
Best Pract Res Clin Haematol
. 2019 Nov;
32(4):101101.
PMID: 31779979
While molecular genetic abnormalities can tell us much about the pathogenesis of acute myeloid leukemia (AML), these molecular genetics do not always explain drug resistance or sensitivity, leaving room for...
27.
Zhang H, Wilmot B, Bottomly D, Dao K, Stevens E, Eide C, et al.
Blood
. 2019 Aug;
134(11):867-879.
PMID: 31366621
Chronic neutrophilic leukemia (CNL), atypical chronic myeloid leukemia (aCML), and myelodysplastic/myeloproliferative neoplasms, unclassifiable (MDS/MPN-U) are a group of rare and heterogeneous myeloid disorders. There is strong morphologic resemblance among these...
28.
Zhang H, Savage S, Schultz A, Bottomly D, White L, Segerdell E, et al.
Nat Commun
. 2019 Jan;
10(1):244.
PMID: 30651561
FLT3 mutations are prevalent in AML patients and confer poor prognosis. Crenolanib, a potent type I pan-FLT3 inhibitor, is effective against both internal tandem duplications and resistance-conferring tyrosine kinase domain...
29.
Tyner J, Tognon C, Bottomly D, Wilmot B, Kurtz S, Savage S, et al.
Nature
. 2018 Oct;
562(7728):526-531.
PMID: 30333627
The implementation of targeted therapies for acute myeloid leukaemia (AML) has been challenging because of the complex mutational patterns within and across patients as well as a dearth of pharmacologic...
30.
Jenkins C, Luty S, Maxson J, Eide C, Abel M, Togiai C, et al.
Sci Signal
. 2018 Jul;
11(539).
PMID: 30018082
The protein tyrosine phosphatase PTPN11 is implicated in the pathogenesis of juvenile myelomonocytic leukemia (JMML), acute myeloid leukemia (AML), and other malignancies. Activating mutations in PTPN11 increase downstream proliferative signaling...