G
George R. Buchanan
Researcher at University of Texas Southwestern Medical Center
Publications - 185
Citations - 7858
George R. Buchanan is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Acute lymphocytic leukemia & Anemia. The author has an hindex of 42, co-authored 185 publications receiving 7340 citations. Previous affiliations of George R. Buchanan include Tennessee Technological University & University of Texas Health Science Center at San Antonio.
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Application of nonlocal continuum models to nanotechnology
TL;DR: In this paper, a nonlocal elasticity theory is employed to develop a non-local Benoulli/Euler beam model and some representative problems are solved to illustrate the magnitude of predicted nonlocal effects.
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American Society of Hematology 2019 guidelines for immune thrombocytopenia
Cindy Neunert,Deirdra R. Terrell,Donald M. Arnold,George R. Buchanan,Douglas B. Cines,Nichola Cooper,Adam Cuker,Jenny M. Despotovic,James N. George,Rachael F. Grace,Thomas Kühne,David J. Kuter,Wendy Lim,Keith R. McCrae,Barbara Pruitt,Hayley Shimanek,Sara K. Vesely +16 more
TL;DR: There was a lack of evidence to support strong recommendations for various management approaches, and a large focus was placed on shared decision-making, especially with regard to second-line therapy.
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The tal gene undergoes chromosome translocation in T cell leukemia and potentially encodes a helix-loop-helix protein.
Qi Chen,Jiin Tsuey Cheng,L.H. Tasi,Nancy R. Schneider,George R. Buchanan,AJ Carroll,W. Crist,B. Ozanne,M. Siciliano,Richard Baer +9 more
TL;DR: Analysis of t(1;14)(p32;q11) chromosome translocations from two patients with T cell acute lymphocytic leukemia has identified sequences within tal that potentially encode an amphipathic helix‐loop‐helix motif, a DNA‐binding domain found in a variety of proteins that control cell growth and differentiation.
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Site-specific recombination of the tal-1 gene is a common occurrence in human T cell leukemia.
Lamorna Brown,Jiin Tsuey Cheng,Qi Chen,Michael J. Siciliano,William M. Crist,William M. Crist,George R. Buchanan,Richard Baer +7 more
TL;DR: T(1;14)(p32;q11) translocations and tald rearrangements disrupt the coding potential of tal‐1 in an equivalent manner, and thereby generate a common genetic lesion shared by a significant proportion of T‐ALL patients.
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Induction by alkylating agents of sister chromatid exchanges and chromatid breaks in Fanconi's anemia.
TL;DR: The results suggest that chromosomal breaks and rearrangements in Fanconi's anemia lymphocytes may result from a defect in a form of repair of DNA damage.