Thomas O’Hare

10.5k total citations · 2 hit papers
116 papers, 5.7k citations indexed

About

Thomas O’Hare is a scholar working on Hematology, Genetics and Rheumatology. According to data from OpenAlex, Thomas O’Hare has authored 116 papers receiving a total of 5.7k indexed citations (citations by other indexed papers that have themselves been cited), including 94 papers in Hematology, 81 papers in Genetics and 40 papers in Rheumatology. Recurrent topics in Thomas O’Hare's work include Chronic Myeloid Leukemia Treatments (85 papers), Chronic Lymphocytic Leukemia Research (70 papers) and Eosinophilic Disorders and Syndromes (40 papers). Thomas O’Hare is often cited by papers focused on Chronic Myeloid Leukemia Treatments (85 papers), Chronic Lymphocytic Leukemia Research (70 papers) and Eosinophilic Disorders and Syndromes (40 papers). Thomas O’Hare collaborates with scholars based in United States, United Kingdom and Germany. Thomas O’Hare's co-authors include Michael W. Deininger, Brian Druker, Christopher A. Eide, Francis Y. Lee, Denise K. Walters, Eric P. Stoffregen, Michael C. Heinrich, Matthew S. Zabriskie, Anna M. Eiring and Amie S. Corbin and has published in prestigious journals such as New England Journal of Medicine, Proceedings of the National Academy of Sciences and Journal of Biological Chemistry.

In The Last Decade

Thomas O’Hare

114 papers receiving 5.6k citations

Hit Papers

align trajectories

What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

In vitro Activity of Bcr-Abl Inhibitors AMN107 and BMS-354825 against Clinically Relevant Imatinib-Resistant Abl Kinase Domain Mutants

2005 812 citations Thomas O’Hare, Denise K. Walters et al. Cancer Research profile →
Ponatinib in Refractory Philadelphia Chromosome–Positive Leukemias

2012 527 citations Jörge E. Cortes, Hagop M. Kantarjian et al. profile →

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name	h						Papers	Cites
Thomas O’Hare United States	37	3.8k	2.9k	1.7k	1.6k	966	116	5.7k
Philippe Rousselot France	46	4.7k 1.2×	2.7k 0.9×	1.7k 1.0×	1.8k 1.1×	1.3k 1.3×	181	6.8k
Javier Pinilla‐Ibarz United States	41	2.6k 0.7×	2.3k 0.8×	986 0.6×	1.9k 1.2×	1.8k 1.8×	236	5.8k
Stephen G. O’Brien United Kingdom	23	3.8k 1.0×	3.1k 1.1×	2.1k 1.2×	487 0.3×	663 0.7×	43	4.5k
Ali G. Turhan France	37	2.0k 0.5×	1.4k 0.5×	509 0.3×	1.5k 0.9×	1.0k 1.1×	184	4.0k
Johan Richter Sweden	36	1.7k 0.5×	1.2k 0.4×	668 0.4×	1.5k 0.9×	851 0.9×	145	4.2k
Mike Scott United Kingdom	24	3.1k 0.8×	4.4k 1.5×	1.8k 1.0×	3.1k 1.9×	776 0.8×	46	5.9k
Robert Ilaria United States	26	1.3k 0.3×	833 0.3×	427 0.3×	1.0k 0.6×	1.1k 1.1×	57	3.1k
Larry D. Cripe United States	30	1.8k 0.5×	1.4k 0.5×	215 0.1×	1.3k 0.8×	1.1k 1.1×	104	4.2k
Anupriya Agarwal United States	28	1.7k 0.5×	1.2k 0.4×	418 0.2×	1.4k 0.8×	497 0.5×	85	3.1k
Denise K. Walters United States	23	1.1k 0.3×	730 0.2×	514 0.3×	719 0.4×	351 0.4×	41	2.0k

Countries citing papers authored by Thomas O’Hare

Since Specialization

Citations

This map shows the geographic impact of Thomas O’Hare's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Thomas O’Hare with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Thomas O’Hare more than expected).

Fields of papers citing papers by Thomas O’Hare

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Thomas O’Hare. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Thomas O’Hare. The network helps show where Thomas O’Hare may publish in the future.

Co-authorship network of co-authors of Thomas O’Hare

This figure shows the co-authorship network connecting the top 25 collaborators of Thomas O’Hare. A scholar is included among the top collaborators of Thomas O’Hare based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Thomas O’Hare. Thomas O’Hare is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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20 of 20 papers shown

Mo, Dan, et al.. (2023). Abstract 6300: Therapeutic potential of EO-3021/SYSA1801, a Claudin18.2 antibody-drug conjugate, for the treatment of CLDN18.2-expressing cancers. Cancer Research. 83(7_Supplement). 6300–6300. 3 indexed citations

Shah, Fenil, Justyna M. Gawel, Yasir S. Raouf, et al.. (2019). Identification and Characterization of AES-135, a Hydroxamic Acid-Based HDAC Inhibitor That Prolongs Survival in an Orthotopic Mouse Model of Pancreatic Cancer. Journal of Medicinal Chemistry. 62(5). 2651–2665. 28 indexed citations

Than, Hein, 義行高橋, Xiaomeng Huang, et al.. (2018). Ongoing clonal evolution in chronic myelomonocytic leukemia on hypomethylating agents: a computational perspective. Leukemia. 32(9). 2049–2054. 5 indexed citations

Eiring, Anna M., Jonathan M. Ahmann, Clinton C. Mason, et al.. (2017). Loss of G0S2 in Kinase-Independent TKI Resistance and Blastic Transformation of CML. Blood. 130. 4173–4173. 1 indexed citations

Pomicter, Anthony D., Clinton C. Mason, Anna M. Eiring, et al.. (2017). Inhibition of Nucleocytoplasmic Export Enhances Selective Elimination of Leukemic Stem Cells in Chronic Myeloid Leukemia. Blood. 130. 42–42.

Patel, Ami B., Thomas O’Hare, & Michael W. Deininger. (2017). Mechanisms of Resistance to ABL Kinase Inhibition in Chronic Myeloid Leukemia and the Development of Next Generation ABL Kinase Inhibitors. Hematology/Oncology Clinics of North America. 31(4). 589–612. 147 indexed citations

Jacob, Thomas, Anupriya Agarwal, Damien Ramunno-Johnson, et al.. (2016). Ultrasensitive proteomic quantitation of cellular signaling by digitized nanoparticle-protein counting. Scientific Reports. 6(1). 28163–28163. 4 indexed citations

Drilon, Alexander, Romel Somwar, Jacob P. Wagner, et al.. (2015). A Novel Crizotinib-Resistant Solvent-Front Mutation Responsive to Cabozantinib Therapy in a Patient with ROS1 -Rearranged Lung Cancer. Clinical Cancer Research. 22(10). 2351–2358. 128 indexed citations

Talpaz, Moshe, Jörge E. Cortes, Hagop M. Kantarjian, et al.. (2015). Four-year minimum follow-up of ongoing patients (pts) with chronic-phase chronic myeloid leukemia (CP-CML) in a phase 1 trial of ponatinib (PON).. Journal of Clinical Oncology. 33(15_suppl). 7047–7047. 6 indexed citations

10.

O’Hare, Thomas, Christopher A. Eide, Anupriya Agarwal, et al.. (2013). Threshold Levels of ABL Tyrosine Kinase Inhibitors Retained in Chronic Myeloid Leukemia Cells Determine Their Commitment to Apoptosis. Cancer Research. 73(11). 3356–3370. 23 indexed citations

11.

Corbin, Amie S., Thomas O’Hare, Zhimin Gu, et al.. (2013). KIT Signaling Governs Differential Sensitivity of Mature and Primitive CML Progenitors to Tyrosine Kinase Inhibitors. Cancer Research. 73(18). 5775–5786. 17 indexed citations

12.

Tyner, Jeffrey, Armand Bankhead, Guang Fan, et al.. (2012). Kinase Pathway Dependence in Primary Human Leukemias Determined by Rapid Inhibitor Screening. Cancer Research. 73(1). 285–296. 100 indexed citations

13.

O’Hare, Thomas, Matthew S. Zabriskie, Anna M. Eiring, & Michael W. Deininger. (2012). Pushing the limits of targeted therapy in chronic myeloid leukaemia. Nature reviews. Cancer. 12(8). 513–526. 227 indexed citations

14.

Eide, Christopher A., Lauren T. Adrian, Jeffrey Tyner, et al.. (2011). The ABL Switch Control Inhibitor DCC-2036 Is Active against the Chronic Myeloid Leukemia Mutant BCR-ABLT315I and Exhibits a Narrow Resistance Profile. Cancer Research. 71(9). 3189–3195. 77 indexed citations

15.

Eiring, Anna M., Matthew S. Zabriskie, Jamshid S. Khorashad, et al.. (2011). Partially or Fully BCR-ABL Independent Mechanisms of in Vitro Resistance to Ponatinib. Blood. 118(21). 2481–2481. 1 indexed citations

16.

O’Hare, Thomas, Christopher A. Eide, Scott Wise, et al.. (2008). Activation switch pocket inhibitors target the T315I mutant of BCR-ABL. Cancer Research. 68. 4867–4867. 1 indexed citations

17.

Agarwal, Anupriya, Thomas G.P. Bumm, Amie S. Corbin, et al.. (2008). Absence of SKP2 expression attenuates BCR-ABL–induced myeloproliferative disease. Blood. 112(5). 1960–1970. 54 indexed citations

18.

O’Hare, Thomas, Christopher A. Eide, & Michael W. Deininger. (2007). Bcr-Abl Kinase Domain Mutations and the Unsettled Problem of Bcr-AblT315I: Looking into the Future of Controlling Drug Resistance in Chronic Myeloid Leukemia. Clinical Lymphoma & Myeloma. 7. S120–S130. 17 indexed citations

19.

O’Hare, Thomas, Denise K. Walters, Eric P. Stoffregen, et al.. (2005). In vitro Activity of Bcr-Abl Inhibitors AMN107 and BMS-354825 against Clinically Relevant Imatinib-Resistant Abl Kinase Domain Mutants. Cancer Research. 65(11). 4500–4505. 812 indexed citations breakdown →

20.

O’Hare, Thomas, et al.. (1995). The current status of academic-mental health linkages in Rhode Island. Community Mental Health Journal. 31(3). 209–214. 5 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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