Thomas Force

25.3k citations
158 papers · 16.9k · 7 hit papers · h-index 67

Impact in

    • Chemotherapy-induced cardiotoxicity and mitigation
    • Cardiac Fibrosis and Remodeling
    • Cardiac electrophysiology and arrhythmias
    • Signaling Pathways in Disease
    • Protein Kinase Regulation and GTPase Signaling
    • Wnt/β-catenin signaling in development and cancer

Papers in

    • Signaling Pathways in Disease 22
    • Protein Kinase Regulation and GTPase Signaling 16
    • Wnt/β-catenin signaling in development and cancer 14
    • Melanoma and MAPK Pathways 14
    • PI3K/AKT/mTOR signaling in cancer 12
    • Chemotherapy-induced cardiotoxicity and mitigation 20
    • Cardiac Fibrosis and Remodeling 19
    • Cardiac electrophysiology and arrhythmias 16

Thomas Force

158 papers receiving 16.6k citations

Thomas Force's Hit Papers

Heart Failure: Preventing Disease and Death Worldwide 2014 · 949 citations
9490+11+22Years since publication250500750

Peers

Thomas Force
Comparison fields: 5 of 156
  • Cardiology and Cardiovascular Medicine 5.8k
  • Molecular Biology 8.1k
  • Oncology 2.8k
  • Hematology 810
  • Pathology and Forensic Medicine 1.1k
Replace Edward T.H. Yeh with:
Edward T.H. Yeh United States
Anthony Rosenzweig United States
Joan Heller Brown United States
Tsutomu Imaizumi Japan
Bradford C. Berk United States
Ziad Mallat France
Johann Bauersachs Germany
Merry L. Lindsey United States
Gavin Y. Oudit Canada
Robert E. Gerszten United States
Thomas Force relative to Edward T.H. Yeh United States Edward T.H. Yeh's profile →
Citations per field
00.5×1.7×
Edward T.H. Yeh · 1×
Citations per year

Countries citing papers authored by Thomas Force

Since Specialization
Citations

This map shows the geographic impact of Thomas Force'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 Force with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Thomas Force more than expected).

Fields of papers citing papers by Thomas Force

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Thomas Force. 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 Force. The network helps show where Thomas Force may publish in the future.

Co-authors

The 25 scholars most cited alongside Thomas Force, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.

Border = papers with Thomas Force Line = papers co-authored together Thomas Force links everyone, so they are left out of the graph.

All Works

20 of 20 papers shown

Showing the 20 most-cited of 158 papers — load more, or switch the sort, to bring in the rest.

#Work
1
Heart Failure: Preventing Disease and Death Worldwide
Hit paper breakdown →
2014949
2
Cardiotoxicity of the cancer therapeutic agent imatinib mesylate
Hit paper breakdown →
2006864
3
Expression cloning of a common receptor for parathyroid hormone and parathyroid hormone-related peptide from rat osteoblast-like cells: a single receptor stimulates intracellular accumulation of both cAMP and inositol trisphosphates and increases intracellular free calcium.
Hit paper breakdown →
1992819
4
Cardiotoxicity associated with tyrosine kinase inhibitor sunitinib
Hit paper breakdown →
2007818
5
Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition
Hit paper breakdown →
2007605
6
Akt Activation Preserves Cardiac Function and Prevents Injury After Transient Cardiac Ischemia In Vivo
Hit paper breakdown →
2001600
7
Mitogen-Activated Protein Kinase Signaling in the Heart: Angels Versus Demons in a Heart-Breaking Tale
Hit paper breakdown →
2010592
8 2005499
9 2001356
10 2000337
11 2010310
12 1998284
13 2008283
14 2011281
15 2004275
16 1994229
17 2003199
18 2008195
19 1995194
20 2000190

About Thomas Force

Thomas Force is a scholar working on Molecular Biology, Cardiology and Cardiovascular Medicine, Oncology, Hematology and Radiology, Nuclear Medicine and Imaging, having authored 158 papers that have together received 16.9k indexed citations. Recurring topics across this work include Signaling Pathways in Disease (22 papers), Chemotherapy-induced cardiotoxicity and mitigation (20 papers), Cardiac Fibrosis and Remodeling (19 papers), Cardiac electrophysiology and arrhythmias (16 papers), Protein Kinase Regulation and GTPase Signaling (16 papers), Wnt/β-catenin signaling in development and cancer (14 papers), Melanoma and MAPK Pathways (14 papers) and PI3K/AKT/mTOR signaling in cancer (12 papers). The work is most often cited by research in Cardiology and Cardiovascular Medicine (5.8k citations), Molecular Biology (8.1k citations), Oncology (2.8k citations), Hematology (810 citations) and Pathology and Forensic Medicine (1.1k citations). Thomas Force has collaborated with scholars based in United States, Canada and United Kingdom. Frequent co-authors include Joseph V. Bonventre, Risto Kerkelä, John Kyriakis, James R. Woodgett, Richard A. Van Etten, Gerald W. Dorn, Anthony Rosenzweig, Roger J. Hajjar, Syed Haq and Daniela S. Krause. Their work appears in journals such as Circulation, Journal of Biological Chemistry, Circulation Research, Molecular and Cellular Biology and Journal of the American College of Cardiology.

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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