Katherine R. Singleton

1.0k total citations
16 papers, 652 citations indexed

About

Katherine R. Singleton is a scholar working on Molecular Biology, Pulmonary and Respiratory Medicine and Oncology. According to data from OpenAlex, Katherine R. Singleton has authored 16 papers receiving a total of 652 indexed citations (citations by other indexed papers that have themselves been cited), including 13 papers in Molecular Biology, 8 papers in Pulmonary and Respiratory Medicine and 4 papers in Oncology. Recurrent topics in Katherine R. Singleton's work include Lung Cancer Treatments and Mutations (8 papers), Fibroblast Growth Factor Research (4 papers) and PI3K/AKT/mTOR signaling in cancer (3 papers). Katherine R. Singleton is often cited by papers focused on Lung Cancer Treatments and Mutations (8 papers), Fibroblast Growth Factor Research (4 papers) and PI3K/AKT/mTOR signaling in cancer (3 papers). Katherine R. Singleton collaborates with scholars based in United States, India and Brazil. Katherine R. Singleton's co-authors include Lynn E. Heasley, Trista K. Hinz, Lindsay A. Marek, Aik Choon Tan, Emily K. Kleczko, David P. Astling, Christopher T. Cummings, B. Helfrich, Douglas K. Graham and Kris C. Wood and has published in prestigious journals such as Journal of Biological Chemistry, Nature Genetics and Bioinformatics.

In The Last Decade

Katherine R. Singleton

16 papers receiving 645 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Katherine R. Singleton United States 11 497 209 190 135 50 16 652
Hideki Terai Japan 15 480 1.0× 297 1.4× 358 1.9× 199 1.5× 45 0.9× 41 778
Christopher Moy United States 12 363 0.7× 270 1.3× 177 0.9× 161 1.2× 47 0.9× 17 618
Yi‐Hung Carol Tan United States 17 344 0.7× 255 1.2× 200 1.1× 90 0.7× 45 0.9× 32 705
Thanh Von United States 10 628 1.3× 289 1.4× 168 0.9× 110 0.8× 59 1.2× 11 808
John P. Gustin United States 11 512 1.0× 206 1.0× 109 0.6× 150 1.1× 54 1.1× 12 641
Rosanna Lacalamita Italy 15 358 0.7× 223 1.1× 97 0.5× 233 1.7× 78 1.6× 30 647
Barbara Lysy United States 7 380 0.8× 192 0.9× 150 0.8× 96 0.7× 30 0.6× 7 568
Davide Torti Italy 12 418 0.8× 304 1.5× 116 0.6× 137 1.0× 77 1.5× 17 677
Elisabeth Llonch Switzerland 2 509 1.0× 214 1.0× 128 0.7× 93 0.7× 106 2.1× 2 651
Leila Dardaei United States 10 333 0.7× 283 1.4× 349 1.8× 160 1.2× 54 1.1× 13 627

Countries citing papers authored by Katherine R. Singleton

Since Specialization
Citations

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

Fields of papers citing papers by Katherine R. Singleton

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Katherine R. Singleton. 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 Katherine R. Singleton. The network helps show where Katherine R. Singleton may publish in the future.

Co-authorship network of co-authors of Katherine R. Singleton

This figure shows the co-authorship network connecting the top 25 collaborators of Katherine R. Singleton. A scholar is included among the top collaborators of Katherine R. Singleton 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 Katherine R. Singleton. Katherine R. Singleton is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

16 of 16 papers shown
1.
Maltas, Jeff, et al.. (2023). Drug dependence in cancer is exploitable by optimally constructed treatment holidays. Nature Ecology & Evolution. 8(1). 147–162. 14 indexed citations
2.
Lin, Kevin, Justine C. Rutter, Abigail Xie, et al.. (2020). Using antagonistic pleiotropy to design a chemotherapy-induced evolutionary trap to target drug resistance in cancer. Nature Genetics. 52(4). 408–417. 39 indexed citations
3.
Liberti, Maria V., Annamarie E. Allen, Vijyendra Ramesh, et al.. (2019). Evolved resistance to partial GAPDH inhibition results in loss of the Warburg effect and in a different state of glycolysis. Journal of Biological Chemistry. 295(1). 111–124. 16 indexed citations
4.
Hinz, Trista K., Emily K. Kleczko, Katherine R. Singleton, et al.. (2019). Functional RNAi Screens Define Distinct Protein Kinase Vulnerabilities in EGFR-Dependent HNSCC Cell Lines. Molecular Pharmacology. 96(6). 862–870. 5 indexed citations
5.
Pilling, Amanda, Jihye Kim, Adriana Estrada‐Bernal, et al.. (2018). ALK is a critical regulator of the MYC-signaling axis in ALK positive lung cancer. Oncotarget. 9(10). 8823–8835. 19 indexed citations
6.
Singleton, Katherine R., et al.. (2017). Analysis of Drug Resistance Using Kinome-Wide Functional Screens. Methods in molecular biology. 1636. 163–177. 2 indexed citations
7.
Singleton, Katherine R. & Kris C. Wood. (2016). Narrowing the focus: a toolkit to systematically connect oncogenic signaling pathways with cancer phenotypes. Genes & Cancer. 7(7-8). 218–228. 4 indexed citations
8.
Singleton, Katherine R., Trista K. Hinz, Emily K. Kleczko, et al.. (2015). Kinome RNAi Screens Reveal Synergistic Targeting of MTOR and FGFR1 Pathways for Treatment of Lung Cancer and HNSCC. Cancer Research. 75(20). 4398–4406. 47 indexed citations
9.
Kleczko, Emily K., Jihye Kim, Stephen B. Keysar, et al.. (2015). An Inducible TGF-β2-TGFβR Pathway Modulates the Sensitivity of HNSCC Cells to Tyrosine Kinase Inhibitors Targeting Dominant Receptor Tyrosine Kinases. PLoS ONE. 10(5). e0123600–e0123600. 6 indexed citations
10.
Kim, Jihye, Vihas T. Vasu, Rangnath Mishra, et al.. (2014). Bioinformatics-driven discovery of rational combination for overcoming EGFR-mutant lung cancer resistance to EGFR therapy. Bioinformatics. 30(17). 2393–2398. 21 indexed citations
11.
Martz, Colin A., Kathleen Ottina, Katherine R. Singleton, et al.. (2014). Systematic identification of signaling pathways with potential to confer anticancer drug resistance. Science Signaling. 7(357). ra121–ra121. 135 indexed citations
12.
Hinz, Trista K., Emily K. Kleczko, Katherine R. Singleton, et al.. (2013). A mechanism of resistance to gefitinib mediated by cellular reprogramming and the acquisition of an FGF2-FGFR1 autocrine growth loop. Oncogenesis. 2(3). e39–e39. 203 indexed citations
13.
14.
Pilling, Amanda, Anh T. Le, Aik Choon Tan, et al.. (2012). Abstract 5594: ALK-driven lung cancer: Potential therapeutic strategies for treatment and prevention of drug resistance. Cancer Research. 72(8_Supplement). 5594–5594. 1 indexed citations
15.
Hinz, Trista K., Scott A. Kono, Katherine R. Singleton, et al.. (2011). Fibroblast Growth Factor Receptors Are Components of Autocrine Signaling Networks in Head and Neck Squamous Cell Carcinoma Cells. Clinical Cancer Research. 17(15). 5016–5025. 84 indexed citations
16.
Singleton, Katherine R., et al.. (2009). Elevated extracellular K+ inhibits apoptosis of corneal epithelial cells exposed to UV-B radiation. Experimental Eye Research. 89(2). 140–151. 26 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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