William H. Chappell

7.0k total citations · 1 hit paper
41 papers, 4.0k citations indexed

About

William H. Chappell is a scholar working on Molecular Biology, Oncology and Pathology and Forensic Medicine. According to data from OpenAlex, William H. Chappell has authored 41 papers receiving a total of 4.0k indexed citations (citations by other indexed papers that have themselves been cited), including 30 papers in Molecular Biology, 19 papers in Oncology and 8 papers in Pathology and Forensic Medicine. Recurrent topics in William H. Chappell's work include PI3K/AKT/mTOR signaling in cancer (19 papers), Cancer-related Molecular Pathways (11 papers) and Melanoma and MAPK Pathways (10 papers). William H. Chappell is often cited by papers focused on PI3K/AKT/mTOR signaling in cancer (19 papers), Cancer-related Molecular Pathways (11 papers) and Melanoma and MAPK Pathways (10 papers). William H. Chappell collaborates with scholars based in United States, Italy and Germany. William H. Chappell's co-authors include James A. McCubrey, Linda S. Steelman, Stephen L. Abrams, Massimo Libra, Alberto M. Martelli, Franca Stivala, Jörg Bäsecke, Brian D. Lehmann, David M. Terrian and Richard A. Franklin and has published in prestigious journals such as Blood, Oncogene and Journal of Virology.

In The Last Decade

William H. Chappell

41 papers receiving 3.9k citations

Hit Papers

Roles of the Raf/MEK/ERK pathway in cell growth, malignan... 2006 2026 2012 2019 2006 500 1000 1.5k

Peers

William H. Chappell
Patrick M. Navolanic United States
Pixu Liu China
Fumin Chang United States
Christopher L. Morton United States
Benjamin D. Hopkins United States
Patrick M. Navolanic United States
William H. Chappell
Citations per year, relative to William H. Chappell William H. Chappell (= 1×) peers Patrick M. Navolanic

Countries citing papers authored by William H. Chappell

Since Specialization
Citations

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

Fields of papers citing papers by William H. Chappell

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by William H. Chappell. 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 William H. Chappell. The network helps show where William H. Chappell may publish in the future.

Co-authorship network of co-authors of William H. Chappell

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

All Works

20 of 20 papers shown
1.
Steelman, Linda S., William H. Chappell, Shaw M. Akula, et al.. (2020). Therapeutic resistance in breast cancer cells can result from deregulated EGFR signaling. Advances in Biological Regulation. 78. 100758–100758. 28 indexed citations
2.
Chappell, William H., Saverio Candido, Stephen L. Abrams, et al.. (2018). Roles of p53, NF-κB and the androgen receptor in controlling NGAL expression in prostate cancer cell lines. Advances in Biological Regulation. 69. 43–62. 19 indexed citations
4.
Sokolosky, Melissa L., William H. Chappell, Kristin M. Stadelman, et al.. (2014). Inhibition of GSK-3β activity can result in drug and hormonal resistance and alter sensitivity to targeted therapy in MCF-7 breast cancer cells. Cell Cycle. 13(5). 820–833. 43 indexed citations
5.
Ciuffreda, Ludovica, Ursula Cesta Incani, Linda S. Steelman, et al.. (2014). Signaling Intermediates (MAPK and PI3K) as Therapeutic Targets in NSCLC. Current Pharmaceutical Design. 20(24). 3944–3957. 52 indexed citations
6.
Chappell, William H., Stephen L. Abrams, Kristin M. Stadelman, et al.. (2012). Increased NGAL (Lnc2) expression after chemotherapeutic drug treatment. Advances in Biological Regulation. 53(1). 146–155. 12 indexed citations
7.
Chappell, William H., Stephen L. Abrams, Richard A. Franklin, et al.. (2012). Ectopic NGAL expression can alter sensitivity of breast cancer cells to EGFR, Bcl-2, CaM-K inhibitors and the plant natural product berberine. Cell Cycle. 11(23). 4447–4461. 21 indexed citations
8.
Steelman, Linda S., Patrick M. Navolanic, William H. Chappell, et al.. (2011). Involvement of Akt and mTOR in chemotherapeutic- and hormonal-based drug resistance and response to radiation in breast cancer cells. Cell Cycle. 10(17). 3003–3015. 70 indexed citations
9.
Steelman, Linda S., Richard A. Franklin, Stephen L. Abrams, et al.. (2011). Roles of the Ras/Raf/MEK/ERK pathway in leukemia therapy. Leukemia. 25(7). 1080–1094. 203 indexed citations
10.
Abrams, Stephen L., Linda S. Steelman, John G. Shelton, et al.. (2010). The Raf/MEK/ERK pathway can govern drug resistance, apoptosis and sensitivity to targeted therapy. Cell Cycle. 9(9). 1781–1791. 103 indexed citations
11.
Abrams, Stephen L., Linda S. Steelman, John G. Shelton, et al.. (2010). Enhancing therapeutic efficacy by targeting non-oncogene addicted cells with combinations of signal transduction inhibitors and chemotherapy. Cell Cycle. 9(9). 1839–1846. 21 indexed citations
12.
McCubrey, James A., William H. Chappell, Stephen L. Abrams, et al.. (2010). Targeting the cancer initiating cell: The Achilles’ heel of cancer. Advances in Enzyme Regulation. 51(1). 152–162. 9 indexed citations
13.
McCubrey, James A., Linda S. Steelman, Steven L. Abrams, et al.. (2009). Emerging Raf inhibitors. Expert Opinion on Emerging Drugs. 14(4). 633–648. 26 indexed citations
14.
Lehmann, Brian D., et al.. (2008). Distinct roles for p107 and p130 in Rb-independent cellular senescence. Cell Cycle. 7(9). 1262–1268. 15 indexed citations
15.
Lee, John Tayu, Brian D. Lehmann, David M. Terrian, et al.. (2008). Targeting prostate cancer based on signal transduction and cell cycle pathways. Cell Cycle. 7(12). 1745–1762. 83 indexed citations
16.
Steelman, Linda S., Kristin M. Stadelman, William H. Chappell, et al.. (2008). Akt as a therapeutic target in cancer. Expert Opinion on Therapeutic Targets. 12(9). 1139–1165. 120 indexed citations
17.
Lee, John Tayu, Linda S. Steelman, William H. Chappell, & James A. McCubrey. (2008). Akt inactivates ERK causing decreased response to chemotherapeutic drugs in advanced CaP cells. Cell Cycle. 7(5). 631–636. 29 indexed citations
18.
McCubrey, James A., Linda S. Steelman, Richard A. Franklin, et al.. (2007). Targeting the RAF/MEK/ERK, PI3K/AKT and P53 pathways in hematopoietic drug resistance. Advances in Enzyme Regulation. 47(1). 64–103. 67 indexed citations
19.
Bertrand, F. E., Linda S. Steelman, William H. Chappell, et al.. (2006). Synergy between an IGF-1R antibody and Raf/MEK/ERK and PI3K/Akt/mTOR pathway inhibitors in suppressing IGF-1R-mediated growth in hematopoietic cells. Leukemia. 20(7). 1254–1260. 68 indexed citations
20.
Chappell, William H., et al.. (2005). Increased Protein Expression of the PTEN Tumor Suppressor in the Presence of Constitutively Active Notch-1. Cell Cycle. 4(10). 1389–1395. 41 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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