John Whysner

2.5k total citations
44 papers, 2.0k citations indexed

About

John Whysner is a scholar working on Cancer Research, Molecular Biology and Health, Toxicology and Mutagenesis. According to data from OpenAlex, John Whysner has authored 44 papers receiving a total of 2.0k indexed citations (citations by other indexed papers that have themselves been cited), including 22 papers in Cancer Research, 14 papers in Molecular Biology and 11 papers in Health, Toxicology and Mutagenesis. Recurrent topics in John Whysner's work include Carcinogens and Genotoxicity Assessment (21 papers), Effects and risks of endocrine disrupting chemicals (7 papers) and Pharmacogenetics and Drug Metabolism (6 papers). John Whysner is often cited by papers focused on Carcinogens and Genotoxicity Assessment (21 papers), Effects and risks of endocrine disrupting chemicals (7 papers) and Pharmacogenetics and Drug Metabolism (6 papers). John Whysner collaborates with scholars based in United States, France and Switzerland. John Whysner's co-authors include Gary M. Williams, Michael J. Iatropoulos, Lynne Verna, C. Clifford Conaway, Boyd W. Harding, Peter Maimon Ross, Gordon C. Hard, M. Vijayaraj Reddy, Marie‐Claude Jaurand and Tom K. Hei and has published in prestigious journals such as Journal of Biological Chemistry, Biochemical and Biophysical Research Communications and Annals of the New York Academy of Sciences.

In The Last Decade

John Whysner

43 papers receiving 1.8k citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
John Whysner United States 25 716 596 395 281 204 44 2.0k
Fumio Furukawa Japan 28 964 1.3× 652 1.1× 307 0.8× 190 0.7× 254 1.2× 163 2.5k
Greg Cosma United States 20 872 1.2× 397 0.7× 334 0.8× 302 1.1× 127 0.6× 38 1.8k
Masamichi Fukuoka Japan 24 752 1.1× 425 0.7× 277 0.7× 159 0.6× 270 1.3× 85 1.6k
Philip Burcham Australia 28 1.0k 1.4× 313 0.5× 324 0.8× 342 1.2× 202 1.0× 64 2.7k
E. Richter Germany 26 610 0.9× 468 0.8× 386 1.0× 188 0.7× 138 0.7× 116 1.7k
A. W. Andrews United States 23 840 1.2× 833 1.4× 424 1.1× 113 0.4× 262 1.3× 70 2.6k
Emerich S. Fiala United States 33 1.9k 2.6× 759 1.3× 238 0.6× 330 1.2× 296 1.5× 89 3.6k
Ronald W. Pero Sweden 29 1.6k 2.2× 638 1.1× 208 0.5× 390 1.4× 259 1.3× 107 2.8k
Francesca Maffei Italy 27 660 0.9× 615 1.0× 349 0.9× 138 0.5× 416 2.0× 79 2.0k
H.P. Witschi United States 20 408 0.6× 287 0.5× 186 0.5× 181 0.6× 223 1.1× 43 1.5k

Countries citing papers authored by John Whysner

Since Specialization
Citations

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

Fields of papers citing papers by John Whysner

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of John Whysner

This figure shows the co-authorship network connecting the top 25 collaborators of John Whysner. A scholar is included among the top collaborators of John Whysner 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 John Whysner. John Whysner 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.
2.
Whysner, John. (2019). The Alchemy of Disease. Columbia University Press eBooks. 1 indexed citations
3.
Huang, Sarah X.L., Marie‐Claude Jaurand, David W. Kamp, John Whysner, & Tom K. Hei. (2011). Role of Mutagenicity in Asbestos Fiber-Induced Carcinogenicity and Other Diseases. Journal of Toxicology and Environmental Health Part B. 14(1-4). 179–245. 118 indexed citations
4.
Gulati, Anthony P., Yang‐Ming Yang, David H. Harter, et al.. (2005). Mutant human tumor suppressor p53 modulates the activation of mitogen‐activated protein kinase and nuclear factor‐κB, but not c‐Jun N‐terminal kinase and activated protein‐1. Molecular Carcinogenesis. 45(1). 26–37. 23 indexed citations
5.
6.
Williams, Gary M., Michael J. Iatropoulos, & John Whysner. (1999). Safety Assessment of Butylated Hydroxyanisole and Butylated Hydroxytoluene as Antioxidant Food Additives. Food and Chemical Toxicology. 37(9-10). 1027–1038. 305 indexed citations
7.
Whysner, John, Peter Maimon Ross, C. Clifford Conaway, Lynne Verna, & Gary M. Williams. (1998). Evaluation of Possible Genotoxic Mechanisms for Acrylonitrile Tumorigenicity. Regulatory Toxicology and Pharmacology. 27(3). 217–239. 26 indexed citations
8.
Whysner, John. (1996). Vinyl chloride mechanistic data and risk assessment: DNA reactivity and cross-species quantitative risk extrapolation. Pharmacology & Therapeutics. 71(1-2). 7–28. 22 indexed citations
9.
Whysner, John & Gary M. Williams. (1996). Saccharin mechanistic data and risk assessment: Urine composition, enhanced cell proliferation, and tumor promotion. Pharmacology & Therapeutics. 71(1-2). 225–252. 39 indexed citations
10.
Whysner, John & Gary M. Williams. (1996). 2,3,7,8-Tetrachlorodibenzo-p-dioxin mechanistic data and risk assessment: Gene regulation, cytotoxicity, enhanced cell proliferation, and tumor promotion. Pharmacology & Therapeutics. 71(1-2). 193–223. 29 indexed citations
11.
Whysner, John, Lynne Verna, & Gary M. Williams. (1996). Benzidine mechanistic data and risk assessment: Species- and organ-specific metabolic activation. Pharmacology & Therapeutics. 71(1-2). 107–126. 45 indexed citations
12.
Williams, Gary M. & John Whysner. (1996). Epigenetic carcinogens: Evaluation and risk assessment. Experimental and Toxicologic Pathology. 48(2-3). 189–195. 50 indexed citations
13.
Whysner, John. (1996). Phenobarbital mechanistic data and risk assessment: Enzyme induction, enhanced cell proliferation, and tumor promotion. Pharmacology & Therapeutics. 71(1-2). 153–191. 188 indexed citations
14.
Whysner, John. (1996). d-Limonene mechanistic data and risk assessment: Absolute species-specific cytotoxicity, enhanced cell proliferation, and tumor promotion. Pharmacology & Therapeutics. 71(1-2). 127–136. 47 indexed citations
15.
Hard, Gordon C. & John Whysner. (1994). Risk Assessment ofd-Limonene: An Example of Male Rat-Specific Renal Tumorigens. Critical Reviews in Toxicology. 24(3). 231–254. 40 indexed citations
16.
Whysner, John, et al.. (1994). Dose response of promotion by butylated hydroxyanisole in chemically initiated tumours of the rat forestomach. Food and Chemical Toxicology. 32(3). 215–222. 70 indexed citations
17.
Whysner, John & Gary M. Williams. (1992). International cancer risk assessment: The impact of biologic mechanisms. Regulatory Toxicology and Pharmacology. 15(1). 41–50. 13 indexed citations
18.
Blaine, Jack, et al.. (1981). CLINICAL STATUS OF METHADYL ACETATE (LAAM). Annals of the New York Academy of Sciences. 362(1). 101–115. 13 indexed citations
19.
Harding, Boyd W., et al.. (1969). Biosynthesis of adrenal corticosteroids: energy metabolism and the hydroxylases. Advances in Enzyme Regulation. 7. 237–257. 24 indexed citations
20.
Whysner, John & Paul R. Saunders. (1966). Purification of the lethal fraction of the venom of the marine snail Conus californicus. Toxicon. 4(3). 177–181. 12 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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