Peter P. Sayeski
- Molecular Biology top 10%
- Oncology top 5%
- Cardiology and Cardiovascular Medicine top 5%
- Genetics top 5%
- Endocrinology, Diabetes and Metabolism top 5%
- Co-authors
- Kenneth E. BernsteinMohammad AliJeffrey E. KudlowEric M. SandbergMario B. MarreroStuart J. FrankXianyue MaDavid J. Hayzer
- Topics
- Cytokine Signaling Pathways and Interactions (44 papers)Myeloproliferative Neoplasms: Diagnosis and Treatment (24 papers)Protein Kinase Regulation and GTPase Signaling (22 papers)
- Partner nations
- United StatesHungaryUnited Kingdom
In The Last Decade
Peter P. Sayeski
75 papers receiving 1.8k citations
Peers
Comparison fields: 5 of 93
- Molecular Biology 980
- Oncology 575
- Cardiology and Cardiovascular Medicine 334
- Genetics 314
- Endocrinology, Diabetes and Metabolism 285
Countries citing papers authored by Peter P. Sayeski
This map shows the geographic impact of Peter P. Sayeski'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 Peter P. Sayeski with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Peter P. Sayeski more than expected).
Fields of papers citing papers by Peter P. Sayeski
This network shows the impact of papers produced by Peter P. Sayeski. 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 Peter P. Sayeski. The network helps show where Peter P. Sayeski may publish in the future.
Co-authorship network of co-authors of Peter P. Sayeski
This figure shows the co-authorship network connecting the top 25 collaborators of Peter P. Sayeski. A scholar is included among the top collaborators of Peter P. Sayeski 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 Peter P. Sayeski. Peter P. Sayeski is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 11 | |
| 2 | 3 | |
| 3 | 55 | |
| 4 | 49 | |
| 5 | 9 | |
| 6 | 8 | |
| 7 | 21 | |
| 8 | 8 | |
| 9 | 10 | |
| 10 | 20 | |
| 11 | 9 | |
| 12 | 26 | |
| 13 | 9 | |
| 14 | 29 | |
| 15 | 45 | |
| 16 | 57 | |
| 17 | 188 | |
| 18 | 6 | |
| 19 | 140 | |
| 20 | 22 |
About Peter P. Sayeski
Peter P. Sayeski is a scholar working on Genetics, Oncology and Pharmacology, having authored 76 papers that have together received 1.8k indexed citations. Recurring topics across this work include Cytokine Signaling Pathways and Interactions (44 papers), Myeloproliferative Neoplasms: Diagnosis and Treatment (24 papers) and Protein Kinase Regulation and GTPase Signaling (22 papers). The work is most often cited by research in Genetics (314 citations), Oncology (575 citations) and Endocrinology, Diabetes and Metabolism (285 citations). Peter P. Sayeski has collaborated with scholars based in United States, Hungary and United Kingdom. Frequent co-authors include Kenneth E. Bernstein, Mohammad Ali, Jeffrey E. Kudlow, Eric M. Sandberg, Mario B. Marrero, Stuart J. Frank, Xianyue Ma, David J. Hayzer, Rebekah Baskin and Kai He. Their work appears in journals such as Nucleic Acids Research, Journal of Biological Chemistry and Blood.
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.