W. David Hankins
- Hematology top 2%
- Molecular Biology
- Genetics top 5%
- Genetics top 2%
- Physiology top 5%
- Co-authors
- Jerry L. SpivakAlison R. MoliternoStephen T. SawyerD H TroxlerSanford B. KrantzThomas A. KostS K RuscettiMark J. Koury
- Topics
- Virus-based gene therapy research (19 papers)Erythrocyte Function and Pathophysiology (18 papers)Erythropoietin and Anemia Treatment (16 papers)
- Cited by
- HematologyGeneticsVirology
- Partner nations
- United StatesUnited KingdomCanada
In The Last Decade
W. David Hankins
56 papers receiving 1.5k citations
Peers
Comparison fields: 5 of 77
- Hematology 584
- Molecular Biology 564
- Genetics 456
- Genetics 385
- Physiology 367
Countries citing papers authored by W. David Hankins
This map shows the geographic impact of W. David Hankins'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 W. David Hankins with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites W. David Hankins more than expected).
Fields of papers citing papers by W. David Hankins
This network shows the impact of papers produced by W. David Hankins. 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 W. David Hankins. The network helps show where W. David Hankins may publish in the future.
Co-authorship network of co-authors of W. David Hankins
This figure shows the co-authorship network connecting the top 25 collaborators of W. David Hankins. A scholar is included among the top collaborators of W. David Hankins 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 W. David Hankins. W. David Hankins is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 0 | |
| 2 | 44 | |
| 3 | 45 | |
| 4 | 16 | |
| 5 | 24 | |
| 6 | 24 | |
| 7 | 235 | |
| 8 | 10 | |
| 9 | 3 | |
| 10 | 9 | |
| 11 | 8 | |
| 12 | 3 | |
| 13 | 20 | |
| 14 | 1 | |
| 15 | Modification of erythropoiesis and hormone sensitivity by RNA tumor viruses. | 3 |
| 16 | 21 | |
| 17 | 21 | |
| 18 | 36 | |
| 19 | 102 | |
| 20 | Production of spleen focus-forming virus and murine leukemia virus by early erythroblasts after Friend virus infection. | 3 |
About W. David Hankins
W. David Hankins is a scholar working on Hematology, Genetics and Virology, having authored 57 papers that have together received 1.5k indexed citations. Recurring topics across this work include Virus-based gene therapy research (19 papers), Erythrocyte Function and Pathophysiology (18 papers) and Erythropoietin and Anemia Treatment (16 papers). The work is most often cited by research in Hematology (584 citations), Genetics (385 citations) and Virology (101 citations). W. David Hankins has collaborated with scholars based in United States, United Kingdom and Canada. Frequent co-authors include Jerry L. Spivak, Alison R. Moliterno, Stephen T. Sawyer, D H Troxler, Sanford B. Krantz, Thomas A. Kost, S K Ruscetti, Mark J. Koury, Edward M. Scolnick and JL Spivak. Their work appears in journals such as Nature, New England Journal of Medicine and Cell.
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.