Stephen K. Tahir
- Molecular Biology top 5%
- Oncology top 5%
- Immunology top 10%
- Genetics top 5%
- Hematology top 5%
- Co-authors
- Saul H. RosenbergChristin TseHaichao ZhangStephen W. FesikXiufen YangMark G. AndersonSteven W. ElmoreSha Jin
- Topics
- Cell death mechanisms and regulation (13 papers)Chronic Lymphocytic Leukemia Research (6 papers)Microtubule and mitosis dynamics (5 papers)
- Cited by
- OncologyMolecular BiologyGenetics
- Partner nations
- United StatesUnited KingdomCanada
In The Last Decade
Stephen K. Tahir
33 papers receiving 3.2k citations
Hit Papers
Peers
Comparison fields: 5 of 105
- Molecular Biology 2.4k
- Oncology 980
- Immunology 391
- Genetics 344
- Hematology 337
Countries citing papers authored by Stephen K. Tahir
This map shows the geographic impact of Stephen K. Tahir'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 Stephen K. Tahir with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Stephen K. Tahir more than expected).
Fields of papers citing papers by Stephen K. Tahir
This network shows the impact of papers produced by Stephen K. Tahir. 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 Stephen K. Tahir. The network helps show where Stephen K. Tahir may publish in the future.
Co-authorship network of co-authors of Stephen K. Tahir
This figure shows the co-authorship network connecting the top 25 collaborators of Stephen K. Tahir. A scholar is included among the top collaborators of Stephen K. Tahir 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 Stephen K. Tahir. Stephen K. Tahir 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 | 9 | |
| 3 | 32 | |
| 4 | 1 | |
| 5 | 55 | |
| 6 | 8 | |
| 7 | 142 | |
| 8 | 43 | |
| 9 | 119 | |
| 10 | 59 | |
| 11 | 100 | |
| 12 | ABT-263: A Potent and Orally Bioavailable Bcl-2 Family Inhibitorbreakdown → | 1513 |
| 13 | 250 | |
| 14 | 53 | |
| 15 | 101 | |
| 16 | Abrogation of G2 checkpoint specifically sensitize p53 defective cells to cancer chemotherapeutic agents. | 28 |
| 17 | 169 | |
| 18 | 7 | |
| 19 | 25 | |
| 20 | 54 |
About Stephen K. Tahir
Stephen K. Tahir is a scholar working on Hematology, Genetics and Oncology, having authored 35 papers that have together received 3.3k indexed citations. Recurring topics across this work include Cell death mechanisms and regulation (13 papers), Chronic Lymphocytic Leukemia Research (6 papers) and Microtubule and mitosis dynamics (5 papers). The work is most often cited by research in Oncology (980 citations), Molecular Biology (2.4k citations) and Genetics (344 citations). Stephen K. Tahir has collaborated with scholars based in United States, United Kingdom and Canada. Frequent co-authors include Saul H. Rosenberg, Christin Tse, Haichao Zhang, Stephen W. Fesik, Xiufen Yang, Mark G. Anderson, Steven W. Elmore, Sha Jin, Alexander R. Shoemaker and Paul Nimmer. Their work appears in journals such as Journal of Biological Chemistry, Blood and Cancer Research.
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.