Diana C. Birle
- Molecular Biology top 10%
- Oncology top 5%
- Pulmonary and Respiratory Medicine top 5%
- Cancer Research top 5%
- Epidemiology top 10%
- Co-authors
- David W. HedleyTomas MustelinJosé BaselgaEileen D. AdamsonStefan S. De BuckThierry VirolleQinhua RuJordi Rodón
- Topics
- PI3K/AKT/mTOR signaling in cancer (7 papers)Protein Kinase Regulation and GTPase Signaling (3 papers)Cancer, Hypoxia, and Metabolism (2 papers)
- Cited by
- Cancer ResearchGeneticsOncology
- Partner nations
- CanadaUnited StatesIndia
In The Last Decade
Diana C. Birle
12 papers receiving 1.8k citations
Hit Papers
Peers
Comparison fields: 5 of 93
- Molecular Biology 1.2k
- Oncology 621
- Pulmonary and Respiratory Medicine 395
- Cancer Research 347
- Epidemiology 269
Countries citing papers authored by Diana C. Birle
This map shows the geographic impact of Diana C. Birle'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 Diana C. Birle with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Diana C. Birle more than expected).
Fields of papers citing papers by Diana C. Birle
This network shows the impact of papers produced by Diana C. Birle. 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 Diana C. Birle. The network helps show where Diana C. Birle may publish in the future.
Co-authorship network of co-authors of Diana C. Birle
This figure shows the co-authorship network connecting the top 25 collaborators of Diana C. Birle. A scholar is included among the top collaborators of Diana C. Birle 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 Diana C. Birle. Diana C. Birle is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 115 | |
| 2 | Phase I, Dose-Escalation Study of BKM120, an Oral Pan-Class I PI3K Inhibitor, in Patients With Advanced Solid Tumorsbreakdown → | 550 |
| 3 | 42 | |
| 4 | 52 | |
| 5 | 260 | |
| 6 | 24 | |
| 7 | 88 | |
| 8 | 138 | |
| 9 | 44 | |
| 10 | Carbonic anhydrase IX expression, hypoxia, and prognosis in patients with uterine cervical carcinomas. | 101 |
| 11 | 62 | |
| 12 | 349 |
About Diana C. Birle
Diana C. Birle is a scholar working on Genetics, Molecular Biology and Cancer Research, having authored 12 papers that have together received 1.8k indexed citations. Recurring topics across this work include PI3K/AKT/mTOR signaling in cancer (7 papers), Protein Kinase Regulation and GTPase Signaling (3 papers) and Cancer, Hypoxia, and Metabolism (2 papers). The work is most often cited by research in Cancer Research (347 citations), Genetics (243 citations) and Oncology (621 citations). Diana C. Birle has collaborated with scholars based in Canada, United States and India. Frequent co-authors include David W. Hedley, Tomas Mustelin, José Baselga, Eileen D. Adamson, Stefan S. De Buck, Thierry Virolle, Qinhua Ru, Jordi Rodón, David Demanse and Ian de Belle. Their work appears in journals such as Journal of Clinical Oncology, The Journal of Immunology and Nature Cell Biology.
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.