Beatrix Versmold
Impact in
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- Neurogenesis and neuroplasticity mechanisms
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- Cancer-related molecular mechanisms research
Papers in
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- DNA Repair Mechanisms 1
- Epigenetics and DNA Methylation 1
- Biomedical Text Mining and Ontologies 1
- Gene expression and cancer classification 1
- Wnt/β-catenin signaling in development and cancer 1
- Cell death mechanisms and regulation 1
- Bioinformatics and Genomic Networks 1
- Oncology 1
- Co-authors
- Rita K. Schmutzler (2 shared papers)Stefan A. Mann (1 shared paper)Irmgard D. Dietzel (1 shared paper)Rolf Heumann (1 shared paper)Susanne Motameny (1 shared paper)Richard E. Berger (1 shared paper)Jörg Felsberg (1 shared paper)Martin Hellmich (1 shared paper)
- Journals
- International Journal of Cancer (2 papers)Journal of Neuroinflammation (1 paper)Lecture notes in computer science (1 paper)
- Partner nations
- GermanyUnited States
In The Last Decade
Beatrix Versmold
4 papers receiving 122 citations
Peers
Comparison fields: 5 of 46
- Developmental Neuroscience 10
- Cancer Research 19
- Neurology 10
- Behavioral Neuroscience 4
- Oncology 27
Countries citing papers authored by Beatrix Versmold
This map shows the geographic impact of Beatrix Versmold'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 Beatrix Versmold with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Beatrix Versmold more than expected).
Fields of papers citing papers by Beatrix Versmold
This network shows the impact of papers produced by Beatrix Versmold. 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 Beatrix Versmold. The network helps show where Beatrix Versmold may publish in the future.
Co-authors
The 25 scholars most cited alongside Beatrix Versmold, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
| # | Work | ||
|---|---|---|---|
| 1 | 2007 | 59 | |
| 2 | 2008 | 39 | |
| 3 | 2008 | 18 | |
| 4 | 2011 | 8 |
About Beatrix Versmold
Beatrix Versmold is a scholar working on Molecular Biology, Oncology, Genetics, Infectious Diseases and Organic Chemistry, having authored 4 papers that have together received 124 indexed citations. Recurring topics across this work include DNA Repair Mechanisms (1 paper), Epigenetics and DNA Methylation (1 paper), Biomedical Text Mining and Ontologies (1 paper), Gene expression and cancer classification (1 paper), Genetic Syndromes and Imprinting (1 paper), Wnt/β-catenin signaling in development and cancer (1 paper), Cell death mechanisms and regulation (1 paper) and Bioinformatics and Genomic Networks (1 paper). The work is most often cited by research in Developmental Neuroscience (10 citations), Cancer Research (19 citations), Neurology (10 citations), Behavioral Neuroscience (4 citations) and Oncology (27 citations). Beatrix Versmold has collaborated with scholars based in Germany and United States. Frequent co-authors include Rita K. Schmutzler, Stefan A. Mann, Irmgard D. Dietzel, Rolf Heumann, Susanne Motameny, Richard E. Berger, Jörg Felsberg, Martin Hellmich, Juergen A. Hampl and Dieter Niederacher. Their work appears in journals such as International Journal of Cancer, Journal of Neuroinflammation and Lecture notes in computer science.
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.