Katia Todoerti
- Molecular Biology top 5%
- Hematology top 1%
- Cancer Research top 2%
- Oncology top 5%
- Pathology and Forensic Medicine top 5%
- Co-authors
- Antonino NeriLuca AgnelliMarta LionettiSonia FabrisLaura MoscaGiorgio La NasaDomenica RonchettiLuigia Lombardi
- Topics
- Multiple Myeloma Research and Treatments (51 papers)Protein Degradation and Inhibitors (19 papers)Chronic Lymphocytic Leukemia Research (14 papers)
- Cited by
- HematologyCancer ResearchGenetics
- Partner nations
- ItalyUnited StatesUnited Kingdom
In The Last Decade
Katia Todoerti
104 papers receiving 2.5k citations
Peers
Comparison fields: 5 of 92
- Molecular Biology 1.8k
- Hematology 944
- Cancer Research 825
- Oncology 594
- Pathology and Forensic Medicine 429
Countries citing papers authored by Katia Todoerti
This map shows the geographic impact of Katia Todoerti'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 Katia Todoerti with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Katia Todoerti more than expected).
Fields of papers citing papers by Katia Todoerti
This network shows the impact of papers produced by Katia Todoerti. 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 Katia Todoerti. The network helps show where Katia Todoerti may publish in the future.
Co-authorship network of co-authors of Katia Todoerti
This figure shows the co-authorship network connecting the top 25 collaborators of Katia Todoerti. A scholar is included among the top collaborators of Katia Todoerti 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 Katia Todoerti. Katia Todoerti is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 3 | |
| 2 | 11 | |
| 3 | 12 | |
| 4 | 40 | |
| 5 | 6 | |
| 6 | 9 | |
| 7 | 16 | |
| 8 | 18 | |
| 9 | 37 | |
| 10 | 11 | |
| 11 | 44 | |
| 12 | 38 | |
| 13 | 10 | |
| 14 | 75 | |
| 15 | 5 | |
| 16 | 33 | |
| 17 | 17 | |
| 18 | 3 | |
| 19 | Transcription repression activity is associated with the type I isoform of the MMSET gene involved in the t(4;14) in multiple myeloma | 1 |
| 20 | 20 |
About Katia Todoerti
Katia Todoerti is a scholar working on Hematology, Cancer Research and Genetics, having authored 104 papers that have together received 2.5k indexed citations. Recurring topics across this work include Multiple Myeloma Research and Treatments (51 papers), Protein Degradation and Inhibitors (19 papers) and Chronic Lymphocytic Leukemia Research (14 papers). The work is most often cited by research in Hematology (944 citations), Cancer Research (825 citations) and Genetics (355 citations). Katia Todoerti has collaborated with scholars based in Italy, United States and United Kingdom. Frequent co-authors include Antonino Neri, Luca Agnelli, Marta Lionetti, Sonia Fabris, Laura Mosca, Giorgio La Nasa, Domenica Ronchetti, Luigia Lombardi, Pierfrancesco Tassone and Fortunato Morabito. Their work appears in journals such as Nucleic Acids Research, Journal of Clinical Oncology 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.