Saeed Eshtad
Impact in
- Cancer Research top 5%
- Cancer Genomics and Diagnostics
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- DNA Repair Mechanisms
- CRISPR and Genetic Engineering
- Epigenetics and DNA Methylation
- Genomics and Chromatin Dynamics
- RNA modifications and cancer
Papers in
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- DNA Repair Mechanisms 3
- Epigenetics and DNA Methylation 2
- RNA modifications and cancer 1
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- Cancer Genomics and Diagnostics 1
- Cancer, Hypoxia, and Metabolism 1
- Co-authors
- Thomas Helleday (2 shared papers)Serena Nik‐Zainal (1 shared paper)Torkild Visnes (1 shared paper)Johan Boström (1 shared paper)Sean G. Rudd (1 shared paper)Mikael Altun (1 shared paper)Josefine Palle (1 shared paper)Husen M. Umer (1 shared paper)
- Journals
- Leukemia (1 paper)Neurology Genetics (1 paper)Oncogenesis (1 paper)Nature Reviews Genetics (1 paper)
- Partner nations
- SwedenNorwayUnited Kingdom
In The Last Decade
Saeed Eshtad
4 papers receiving 576 citations
Saeed Eshtad's Hit Papers
Peers
Comparison fields: 5 of 64
- Cancer Research 325
- Molecular Biology 384
- Pathology and Forensic Medicine 98
- Oncology 135
- Genetics 120
Countries citing papers authored by Saeed Eshtad
This map shows the geographic impact of Saeed Eshtad'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 Saeed Eshtad with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Saeed Eshtad more than expected).
Fields of papers citing papers by Saeed Eshtad
This network shows the impact of papers produced by Saeed Eshtad. 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 Saeed Eshtad. The network helps show where Saeed Eshtad may publish in the future.
Co-authors
The 25 scholars most cited alongside Saeed Eshtad, 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 | Mechanisms underlying mutational signatures in human cancers Hit paper breakdown → | 2014 | 551 |
| 2 | 2016 | 15 | |
| 3 | 2022 | 14 | |
| 4 | 2021 | 2 |
About Saeed Eshtad
Saeed Eshtad is a scholar working on Molecular Biology, Cancer Research, Cellular and Molecular Neuroscience, Public Health, Environmental and Occupational Health and Hematology, having authored 4 papers that have together received 582 indexed citations. Recurring topics across this work include DNA Repair Mechanisms (3 papers), Epigenetics and DNA Methylation (2 papers), Cancer Genomics and Diagnostics (1 paper), Cancer, Hypoxia, and Metabolism (1 paper), Acute Myeloid Leukemia Research (1 paper), Genetic Neurodegenerative Diseases (1 paper), Acute Lymphoblastic Leukemia research (1 paper) and RNA modifications and cancer (1 paper). The work is most often cited by research in Cancer Research (325 citations), Molecular Biology (384 citations), Pathology and Forensic Medicine (98 citations), Oncology (135 citations) and Genetics (120 citations). Saeed Eshtad has collaborated with scholars based in Sweden, Norway and United Kingdom. Frequent co-authors include Thomas Helleday, Serena Nik‐Zainal, Torkild Visnes, Johan Boström, Sean G. Rudd, Mikael Altun, Josefine Palle, Husen M. Umer, Janne Lehtiö and Anna Eriksson. Their work appears in journals such as Leukemia, Neurology Genetics, Oncogenesis and Nature Reviews Genetics.
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.