Sébastien Cagnol
- Molecular Biology top 5%
- Melanoma and MAPK Pathways 5
- Cell death mechanisms and regulation 4
- Protein Tyrosine Phosphatases 3
- PI3K/AKT/mTOR signaling in cancer 2
- Protein Kinase Regulation and GTPase Signaling 2
- Cancer Research top 10%
- Oncology top 5%
- Cancer Cells and Metastasis 2
- Toxicology top 5%
- Immunology top 10%
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- Cell Adhesion Molecules Research 3
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- Genetic factors in colorectal cancer 2
- Co-authors
- Jean‐Claude ChambardNathalie RivardJulie CarrierGilles PagèsPascal ColosettiFrédéric LucianoMagali HerrantArnaud Jacquel
- Partner nations
- CanadaFranceUnited States
In The Last Decade
Sébastien Cagnol
17 papers receiving 2.3k citations
Hit Papers
Peers
Comparison fields: 5 of 110
- Molecular Biology 1.5k
- Cancer Research 305
- Oncology 489
- Toxicology 50
- Immunology 308
Countries citing papers authored by Sébastien Cagnol
This map shows the geographic impact of Sébastien Cagnol'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 Sébastien Cagnol with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Sébastien Cagnol more than expected).
Fields of papers citing papers by Sébastien Cagnol
This network shows the impact of papers produced by Sébastien Cagnol. 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 Sébastien Cagnol. The network helps show where Sébastien Cagnol may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Sébastien Cagnol, 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 | 2020 | 5 | |
| 2 | 2019 | 19 | |
| 3 | 2018 | 24 | |
| 4 | 2015 | 131 | |
| 5 | 2014 | 142 | |
| 6 | 2013 | 16 | |
| 7 | 2013 | 36 | |
| 8 | 2012 | 68 | |
| 9 | 2011 | 57 | |
| 10 | 2010 | 14 | |
| 11 | 2010 | 57 | |
| 12 | ERK and cell death: Mechanisms of ERK‐induced cell death – apoptosis, autophagy and senescencebreakdown → | 2009 | 1080 |
| 13 | 2008 | 97 | |
| 14 | 2008 | 10 | |
| 15 | 2006 | 78 | |
| 16 | 2006 | 45 | |
| 17 | 2003 | 395 |
About Sébastien Cagnol
Sébastien Cagnol is a scholar working on Immunology and Allergy, Oncology and Molecular Biology, having authored 17 papers that have together received 2.3k indexed citations. Recurring topics across this work include Melanoma and MAPK Pathways (5 papers), Cell death mechanisms and regulation (4 papers), Protein Tyrosine Phosphatases (3 papers), Cell Adhesion Molecules Research (3 papers), Genetic factors in colorectal cancer (2 papers), PI3K/AKT/mTOR signaling in cancer (2 papers), Cancer Cells and Metastasis (2 papers) and Protein Kinase Regulation and GTPase Signaling (2 papers). The work is most often cited by research in Molecular Biology (1.5k citations), Cancer Research (305 citations) and Oncology (489 citations). Sébastien Cagnol has collaborated with scholars based in Canada, France and United States. Frequent co-authors include Jean‐Claude Chambard, Nathalie Rivard, Julie Carrier, Gilles Pagès, Pascal Colosetti, Frédéric Luciano, Magali Herrant, Arnaud Jacquel, Patrick Auberger and Ellen Van Obberghen‐Schilling. Their work appears in journals such as Molecular and Cellular Biology, Oncogene and The FASEB Journal.
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.