Matthew Rowley
Impact in
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- Cancer Genomics and Diagnostics
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- Pancreatic and Hepatic Oncology Research
- Cancer-related Molecular Pathways
Papers in
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- DNA Repair Mechanisms 4
- Epigenetics and DNA Methylation 2
- Congenital heart defects research 2
- Signaling Pathways in Disease 1
- Protein Degradation and Inhibitors 1
- Developmental Biology and Gene Regulation 1
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- Microtubule and mitosis dynamics 3
- Co-authors
- Fergus J. Couch (5 shared papers)Gourish Mondal (4 shared papers)Ali Naderi (1 shared paper)Colleen Sinclair (1 shared paper)Jianmin Wu (2 shared papers)V. Shane Pankratz (2 shared papers)Akihiro Ohashi (2 shared papers)Lucia Guidugli (1 shared paper)
- Journals
- Developmental Cell (1 paper)Molecular Cell (1 paper)Breast Cancer Research and Treatment (1 paper)Leukemia Research (1 paper)Journal of Mammary Gland Biology and Neoplasia (1 paper)
- Partner nations
- United StatesFrance
In The Last Decade
Matthew Rowley
7 papers receiving 403 citations
Peers
Comparison fields: 5 of 53
- Cancer Research 89
- Oncology 140
- Cell Biology 78
- Molecular Biology 303
- Genetics 92
Countries citing papers authored by Matthew Rowley
This map shows the geographic impact of Matthew Rowley'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 Matthew Rowley with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Matthew Rowley more than expected).
Fields of papers citing papers by Matthew Rowley
This network shows the impact of papers produced by Matthew Rowley. 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 Matthew Rowley. The network helps show where Matthew Rowley may publish in the future.
Co-authors
The 25 scholars most cited alongside Matthew Rowley, 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 | 2003 | 111 | |
| 2 | 2004 | 81 | |
| 3 | 2012 | 68 | |
| 4 | 2011 | 59 | |
| 5 | 2009 | 43 | |
| 6 | 2012 | 37 | |
| 7 | 2007 | 8 |
About Matthew Rowley
Matthew Rowley is a scholar working on Molecular Biology, Cell Biology, Neurology, Oncology and Genetics, having authored 7 papers that have together received 407 indexed citations. Recurring topics across this work include DNA Repair Mechanisms (4 papers), Microtubule and mitosis dynamics (3 papers), Epigenetics and DNA Methylation (2 papers), Congenital heart defects research (2 papers), Signaling Pathways in Disease (1 paper), BRCA gene mutations in cancer (1 paper), Protein Degradation and Inhibitors (1 paper) and Developmental Biology and Gene Regulation (1 paper). The work is most often cited by research in Cancer Research (89 citations), Oncology (140 citations), Cell Biology (78 citations), Molecular Biology (303 citations) and Genetics (92 citations). Matthew Rowley has collaborated with scholars based in United States and France. Frequent co-authors include Fergus J. Couch, Gourish Mondal, Ali Naderi, Colleen Sinclair, Jianmin Wu, V. Shane Pankratz, Akihiro Ohashi, Lucia Guidugli, Fergus J. Couch and Lin Yang. Their work appears in journals such as Developmental Cell, Molecular Cell, Breast Cancer Research and Treatment, Leukemia Research and Journal of Mammary Gland Biology and Neoplasia.
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.