Walid Awad
- Immunology top 5%
- Immune Cell Function and Interaction 8
- T-cell and B-cell Immunology 4
- Oncology top 10%
- CAR-T cell therapy research 3
- Cancer Immunotherapy and Biomarkers 2
- Cell Biology top 10%
- Endoplasmic Reticulum Stress and Disease 3
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- Diabetes and associated disorders 4
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- Research on Leishmaniasis Studies 1
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- Autophagy in Disease and Therapy 1
- Co-authors
- Linda M. HendershotPaul G. ThomasPradyot DashGeoffrey NealeBen YoungbloodArdiana MoustakiHossam A. AbdelsamedYiping Fan
- Cited by
- ImmunologyOncologyCell Biology
- Journals
- Science Translational Medicine (1 paper)The EMBO Journal (1 paper)Science Immunology (1 paper)
- Partner nations
- United StatesSouth KoreaUnited Kingdom
In The Last Decade
Walid Awad
10 papers receiving 1.1k citations
Hit Papers
Peers
Comparison fields: 5 of 78
- Immunology 586
- Oncology 405
- Cell Biology 158
- Cancer Research 107
- Molecular Biology 437
Countries citing papers authored by Walid Awad
This map shows the geographic impact of Walid Awad'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 Walid Awad with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Walid Awad more than expected).
Fields of papers citing papers by Walid Awad
This network shows the impact of papers produced by Walid Awad. 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 Walid Awad. The network helps show where Walid Awad may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Walid Awad, 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 | 2025 | 0 | |
| 2 | 2025 | 0 | |
| 3 | 2024 | 10 | |
| 4 | 2022 | 1 | |
| 5 | 2019 | 59 | |
| 6 | 2018 | 62 | |
| 7 | Metabolic signaling directs the reciprocal lineage decisions of αβ and γδ T cells | 2018 | 14 |
| 8 | 2018 | 86 | |
| 9 | De Novo Epigenetic Programs Inhibit PD-1 Blockade-Mediated T Cell Rejuvenationbreakdown → | 2017 | 567 |
| 10 | 2013 | 154 | |
| 11 | 2008 | 67 | |
| 12 | 2008 | 53 |
About Walid Awad
Walid Awad is a scholar working on Immunology, Cell Biology and Genetics, having authored 12 papers that have together received 1.1k indexed citations. Recurring topics across this work include Immune Cell Function and Interaction (8 papers), Diabetes and associated disorders (4 papers), T-cell and B-cell Immunology (4 papers), CAR-T cell therapy research (3 papers), Endoplasmic Reticulum Stress and Disease (3 papers), Cancer Immunotherapy and Biomarkers (2 papers), Research on Leishmaniasis Studies (1 paper) and Autophagy in Disease and Therapy (1 paper). The work is most often cited by research in Immunology (586 citations), Oncology (405 citations) and Cell Biology (158 citations). Walid Awad has collaborated with scholars based in United States, South Korea and United Kingdom. Frequent co-authors include Linda M. Hendershot, Paul G. Thomas, Pradyot Dash, Geoffrey Neale, Ben Youngblood, Ardiana Moustaki, Hossam A. Abdelsamed, Yiping Fan, Robert Carter and Hazem E. Ghoneim. Their work appears in journals such as Science Translational Medicine, The EMBO Journal, Science Immunology, The Journal of Immunology and Journal of Biological Chemistry.
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.