Barbara Ikejiri
- Cancer Research top 10%
- Cancer, Hypoxia, and Metabolism 5
- Genetics top 10%
- Glioma Diagnosis and Treatment 3
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- Immune Cell Function and Interaction 7
- Immunotherapy and Immune Responses 5
- Oncology top 10%
- Cancer-related Molecular Pathways 4
- CAR-T cell therapy research 2
- Neurology top 10%
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- Hedgehog Signaling Pathway Studies 2
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- Endoplasmic Reticulum Stress and Disease 2
- Co-authors
- Edward H. OldfieldZhengping ZhuangEli KedarAbha SaxenaJ T RobertsonRussell R. LonserAlexander O. VortmeyerRonald B. Herberman
- Cited by
- Cancer ResearchGeneticsImmunology
- Partner nations
- United StatesUnited KingdomMalaysia
In The Last Decade
Barbara Ikejiri
28 papers receiving 874 citations
Peers
Comparison fields: 5 of 79
- Cancer Research 233
- Genetics 92
- Immunology 182
- Oncology 233
- Neurology 105
Countries citing papers authored by Barbara Ikejiri
This map shows the geographic impact of Barbara Ikejiri'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 Barbara Ikejiri with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Barbara Ikejiri more than expected).
Fields of papers citing papers by Barbara Ikejiri
This network shows the impact of papers produced by Barbara Ikejiri. 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 Barbara Ikejiri. The network helps show where Barbara Ikejiri may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Barbara Ikejiri, 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 | 2015 | 21 | |
| 2 | 2012 | 69 | |
| 3 | 2009 | 27 | |
| 4 | 2008 | 33 | |
| 5 | 2006 | 35 | |
| 6 | 2006 | 11 | |
| 7 | 2006 | 30 | |
| 8 | 2005 | 7 | |
| 9 | 2005 | 50 | |
| 10 | Developmental arrest of angioblastic lineage initiates tumorigenesis in von Hippel-Lindau disease. | 2003 | 80 |
| 11 | 2001 | 25 | |
| 12 | 1994 | 2 | |
| 13 | 1989 | 7 | |
| 14 | 1988 | 19 | |
| 15 | Opiate receptor mediated regulation of the immune response in vivo. | 1987 | 33 |
| 16 | 1986 | 15 | |
| 17 | 1983 | 11 | |
| 18 | 1982 | 50 | |
| 19 | 1982 | 30 | |
| 20 | 1976 | 15 |
About Barbara Ikejiri
Barbara Ikejiri is a scholar working on Developmental Neuroscience, Immunology and Cancer Research, having authored 28 papers that have together received 901 indexed citations. Recurring topics across this work include Immune Cell Function and Interaction (7 papers), Cancer, Hypoxia, and Metabolism (5 papers), Immunotherapy and Immune Responses (5 papers), Cancer-related Molecular Pathways (4 papers), Glioma Diagnosis and Treatment (3 papers), Hedgehog Signaling Pathway Studies (2 papers), CAR-T cell therapy research (2 papers) and Endoplasmic Reticulum Stress and Disease (2 papers). The work is most often cited by research in Cancer Research (233 citations), Genetics (92 citations) and Immunology (182 citations). Barbara Ikejiri has collaborated with scholars based in United States, United Kingdom and Malaysia. Frequent co-authors include Edward H. Oldfield, Zhengping Zhuang, Eli Kedar, Abha Saxena, J T Robertson, Russell R. Lonser, Alexander O. Vortmeyer, Ronald B. Herberman, Chunzhang Yang and W. Craig Clark.
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.