B Bödey
Impact in
- Genetics top 5%
- Virus-based gene therapy research
- Glioma Diagnosis and Treatment
- Immunology top 5%
- Immunotherapy and Immune Responses
- T-cell and B-cell Immunology
Papers in
- Genetics 18
- Glioma Diagnosis and Treatment 18
- Immunology 20
- T-cell and B-cell Immunology 16
- Immunotherapy and Immune Responses 4
- Co-authors
- Stuart E. Siegel (32 shared papers)Hans Elmar Kaiser (25 shared papers)H. E. Kaiser (10 shared papers)László K. Csatáry (4 shared papers)József Szeberényi (2 shared papers)Zsolt Fábián (2 shared papers)Georg Gosztonyi (1 shared paper)H E Kaiser (6 shared papers)
- Journals
- Expert Opinion on Biological Therapy (7 papers)Cancer (2 papers)Expert Opinion on Therapeutic Targets (1 paper)Journal of Neuro-Oncology (1 paper)Critical Reviews in Oncology/Hematology (1 paper)
- Partner nations
- United StatesGermanyHungary
In The Last Decade
B Bödey
93 papers receiving 2.0k citations
Peers
Comparison fields: 5 of 71
- Genetics 205
- Immunology 328
- Cancer Research 131
- Genetics 232
- Oncology 172
Countries citing papers authored by B Bödey
This map shows the geographic impact of B Bödey'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 B Bödey with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites B Bödey more than expected).
Fields of papers citing papers by B Bödey
This network shows the impact of papers produced by B Bödey. 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 B Bödey. The network helps show where B Bödey may publish in the future.
Co-authors
The 25 scholars most cited alongside B Bödey, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
Showing the 20 most-cited of 93 papers — load more, or switch the sort, to bring in the rest.
| # | Work | ||
|---|---|---|---|
| 1 | 2004 | 170 | |
| 2 | Involution of the mammalian thymus, one of the leading regulators of aging. | 1998 | 124 |
| 3 | Failure of cancer vaccines: the significant limitations of this approach to immunotherapy. | 2000 | 124 |
| 4 | Attenuated veterinary virus vaccine for the treatment of cancer. | 1993 | 98 |
| 5 | Over-expression of endoglin (CD105): a marker of breast carcinoma-induced neo-vascularization. | 1998 | 82 |
| 6 | Clinical and prognostic significance of the expression of the c-erbB-2 and c-erbB-3 oncoproteins in primary and metastatic malignant melanomas and breast carcinomas. | 1997 | 57 |
| 7 | Invasion and metastasis: the expression and significance of matrix metalloproteinases in carcinomas of the lung. | 2001 | 50 |
| 8 | Matrix metalloproteinase expression in malignant melanomas: tumor-extracellular matrix interactions in invasion and metastasis. | 2001 | 49 |
| 9 | Immunocytochemical detection of endoglin is indicative of angiogenesis in malignant melanoma. | 1998 | 47 |
| 10 | 2000 | 46 | |
| 11 | 2002 | 44 | |
| 12 | Induction of apoptosis by a Newcastle disease virus vaccine (MTH-68/H) in PC12 rat phaeochromocytoma cells. | 2001 | 38 |
| 13 | Upregulation of endoglin (CD105) expression during childhood brain tumor-related angiogenesis. Anti-angiogenic therapy. | 1998 | 36 |
| 14 | Novel insights into the function of the thymic Hassall's bodies. | 2000 | 36 |
| 15 | Immunophenotypically varied cell subpopulations in primary and metastatic human melanomas. Monoclonal antibodies for diagnosis, detection of neoplastic progression and receptor directed immunotherapy. | 1996 | 35 |
| 16 | Spontaneous neoplastic regression: the significance of apoptosis. | 2001 | 34 |
| 17 | Dendritic type, accessory cells within the mammalian thymic microenvironment. Antigen presentation in the dendritic neuro-endocrine-immune cellular network. | 1997 | 32 |
| 18 | Epidermal growth factor receptor (EGFR) expression in childhood brain tumors. | 2005 | 32 |
| 19 | 1992 | 31 | |
| 20 | Immunocytochemical detection of the homeobox B3, B4, and C6 gene products in childhood medulloblastomas/primitive neuroectodermal tumors. | 2000 | 31 |
About B Bödey
B Bödey is a scholar working on Genetics, Immunology, Cancer Research, Oncology and Molecular Biology, having authored 93 papers that have together received 2.1k indexed citations. Recurring topics across this work include Glioma Diagnosis and Treatment (18 papers), T-cell and B-cell Immunology (16 papers), Protease and Inhibitor Mechanisms (10 papers), Cell death mechanisms and regulation (5 papers), Angiogenesis and VEGF in Cancer (4 papers), Immunotherapy and Immune Responses (4 papers), Monoclonal and Polyclonal Antibodies Research (3 papers) and Sarcoma Diagnosis and Treatment (2 papers). The work is most often cited by research in Genetics (205 citations), Immunology (328 citations), Cancer Research (131 citations), Genetics (232 citations) and Oncology (172 citations). B Bödey has collaborated with scholars based in United States, Germany and Hungary. Frequent co-authors include Stuart E. Siegel, Hans Elmar Kaiser, H. E. Kaiser, László K. Csatáry, József Szeberényi, Zsolt Fábián, Georg Gosztonyi, H E Kaiser, James V. Luck and C R Taylor. Their work appears in journals such as Expert Opinion on Biological Therapy, Cancer, Expert Opinion on Therapeutic Targets, Journal of Neuro-Oncology and Critical Reviews in Oncology/Hematology.
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.