A.M. Ford
Impact in
- Hematology top 10%
- Acute Myeloid Leukemia Research
-
- Immune Cell Function and Interaction
- T-cell and B-cell Immunology
Papers in
- Oncology 4
- Cancer-related Molecular Pathways 1
-
- Glycosylation and Glycoproteins Research 2
- Co-authors
- H. V. Molgaard (3 shared papers)Melvyn F. Greaves (2 shared papers)Andrew J. Furley (3 shared papers)Shuki Mizutani (3 shared papers)Sy Ha (3 shared papers)Hannah J. Gould (1 shared paper)M. F. Greaves (3 shared papers)Barry Toyonaga (1 shared paper)
- Journals
- The EMBO Journal (2 papers)Cancer (1 paper)British Journal of Cancer (1 paper)International Journal of Cancer (1 paper)Cell (1 paper)
- Partner nations
- United KingdomUnited StatesCanada
In The Last Decade
A.M. Ford
10 papers receiving 420 citations
Peers
Comparison fields: 5 of 36
- Hematology 133
- Immunology 215
- Genetics 94
- Pathology and Forensic Medicine 88
- Public Health, Environmental and Occupational Health 138
Countries citing papers authored by A.M. Ford
This map shows the geographic impact of A.M. Ford'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 A.M. Ford with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites A.M. Ford more than expected).
Fields of papers citing papers by A.M. Ford
This network shows the impact of papers produced by A.M. Ford. 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 A.M. Ford. The network helps show where A.M. Ford may publish in the future.
Co-authors
The 25 scholars most cited alongside A.M. Ford, 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 | 1986 | 181 | |
| 2 | 1983 | 92 | |
| 3 | 1986 | 44 | |
| 4 | Rapid intraclonal switch of lineage dominance in congenital leukaemia with a MLL gene rearrangement. | 1995 | 38 |
| 5 | 1986 | 26 | |
| 6 | 1999 | 24 | |
| 7 | 1988 | 21 | |
| 8 | 1992 | 19 | |
| 9 | 1992 | 2 | |
| 10 | 2000 | 1 |
About A.M. Ford
A.M. Ford is a scholar working on Oncology, Molecular Biology, Hematology, Immunology and Genetics, having authored 10 papers that have together received 448 indexed citations. Recurring topics across this work include Acute Myeloid Leukemia Research (3 papers), Immune Cell Function and Interaction (2 papers), Glycosylation and Glycoproteins Research (2 papers), T-cell and B-cell Immunology (2 papers), Lymphoma Diagnosis and Treatment (1 paper), Mast cells and histamine (1 paper), Chronic Myeloid Leukemia Treatments (1 paper) and Cancer-related Molecular Pathways (1 paper). The work is most often cited by research in Hematology (133 citations), Immunology (215 citations), Genetics (94 citations), Pathology and Forensic Medicine (88 citations) and Public Health, Environmental and Occupational Health (138 citations). A.M. Ford has collaborated with scholars based in United Kingdom, United States and Canada. Frequent co-authors include H. V. Molgaard, Melvyn F. Greaves, Andrew J. Furley, Shuki Mizutani, Sy Ha, Hannah J. Gould, M. F. Greaves, Barry Toyonaga, Cox Terhorst and Peter J. van den Elsen. Their work appears in journals such as The EMBO Journal, Cancer, British Journal of Cancer, International Journal of Cancer and Cell.
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.