John T. Isaacs
Impact in
- Pulmonary and Respiratory Medicine top 0.05%
- Prostate Cancer Treatment and Research
- Prostate Cancer Diagnosis and Treatment
- Cancer Research top 0.2%
- Cancer, Lipids, and Metabolism
Papers in
-
- Prostate Cancer Treatment and Research 144
- Prostate Cancer Diagnosis and Treatment 35
-
- Cell death mechanisms and regulation 19
- Ubiquitin and proteasome pathways 13
- DNA Repair Mechanisms 12
- Co-authors
- Samuel R. Denmeade (84 shared papers)Natasha Kyprianou (8 shared papers)Donald S. Coffey (19 shared papers)Hugh F. English (7 shared papers)Natasha Kyprianou (15 shared papers)W. Nathaniel Brennen (27 shared papers)Jin‐Tang Dong (12 shared papers)Jasminka Vukanovic (7 shared papers)
- Journals
- The Prostate (79 papers)The Journal of Urology (19 papers)Cancer Research (14 papers)Endocrinology (9 papers)Journal of Medicinal Chemistry (4 papers)
- Partner nations
- United StatesJapanNetherlands
In The Last Decade
John T. Isaacs
323 papers receiving 21.7k citations
John T. Isaacs's Hit Papers
Peers
Comparison fields: 5 of 157
- Pulmonary and Respiratory Medicine 7.7k
- Cancer Research 3.3k
- Oncology 5.1k
- Urology 980
- Endocrinology, Diabetes and Metabolism 2.4k
Countries citing papers authored by John T. Isaacs
This map shows the geographic impact of John T. Isaacs'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 John T. Isaacs with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites John T. Isaacs more than expected).
Fields of papers citing papers by John T. Isaacs
This network shows the impact of papers produced by John T. Isaacs. 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 John T. Isaacs. The network helps show where John T. Isaacs may publish in the future.
Co-authors
The 25 scholars most cited alongside John T. Isaacs, 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 328 papers — load more, or switch the sort, to bring in the rest.
| # | Work | ||
|---|---|---|---|
| 1 | Hedgehog signalling in prostate regeneration, neoplasia and metastasis Hit paper breakdown → | 2004 | 828 |
| 2 | KAI1 , a Metastasis Suppressor Gene for Prostate Cancer on Human Chromosome 11p11.2 Hit paper breakdown → | 1995 | 678 |
| 3 | Activation of Programmed Cell Death in the Rat Ventral Prostate after Castration* Hit paper breakdown → | 1988 | 637 |
| 4 | 2002 | 468 | |
| 5 | Conversion of lytic to persistent alphavirus infection by the bcl-2 cellular oncogene Hit paper breakdown → | 1993 | 455 |
| 6 | Etiology and disease process of benign prostatic hyperplasia Hit paper breakdown → | 1989 | 449 |
| 7 | Programmed cell death during regression of PC-82 human prostate cancer following androgen ablation. | 1990 | 438 |
| 8 | Programmed cell death during regression of the MCF-7 human breast cancer following estrogen ablation. | 1991 | 398 |
| 9 | Establishment and characterization of seven dunning rat prostatic cancer cell lines and their use in developing methods for predicting metastatic abilities of prostatic cancers Hit paper breakdown → | 1986 | 374 |
| 10 | 1996 | 368 | |
| 11 | Adaptation versus selection as the mechanism responsible for the relapse of prostatic cancer to androgen ablation therapy as studied in the Dunning R-3327-H adenocarcinoma. | 1981 | 322 |
| 12 | 1984 | 306 | |
| 13 | Implication of cell kinetic changes during the progression of human prostatic cancer. | 1995 | 300 |
| 14 | The role of calcium, pH, and cell proliferation in the programmed (apoptotic) death of androgen-independent prostatic cancer cells induced by thapsigargin. | 1994 | 279 |
| 15 | 1989 | 237 | |
| 16 | Down-regulation of the KAI1 metastasis suppressor gene during the progression of human prostatic cancer infrequently involves gene mutation or allelic loss. | 1996 | 236 |
| 17 | 2012 | 229 | |
| 18 | 1990 | 214 | |
| 19 | 2008 | 208 | |
| 20 | 1990 | 206 |
About John T. Isaacs
John T. Isaacs is a scholar working on Pulmonary and Respiratory Medicine, Molecular Biology, Oncology, Endocrinology, Diabetes and Metabolism and Cancer Research, having authored 328 papers that have together received 22.6k indexed citations. Recurring topics across this work include Prostate Cancer Treatment and Research (144 papers), Hormonal and reproductive studies (50 papers), Prostate Cancer Diagnosis and Treatment (35 papers), Cancer, Lipids, and Metabolism (20 papers), Cell death mechanisms and regulation (19 papers), Cancer-related Molecular Pathways (16 papers), Ubiquitin and proteasome pathways (13 papers) and DNA Repair Mechanisms (12 papers). The work is most often cited by research in Pulmonary and Respiratory Medicine (7.7k citations), Cancer Research (3.3k citations), Oncology (5.1k citations), Urology (980 citations) and Endocrinology, Diabetes and Metabolism (2.4k citations). John T. Isaacs has collaborated with scholars based in United States, Japan and Netherlands. Frequent co-authors include Samuel R. Denmeade, Natasha Kyprianou, Donald S. Coffey, Hugh F. English, Natasha Kyprianou, W. Nathaniel Brennen, Jin‐Tang Dong, Jasminka Vukanovic, Yuzo Furuya and Susan L. Dalrymple. Their work appears in journals such as The Prostate, The Journal of Urology, Cancer Research, Endocrinology and Journal of Medicinal 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.