Petia Mitchell

12 papers receiving 493 citations

Peers

Petia Mitchell
Comparison fields: 5 of 55
  • Endocrinology, Diabetes and Metabolism 132
  • Oncology 178
  • Cancer Research 63
  • Cell Biology 56
  • Immunology 68
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Peter M. Broad United Kingdom
Michael Conner United States
Suja Pillai Australia
Siyang Dong China
Adviti Naik Qatar
Irene Delgado‐Sainz Spain
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Melanie A. Girondo United States
Jo Yeargin United States
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Countries citing papers authored by Petia Mitchell

Since Specialization
Citations

This map shows the geographic impact of Petia Mitchell'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 Petia Mitchell with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Petia Mitchell more than expected).

Fields of papers citing papers by Petia Mitchell

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Petia Mitchell. 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 Petia Mitchell. The network helps show where Petia Mitchell may publish in the future.

Co-authors

The 25 scholars most cited alongside Petia Mitchell, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.

Border = papers with Petia Mitchell Line = papers co-authored together Petia Mitchell links everyone, so they are left out of the graph.

All Works

12 of 12 papers shown
#Work
1 2009120
2 201790
3 201577
4 201173
5 201447
6 201331
7 201421
8 201519
9 202310
10 20157
11
AMG 479, a fully human anti IGF-1 receptor monoclonal antibody, is efficacious against Ewing’s sarcoma and osteosarcoma xenografts
20076
12
Inhibition of endocrine IGF-1 signaling in normal murine tissues and human tumor xenografts with AMG 479, a fully human anti IGF-1R monoclonal antibody
20074

About Petia Mitchell

Petia Mitchell is a scholar working on Endocrinology, Diabetes and Metabolism, Cancer Research, Oncology, Pulmonary and Respiratory Medicine and Molecular Biology, having authored 12 papers that have together received 505 indexed citations. Recurring topics across this work include Growth Hormone and Insulin-like Growth Factors (6 papers), Cancer, Hypoxia, and Metabolism (5 papers), Sarcoma Diagnosis and Treatment (2 papers), CAR-T cell therapy research (2 papers), Immunotherapy and Immune Responses (2 papers), Virus-based gene therapy research (2 papers), Metabolism, Diabetes, and Cancer (2 papers) and Neuroblastoma Research and Treatments (1 paper). The work is most often cited by research in Endocrinology, Diabetes and Metabolism (132 citations), Oncology (178 citations), Cancer Research (63 citations), Cell Biology (56 citations) and Immunology (68 citations). Petia Mitchell has collaborated with scholars based in United States, Germany and China. Frequent co-authors include Pedro Jose Beltran, Elaina E Cajulis, Frank J. Calzone, Robert Radinsky, Richard L. Kendall, Steven L. Vonderfecht, Brian Belmontes, Gordon E. Moody, John M. Lu and Joanne Man-Wai Ho. Their work appears in journals such as Molecular Cancer Therapeutics, Clinical Cancer Research, Journal for ImmunoTherapy of Cancer, Journal of Endocrinology and Journal of Pharmacology and Experimental Therapeutics.

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.

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