Peter C. Adamson
· Assistant ProfessorVerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 1984–2025
About
Peter C. Adamson, MD, is an Emeritus Professor and the Chief of Pediatrics (Oncology) at the University of Pennsylvania's Perelman School of Medicine. His primary research focus has been on pediatric cancer drug development, specifically early phase clinical trials and clinical pharmacologic studies. He has contributed significantly to the field of pediatric oncology, with expertise in clinical pharmacology and drug development. Dr. Adamson has been involved in advancing therapies for children with refractory solid tumors and leukemia, and his work includes the development and testing of novel drugs and treatment protocols. He is also recognized for his leadership in pediatric oncology research and his role as the Global Head of Oncology Development & Pediatric Innovation at Sanofi.
Research topics
- Medicine
- Oncology
- Internal medicine
- Computer Science
- Biology
- Cancer research
- Genetics
- Immunology
Selected publications
Enhanced retinal pigment epithelial cells as a delivery vehicle for retinal disease
Molecular Therapy — Methods & Clinical Development · 2025-03-14
articleOpen accessAge-related macular degeneration (AMD) represents a major global health burden, with current estimates suggesting that up to 200 million people are affected globally. While effective treatments exist for the exudative form of the disease termed choroidal neovascular AMD, there remain challenges associated with long-term responses to treatment and the ongoing parallel development of the non-exudative form of AMD. Here, we sought to develop an approach for long-term delivery of both aflibercept, a decoy receptor that neutralises vascular endothelial growth factor and a concomitant treatment focused on treating the non-exudative form of AMD. To this end, we developed a series of induced pluripotent stem cell (iPS)-derived retinal pigment epithelial (RPE) cell lines that stably expressed aflibercept and/or sCD59. These cell lines were shown to produce high concentrations of both proteins. Sub-retinal injection of enhanced RPE cells potently prevented leakage of neovascular lesions in the JR5558 mouse model of retinal and choroidal neovascularization. Early results described here suggest that enhanced iPS-derived RPE cells could represent a novel approach to the long-term delivery of therapeutic agents to the eye.
Collaborative Innovations in Childhood Cancer Therapies
Handbook of experimental pharmacology · 2024-01-01
reviewSenior authorArchiv für Geschichte der Philosophie · 2024-03-05
articleOpen accessHeart Lung and Circulation · 2024-07-28 · 2 citations
articleOpen accessSenior authorArchiv für Geschichte der Philosophie · 2024-06-06
articleOpen access2023-03-31
preprintOpen access<p>Supp Table 1</p>
2023-03-31
preprintOpen access<p>PDF file, 38K, Plasma soluble VEGFR2 (A) and Placental Growth Factor (B) concentrations prior to therapy (baseline) and at the end of cycle 1 (steady state).</p>
2023-03-31
preprintOpen access<div>AbstractPurpose:<p>Anaplastic lymphoma kinase (ALK) aberrations are a promising target for patients with neuroblastoma. We assessed the activity of first-generation ALK inhibitor crizotinib in patients with no known curative treatments and whose tumors harbored an activating ALK alteration.</p>Patients and Methods:<p>Twenty patients with relapsed/refractory ALK-positive neuroblastoma received crizotinib at the recommended phase II dose of 280 mg/m<sup>2</sup>/dose. A Simon two-stage design was used to evaluate the antitumor activity of crizotinib monotherapy. Response evaluation occurred after cycles 1, 3, 5, 7, and then every 3 cycles. Correlation of ALK status and response was a secondary aim of the study.</p>Results:<p>The objective response rate for patients with neuroblastoma was 15% [95% confidence interval (CI): 3.3%–34.3%]: two with partial responses and 1 with a complete response. All three patients had a somatic ALK Arg1275Gln mutation, the most common ALK hotspot mutation observed in neuroblastoma and the only mutation predicted to be sensitive to ALK inhibition with crizotinib. Two patients had prolonged stable disease (10 and 13 cycles, respectively); both harbored an ALK Arg1275Gln mutation. Three patients with ALK Phe1174Leu mutations progressed during cycle 1 of therapy, and one patient with an ALK Phe1174Val received three cycles before disease progression. The two patients with ALK amplification had no response. The most common adverse event was a decrease in neutrophil count.</p>Conclusions:<p>Despite limited activity seen in this trial, we conclude that this is more likely due to an inability to reach the higher concentrations of crizotinib needed to overcome the competing ATP affinity.</p><p><i>See related commentary by Schulte and Eggert, p. 3507</i></p></div>
2023-03-31
preprintOpen access<div>AbstractPurpose:<p>Anaplastic lymphoma kinase (ALK) aberrations are a promising target for patients with neuroblastoma. We assessed the activity of first-generation ALK inhibitor crizotinib in patients with no known curative treatments and whose tumors harbored an activating ALK alteration.</p>Patients and Methods:<p>Twenty patients with relapsed/refractory ALK-positive neuroblastoma received crizotinib at the recommended phase II dose of 280 mg/m<sup>2</sup>/dose. A Simon two-stage design was used to evaluate the antitumor activity of crizotinib monotherapy. Response evaluation occurred after cycles 1, 3, 5, 7, and then every 3 cycles. Correlation of ALK status and response was a secondary aim of the study.</p>Results:<p>The objective response rate for patients with neuroblastoma was 15% [95% confidence interval (CI): 3.3%–34.3%]: two with partial responses and 1 with a complete response. All three patients had a somatic ALK Arg1275Gln mutation, the most common ALK hotspot mutation observed in neuroblastoma and the only mutation predicted to be sensitive to ALK inhibition with crizotinib. Two patients had prolonged stable disease (10 and 13 cycles, respectively); both harbored an ALK Arg1275Gln mutation. Three patients with ALK Phe1174Leu mutations progressed during cycle 1 of therapy, and one patient with an ALK Phe1174Val received three cycles before disease progression. The two patients with ALK amplification had no response. The most common adverse event was a decrease in neutrophil count.</p>Conclusions:<p>Despite limited activity seen in this trial, we conclude that this is more likely due to an inability to reach the higher concentrations of crizotinib needed to overcome the competing ATP affinity.</p><p><i>See related commentary by Schulte and Eggert, p. 3507</i></p></div>
2023-03-31
preprintOpen accessCCR Translation for This Article from A Phase I Trial and Pharmacokinetic Study of Aflibercept (VEGF Trap) in Children with Refractory Solid Tumors: A Children's Oncology Group Phase I Consortium Report
Recent grants
COG NCTN Network Group Operations Center - Year 11 STAR Act MCI and PEC Supplement
NIH · $398.6M · 2014–2026
NIH · $28.2M · 2012
NIH · $1.4M · 2016
NIH · $1.6M · 2003
NIH · $335.5M · 2015
Frequent coauthors
- 1500 shared
Susan M. Blaney
Children's Cancer Center
- 832 shared
Ashish M. Ingle
- 617 shared
Joel M. Reid
Mayo Clinic in Florida
- 512 shared
Mark Krailo
- 450 shared
Charlotte H. Ahern
- 436 shared
Julia L. Glade Bender
Memorial Sloan Kettering Cancer Center
- 432 shared
Sylvain Baruchel
University of Toronto
- 384 shared
Frank M. Balis
Children's Hospital of Philadelphia
Education
- 1980
B.A., Chemistry
Wesleyan University
- 1984
M.D., Medicine
Cornell University Medical College
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