Priscila Villalvazo
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Priscila Villalvazo has a total of 14 co-authors. Here are the top co-authors by number of shared publications:
- Aitana Calvo
Servicio de Oncología Médica, Instituto de Investigación Sanitaria Gregorio Marañón, CiberOnc, Hospital General Universitario Gregorio Marañón, Universidad Complutense de Madrid, 28007 Madrid, Spain
1 shared publication - Belen Marzal-Alfaro
Servicio de Farmacia, Instituto de Investigación Sanitaria Gregorio Marañón, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain
1 shared publication - Fabienne Thomas
Department of Pharmacology, Institut Claudius-Regaud, CRCT, Université de Toulouse, Inserm, UPS, 20-24, 31300 Toulouse, France
1 shared publication - Flora López-López
Servicio de Oncología Médica, Fundación de Investigación Sanitaria Doce de Octubre, Hospital Universitario Doce de Octubre, 28041 Madrid, Spain
1 shared publication - Iker Aguilar
Servicio de Oncología Médica, Instituto de Investigación Sanitaria Ramón y Cajal, Hospital Universitario Ramón y Cajal, 28034 Madrid, Spain
1 shared publication - José Luis Revuelta-Herrero
Hospital General Universitario Gregorio Marañón
1 shared publication
Latest Publications
- Open Access
- 13 August 2021
- Published by MDPI AG in Journal of Personalized Medicine
- Vol. 11 (8) , 792
DPYD Exome, mRNA Expression and Uracil Levels in Early Severe Toxicity to Fluoropyrimidines: An Extreme Phenotype Approach
Dihydropyrimidine dehydrogenase deficiency is a major cause of severe fluoropyrimidine-induced toxicity and could lead to interruption of chemotherapy or life-threatening adverse reactions. This study aimed to characterize the DPYD exon sequence, mRNA expression and in vivo DPD activity by plasma uracil concentration. It was carried out in two groups of patients with extreme phenotypes (toxicity versus control) newly treated with a fluoropyrimidine, during the first three cycles of treatment. A novel nonsense gene variant (c.2197insA) was most likely responsible for fluoropyrimidine-induced toxicity in one patient, while neither DPYD mRNA expression nor plasma uracil concentration was globally associated with early toxicity. Our present work may help improve pharmacogenetic testing to avoid severe and undesirable adverse reactions to fluoropyrimidine treatment and it also supports the idea of looking beyond DPYD.
- 13 August 2021
- Published by MDPI AG in Journal of Personalized Medicine
- Vol. 11 (8) , 792
Open AccessDPYD Exome, mRNA Expression and Uracil Levels in Early Severe Toxicity to Fluoropyrimidines: An Extreme Phenotype Approach
Dihydropyrimidine dehydrogenase deficiency is a major cause of severe fluoropyrimidine-induced toxicity and could lead to interruption of chemotherapy or life-threatening adverse reactions. This study aimed to characterize the DPYD exon sequence, mRNA expression and in vivo DPD activity by plasma uracil concentration. It was carried out in two groups of patients with extreme phenotypes (toxicity versus control) newly treated with a fluoropyrimidine, during the first three cycles of treatment. A novel nonsense gene variant (c.2197insA) was most likely responsible for fluoropyrimidine-induced toxicity in one patient, while neither DPYD mRNA expression nor plasma uracil concentration was globally associated with early toxicity. Our present work may help improve pharmacogenetic testing to avoid severe and undesirable adverse reactions to fluoropyrimidine treatment and it also supports the idea of looking beyond DPYD.