L
Luis J Leandro-García
Researcher at Memorial Sloan Kettering Cancer Center
Publications - 38
Citations - 2430
Luis J Leandro-García is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Paraganglioma & Medicine. The author has an hindex of 19, co-authored 32 publications receiving 2132 citations. Previous affiliations of Luis J Leandro-García include Autonomous University of Madrid & Carlos III Health Institute.
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Journal ArticleDOI
Exome sequencing identifies MAX mutations as a cause of hereditary pheochromocytoma
Iñaki Comino-Méndez,Francisco Javier Gracia-Aznarez,Francesca Schiavi,Iñigo Landa,Luis J Leandro-García,Rocío Letón,Emiliano Honrado,Rocío Ramos-Medina,Daniela Caronia,Guillermo Pita,Álvaro Gómez-Graña,Aguirre A. de Cubas,Lucía Inglada-Pérez,Agnieszka Maliszewska,Elisa Taschin,Sara Bobisse,Giuseppe Pica,Paola Loli,Rafael Hernández-Lavado,José Ángel Díaz,Mercedes Gómez-Morales,Anna González-Neira,Giovanna Roncador,Cristina Rodríguez-Antona,Javier Benitez,Massimo Mannelli,Giuseppe Opocher,Mercedes Robledo,Alberto Cascón +28 more
TL;DR: The involvement of the MYC-MAX-MXD1 network in the development and progression of neural crest cell tumors is supported and the lack of functional MAX in rat PCC (PC12) cells is supported, which suggests that loss of MAX function is correlated with metastatic potential.
Journal ArticleDOI
Tumoral and tissue-specific expression of the major human beta-tubulin isotypes.
Luis J Leandro-García,Susanna Leskelä,Iñigo Landa,Cristina Montero-Conde,Elena López-Jiménez,Rocío Letón,Alberto Cascón,Mercedes Robledo,Cristina Rodríguez-Antona +8 more
TL;DR: A quantitative RT‐PCR technique is developed that accurately determines the mRNA expression of the eight human β‐tubulin isotypes, encoding class I, IIa, IIb, III, IVa, IVb, V, and VI and applied to 21 nontumoral tissues and 79 tumor samples belonging to seven cancer types.
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Single nucleotide polymorphism associations with response and toxic effects in patients with advanced renal-cell carcinoma treated with first-line sunitinib: a multicentre, observational, prospective study
Jesús García-Donas,Emilio Esteban,Luis J Leandro-García,Daniel Castellano,Aranzazu Gonzalez del Alba,Miguel Angel Climent,Jose Angel Arranz,Enrique Gallardo,Javier Puente,Joaquim Bellmunt,Begoña Mellado,Esther Martínez,Fernando Salvador Moreno,Albert Font,Mercedes Robledo,Cristina Rodríguez-Antona +15 more
TL;DR: Polymorphisms in VEGFR3 and CYP3A5*1 might be able to define a subset of patients with renal-cell carcinoma with decreased sunitinib response and tolerability, and should promote interventional studies testing alternative therapeutic approaches for patients with such variants.
Journal ArticleDOI
The miR-200 family controls beta-tubulin III expression and is associated with paclitaxel-based treatment response and progression-free survival in ovarian cancer patients.
Susanna Leskelä,Luis J Leandro-García,Marta Mendiola,Jorge Barriuso,Lucía Inglada-Pérez,Iván Muñoz,Beatriz Martinez-Delgado,Andrés Redondo,Javier De Santiago,Mercedes Robledo,David Hardisson,Cristina Rodríguez-Antona +11 more
TL;DR: It is demonstrated that patients with a high expression of the miR-200 family show low levels of β-tubulin class III in ovarian carcinomas, and these microRNAs might constitute the biomarkers of response to paclitaxel-based treatments and relapse/progression of advanced stage ovarian carcinoma patients.
Journal ArticleDOI
Tumoral EPAS1 (HIF2A) mutations explain sporadic pheochromocytoma and paraganglioma in the absence of erythrocytosis
Iñaki Comino-Méndez,Aguirre A. de Cubas,Carmen Bernal,Cristina Álvarez-Escolá,Carolina Sánchez-Malo,César L. Ramírez-Tortosa,Susana Pedrinaci,Elena Rapizzi,Tonino Ercolino,Giampaolo Bernini,Alessandra Bacca,Rocío Letón,Guillermoó Pita,María R Alonso,Luis J Leandro-García,Álvaro Gómez-Graña,Lucía Inglada-Pérez,Veronika Mancikova,Cristina Rodríguez-Antona,Massimo Mannelli,Mercedes Robledo,Alberto Cascón +21 more
TL;DR: The finding that EPAS1 is involved in the sporadic presentation of the disease not only increases the percentage of PCCs/PGLs with known driver mutations, but also highlights the relevance of studying other hypoxia-related genes in apparently sporadic tumors.