Marta Benet
New York University
6 Papers
20 Citations
Marta Benet is an academic researcher from New York University. The author has contributed to research in topics: Gene & Tumor suppressor gene. The author has an hindex of 4, co-authored 6 publications.
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Papers
Using Sindbis Viral Vectors for Specific Detection and Suppression of Advanced Ovarian Cancer in Animal Models
Jen-Chieh Tseng,Alicia Hurtado,Herman Yee,Brandi Levin,Christopher Boivin,Marta Benet,Stephanie V. Blank,Angel Pellicer,Daniel Meruelo +8 more
TL;DR: It is demonstrated through imaging, histologic, and molecular data that Sindbis vectors systemically and specifically infect/detect and kill metastasized tumors in the peritoneal cavity, leading to significant suppression of the carcinomatosis in both animal models.
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•Journal Article
rgr oncogene: activation by elimination of translational controls and mislocalization.
Inmaculada Hernandez-Muñoz,Marta Benet,Miguel Calero,Maria Jimenez,Roberto Diaz,Angel Pellicer +5 more
TL;DR: Results indicate that rgr is activated when its tight translational controls are eliminated and increased expression allows its relocation to the plasma membrane, where efficient activation of RAS occurs.
16
Endothelin-1-Mediated Drug Resistance in EGFR -Mutant Non-Small Cell Lung Carcinoma.
Ines Pulido,Stephen L. Ollosi,Salvador Aparisi,Jeffrey H. Becker,Alicia Aliena-Valero,Marta Benet,Maria L. Rodriguez,Adrián López,Eva Tamayo-Torres,Lourdes Chuliá-Peris,Juan Carlos García-Cañaveras,Margaret Soucheray,Annika Dalheim,Juan B. Salom,Wei Qiu,Simon Kaja,Javier Alcácer Fernández-Coronado,Sandra Alandes,Javier Alcácer,Fatima Al-Shahrour,Jeffrey A. Borgia,Oscar Juan,Michael I. Nishimura,Agustín Lahoz,Julian Carretero,Takeshi Shimamura +25 more
TL;DR: A simplistic endogenous yet previously unrealized resistance mechanism inherent to a subset of EGFR-mutant NSCLC to attenuate tyrosine kinase inhibitor delivery to the tumors by limiting drug-carrying blood flow and the drug concentration in tumors is described.
13
The Rgr oncogene induces tumorigenesis in transgenic mice.
Maria Jimenez,Ignacio Pérez de Castro,Marta Benet,Juan F. García,Giorgio Inghirami,Angel Pellicer +5 more
TL;DR: It is demonstrated that oncogenic Rgr can induce expression of p15ink4b and, more importantly, that both Rgr and p15INK4b cooperate in the malignant phenotype in vivo and are shown to act as a tumor suppressor gene.
13
Mouse p10, an alternative spliced form of p15INK4b, inhibits cell cycle progression and malignant transformation.
Ignacio Pérez de Castro,Marta Benet,Maria Jimenez,Saba Alzabin,Marcos Malumbres,Angel Pellicer +5 more
TL;DR: It is shown that mouse p10 is able to induce cell cycle arrest in a p53-dependent manner, and that these antitransforming properties of mouse p 10 are also p 53-dependent.
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