The MAD1 1673 G→A polymorphism alters the function of the mitotic spindle assembly checkpoint and is associated with a worse response to induction chemotherapy and sensitivity to treatment in patients with advanced epithelial ovarian cancer

BACKGROUNDMitotic arrest deficient 1 (MAD1), a protein of the mitotic spindle assembly checkpoint (SAC), recognizes MAD2 through two leucine zippers, transporting and activating MAD2, which promotes a metaphase arrest signal. A single nucleotide polymorphism of MAD1 was found to affect the SAC funct...

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Veröffentlicht in:	Pharmacogenetics and genomics 2013-04, Vol.23 (4), p.190-199
Hauptverfasser:	Santibáñez, Miguel, Gallardo, Dolores, Morales, Flavia, López, Alejandro, Prada, Diddier, Mendoza, Julia, Castro, Clementina, de León, David Cantú, Oñate, Luis F, Perez, Delia, Mohar, Alejandro, Herrera, Luis A
Format:	Artikel
Sprache:	eng
Schlagworte:	Biomarkers, Pharmacological Calcium-Binding Proteins - genetics Carcinoma, Ovarian Epithelial Cell Cycle Proteins - genetics Chromosomal Instability - drug effects Chromosomal Instability - genetics Female Genetic Association Studies Humans M Phase Cell Cycle Checkpoints - drug effects M Phase Cell Cycle Checkpoints - genetics Mad2 Proteins Microtubules - pathology Neoplasm Staging Neoplasms, Glandular and Epithelial - drug therapy Neoplasms, Glandular and Epithelial - genetics Neoplasms, Glandular and Epithelial - pathology Nocodazole - pharmacology Nuclear Proteins - genetics Ovarian Neoplasms - drug therapy Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology Paclitaxel - pharmacology Polymorphism, Single Nucleotide Repressor Proteins - genetics
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