• Antonio Bandala-Jacques, Irwin A Hernández-Cruz, Clementina Castro-Hernández, José Díaz-Chávez, Cristian Arriaga-Canon, Salim A Barquet-Muñoz, Diddier G Prada-Ortega, David Cantú-de León, and Luis A Herrera.
• Cancer Biomedical Research Unit, Instituto Nacional de Cancerología, SSA-Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México (UNAM), Mexico City, Mexico.
• Rev Invest Clin. 2020 Dec 22; 72 (6): 372-379.

BackgroundOvarian cancer is the most lethal gynecologic cancer. Although most patients respond adequately to the first-line therapy, up to 85% experience a recurrence of disease, which carries a poor prognosis. Mitotic arrest deficiency 1 is a protein that helps in the assembly of the mitotic spindle assembly checkpoint by preventing anaphase until all chromatids are properly aligned. A single-nucleotide polymorphism in the MAD1L1 gene is prevalent in patients with advanced epithelial ovarian cancer and alters the way in which it responds to chemotherapy.ObjectiveThe objective of the study was to study the relationship between the rs1801368 polymorphism of MAD1L1 and prognosis of ovarian adenocarcinoma.MethodsA total of 118 patients in whom the MAD1L1 gene was sequenced were analyzed using descriptive and comparative statistics.ResultsPatients carrying the wild-type genotype had a higher distribution of early-stage disease. Having a MAD1L1 polymorphic allele increased the risk of being non-sensitive to chemotherapy. The median disease-free survival for patients with the wild-type MAD1L1 was 46.93 months, compared to 10.4 months for patients with at least one polymorphic allele.ConclusionsThe rs1801368 polymorphism of MAD1L1 gene worsens prognosis in patients with ovarian adenocarcinoma. Traditional therapy for ovarian cancer might not be optimal in patients carrying this polymorphism.

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