PARP Inhibitors in Ovarian Cancer

To the Editor: In the PRIMA (PRIMA/ENGOT-OV26/GOG-3012) trial conducted by González-Martín et al. (Dec. 19 issue), 1 the test used to define homologous-recombination deficiency (HRD) was based on the sum of three scores that identify specific structural variations in the genome attributable to HRD....

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Published inThe New England journal of medicine Vol. 382; no. 16; pp. 1572 - 1575
Main Authors da Costa, Alexandre, Haines, Ian E, Gabor Miklos, George L, Dekker, Tim J.A, González-Martín, Antonio, Monk, Bradley J, Ray-Coquard, Isabelle, Pérol, David, Pujade-Lauraine, Eric
Format Journal Article
LanguageEnglish
Published United States Massachusetts Medical Society 16.04.2020
Subjects
Breast cancer
Female
Genomes
Heterozygosity
Homologous recombination
Humans
Indazoles
Loss of heterozygosity
Mutation
Ovarian cancer
Ovarian Neoplasms
Piperidines
Platinum
Poly(ADP-ribose) polymerase
Poly(ADP-ribose) Polymerase Inhibitors
Tumors
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Summary:To the Editor: In the PRIMA (PRIMA/ENGOT-OV26/GOG-3012) trial conducted by González-Martín et al. (Dec. 19 issue), 1 the test used to define homologous-recombination deficiency (HRD) was based on the sum of three scores that identify specific structural variations in the genome attributable to HRD. 2 In the absence of a standard test or marker of HRD, in previous studies, investigators created these scores using BRCA mutations and platinum sensitivity as surrogate markers of HRD to determine whether a sample had HRD. Scores were based on patterns of large-scale state transitions, 3 loss of heterozygosity, 4 and telomeric allele imbalance 5 that were associated with the . . .
Bibliography:SourceType-Other Sources-1
content type line 63
ObjectType-Correspondence-1
ObjectType-Commentary-2
ISSN:0028-4793
1533-4406
DOI:10.1056/NEJMc2000644