Genomic Instability andTP53Genomic Alterations Associate With Poor Antiproliferative Response and Intrinsic Resistance to Aromatase Inhibitor Treatment | Zendy

Eugene F. Schuster | Zendy; Pascal Gellert | Zendy; Corrinne V. Segal | Zendy; Elena LópezKnowles | Zendy; Richard Buus | Zendy; Maggie C.U. Cheang | Zendy; James P. Morden | Zendy; J.F.R. Robertson | Zendy; Judith M. Bliss | Zendy; Ian Smith | Zendy; Mitch Dowsett | Zendy

Open Access

Genomic Instability andTP53Genomic Alterations Associate With Poor Antiproliferative Response and Intrinsic Resistance to Aromatase Inhibitor Treatment

Author(s) -

Eugene F. Schuster,

Pascal Gellert,

Corrinne V. Segal,

Elena LópezKnowles,

Richard Buus,

Maggie C.U. Cheang,

James P. Morden,

J.F.R. Robertson,

Judith M. Bliss,

Ian Smith,

Mitch Dowsett

Publication year - 2019

Publication title -

jco precision oncology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.405

H-Index - 22

ISSN - 2473-4284

DOI - 10.1200/po.18.00286

Subject(s) - loss of heterozygosity , genome instability , breast cancer , genotype , somatic cell , cancer , medicine , biology , oncology , cancer research , genetics , gene , allele , dna , dna damage

Although aromatase inhibitor (AI) treatment is effective in estrogen receptor-positive postmenopausal breast cancer, resistance is common and incompletely explained. Genomic instability, as measured by somatic copy number alterations (SCNAs), is important in breast cancer development and prognosis. SCNAs to specific genes may drive intrinsic resistance, or high genomic instability may drive tumor heterogeneity, which allows differential response across tumors and surviving cells to evolve resistance to treatment rapidly. We therefore evaluated the relationship between SCNAs and intrinsic resistance to treatment as measured by a poor antiproliferative response.

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