The Genomic Landscape of Endocrine-Resistant Advanced Breast Cancers
By P. Razavi, Matthew T. Chang, Guotai Xu, C. Bandlamudi, D. Ross, N. Vasan, Yanyan Cai, C. Bielski, M. Donoghue, P. Jonsson and 35 more. Cancer Cell, 2018
851 citations recorded by the source corpus.
SUMMARY We integrated the genomic sequencing of 1,918 breast cancers, including 1,501 hormone receptor-positive tumors, with detailed clinical information and treatment outcomes. In 692 tumors previously exposed to hormonal therapy, we identified an increased number of alterations in genes involved in the mitogen-activated protein kinase (MAPK) pathway and in the estrogen receptor transcriptional machinery. Activating ERBB2 mutations and NF1 loss-of-function mutations were more than twice as common in endocrine resistant tumors. Alterations in other MAPK pathway genes (EGFR, KRAS, among others) and estrogen receptor transcriptional regulators (MYC, CTCF, FOXA1, and TBX3) were also enriched. Altogether, these alterations were present in 22% of tumors, mutually exclusive with ESR1 mutations, and associated with a shorter duration of response to subsequent hormonal therapies
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/b3d2d6af31a0b5739246bdc30e7e2346bd764558
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Citations in the corpus
- Harnessing multimodal data integration to advance precision oncology (2021, background): “This leads to further understanding of the cancer genome, drug sensitivity 2 and resistance mechanisms 3 , and prognostic associations 4,5 .”
- Overcoming Endocrine Resistance in Breast Cancer (2020, neutral): “also reported acquired hotspot alterations in KRAS, BRAF, and MAP2K1 (the gene encoding MEK1) in posttreatment biopsies compared to matched pre-treatment tumors (Razavi et al., 2018).”