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UID:994@biotech.technion.ac.il
DTSTART;TZID=Asia/Jerusalem:20210112T173000
DTEND;TZID=Asia/Jerusalem:20220202T164952
DTSTAMP:20220512T124719Z
URL:https://biotech.technion.ac.il/events/uncovering-evolving-drug-resista
 nt-cell-states-in-metastatic-breast-cancer-2/
SUMMARY:Uncovering Evolving Drug-resistant Cell-states in Metastatic Breast
  Cancer
DESCRIPTION:Notwithstanding the rapidly growing armamentarium of therapeuti
 cs in metastatic malignancies\n-finding therapeutic combinations that resu
 lt in a durable response remains a stubbornly\nintractable challenge. Thus
 \, I dedicated my postdoctoral research to finding strategies that\nmay ad
 vance our understanding of this problem.\nMy work led to the identificatio
 n of novel resistance alterations to CDK4/6 inhibition in\nmetastatic brea
 st cancer (Wander*\, Cohen* et al.\, Cancer Discovery\, 2020)\, identifica
 tion of\nevolutionary acquired point mutations in HER2 as a novel resistan
 ce mechanism (Nayar\,*\nCohen* et al. Nature Genetics\, 2019)\, and acquir
 ed FGF/R pathways alterations as a prevalent\nmode of resistance (Mao*\, C
 ohen* et al. Clin Cancer Res 2020).\nMy ongoing work and future research a
 re focused on studying evolved resistance while\nconsidering both clonal d
 ynamics (mutations) and cellular-rewiring (regulation). For this\, I had\n
 developed a schema for jointly analyzing exome and transcriptome profiles\
 , combining both\nbulk and single-cell RNA-seq profiles towards a "cell-st
 ates" outlook (representing distinctive\ngene-expression and phenotypic ch
 aracteristics). Recently\, I had exemplified this strategy by\nuncovering 
 the transcriptional convergence in acquired resistance via activated recep
 tor\ntyrosine kinases both in-vitro and in-vivo (Cohen et al.\, SABCS 2019
 \, Abstract GS2-02)\, and\nby revealing the ER-axis transcriptional progra
 m with single-cell analysis of drug-resistant\nmetastatic tumors (Cohen et
  al.\, SABCS\, 2019\, Abstract GS6-05).\n\nFull Abstract
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