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Targeting Recurrence in Glioblastoma.

Blomquist, Mylan Rachel.

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Targeting Recurrence in Glioblastoma.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Targeting Recurrence in Glioblastoma./
Author:	Blomquist, Mylan Rachel.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2023,
Description:	165 p.
Notes:	Source: Dissertations Abstracts International, Volume: 85-04, Section: B.
Contained By:	Dissertations Abstracts International85-04B.
Subject:	Cellular biology. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30640635
ISBN:	9798380589901

Targeting Recurrence in Glioblastoma.
Blomquist, Mylan Rachel.

Targeting Recurrence in Glioblastoma. - Ann Arbor : ProQuest Dissertations & Theses, 2023 - 165 p.

Source: Dissertations Abstracts International, Volume: 85-04, Section: B.

Thesis (Ph.D.)--College of Medicine - Mayo Clinic, 2023.

Glioblastoma (GBM), the most common primary brain tumor in adults, confers a dismal 5% five-year survival rate to newly diagnosed patients. Despite extensive efforts to characterize the molecular features of GBM tumors, the standard of care for GBM has not changed in more than 20 years, and no targeted therapies have improved GBM patient survival thus far. Despite therapeutic measures, all GBM tumors inevitably recur due to diffuse invasion of cancer cells distantly into the brain parenchyma. There is currently no standard of care for GBM recurrence. This dissertation seeks to characterize the signaling pathways that remain active at GBM recurrence and assess this activity as a therapeutic target in the setting of recurrence. Chapter I reviews the current literature on why GBM recurs, treatment strategies for recurrent GBM, molecular characteristics of recurrent GBM, and the oncogenic role of EGFR and STAT pathway activation in GBM cells. Chapter II uses GBM samples collected over recurrences and in spatially distinct regions to demonstrate that common signaling pathways remain active at GBM recurrence despite therapeutic intervention. Chapter III details the spatial genomic heterogeneity of driver alterations, specifically at the EGFR locus, emphasizing the need for targeting common downstream pathways over specific oncogenic drivers. Chapter IV demonstrates that STAT5, despite almost never undergoing genomic alteration in GBM, represents a viable therapeutic target. Chapter V provides overall conclusions of the work and future directions.

ISBN: 9798380589901Subjects--Topical Terms:

3172791
Cellular biology.
Subjects--Index Terms:

Genomics

Targeting Recurrence in Glioblastoma.
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300 $a 165 p.
500 $a Source: Dissertations Abstracts International, Volume: 85-04, Section: B.
500 $a Advisor: Tran, Nhan.
502 $a Thesis (Ph.D.)--College of Medicine - Mayo Clinic, 2023.
520 $a Glioblastoma (GBM), the most common primary brain tumor in adults, confers a dismal 5% five-year survival rate to newly diagnosed patients. Despite extensive efforts to characterize the molecular features of GBM tumors, the standard of care for GBM has not changed in more than 20 years, and no targeted therapies have improved GBM patient survival thus far. Despite therapeutic measures, all GBM tumors inevitably recur due to diffuse invasion of cancer cells distantly into the brain parenchyma. There is currently no standard of care for GBM recurrence. This dissertation seeks to characterize the signaling pathways that remain active at GBM recurrence and assess this activity as a therapeutic target in the setting of recurrence. Chapter I reviews the current literature on why GBM recurs, treatment strategies for recurrent GBM, molecular characteristics of recurrent GBM, and the oncogenic role of EGFR and STAT pathway activation in GBM cells. Chapter II uses GBM samples collected over recurrences and in spatially distinct regions to demonstrate that common signaling pathways remain active at GBM recurrence despite therapeutic intervention. Chapter III details the spatial genomic heterogeneity of driver alterations, specifically at the EGFR locus, emphasizing the need for targeting common downstream pathways over specific oncogenic drivers. Chapter IV demonstrates that STAT5, despite almost never undergoing genomic alteration in GBM, represents a viable therapeutic target. Chapter V provides overall conclusions of the work and future directions.
590 $a School code: 1542.
650 4 $a Cellular biology. $3 3172791
650 4 $a Medicine. $3 641104
650 4 $a Molecular biology. $3 517296
653 $a Genomics
653 $a Glioblastoma
653 $a Saracatinib
653 $a STAT5
653 $a Tumor heterogeneity
690 $a 0379
690 $a 0564
690 $a 0307
710 2 $a College of Medicine - Mayo Clinic. $b Molecular Pharmacology and Experimental Therapeutics. $3 3697704
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