國立虎尾科技大學 |

Targeting Recurrence in Glioblastoma.

紀錄類型:	書目-語言資料,手稿 : Monograph/item
正題名/作者:	Targeting Recurrence in Glioblastoma./
作者:	Blomquist, Mylan Rachel.
面頁冊數:	1 online resource (165 pages)
附註:	Source: Dissertations Abstracts International, Volume: 85-04, Section: B.
Contained By:	Dissertations Abstracts International85-04B.
標題:	Molecular biology. -
電子資源:	click for full text (PQDT)
ISBN:	9798380589901

Targeting Recurrence in Glioblastoma.
Blomquist, Mylan Rachel.

Targeting Recurrence in Glioblastoma. - 1 online resource (165 pages)

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

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

Includes bibliographical references

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.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024

Mode of access: World Wide Web

ISBN: 9798380589901Subjects--Topical Terms:

583443
Molecular biology.
Subjects--Index Terms:

GenomicsIndex Terms--Genre/Form:

554714
Electronic books.

Targeting Recurrence in Glioblastoma.
LDR:02883ntm a22003977 4500 001 1149377
005 20241015112533.5
006 m o d
007 cr bn ---uuuuu
008 250605s2023 xx obm 000 0 eng d
020 $a 9798380589901
035 $a (MiAaPQ)AAI30640635
035 $a AAI30640635
040 $a MiAaPQ $b eng $c MiAaPQ $d NTU
100 1 $a Blomquist, Mylan Rachel. $3 1475583
245 1 0 $a Targeting Recurrence in Glioblastoma.
264 0 $c 2023
300 $a 1 online resource (165 pages)
336 $a text $b txt $2 rdacontent
337 $a computer $b c $2 rdamedia
338 $a online resource $b cr $2 rdacarrier
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.
504 $a Includes bibliographical references
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.
533 $a Electronic reproduction. $b Ann Arbor, Mich. : $c ProQuest, $d 2024
538 $a Mode of access: World Wide Web
650 4 $a Molecular biology. $3 583443
650 4 $a Medicine. $3 644133
650 4 $a Cellular biology. $3 1148666
653 $a Genomics
653 $a Glioblastoma
653 $a Saracatinib
653 $a STAT5
653 $a Tumor heterogeneity
655 7 $a Electronic books. $2 local $3 554714
690 $a 0379
690 $a 0564
690 $a 0307
710 2 $a College of Medicine - Mayo Clinic. $b Molecular Pharmacology and Experimental Therapeutics. $3 1475584
710 2 $a ProQuest Information and Learning Co. $3 1178819
773 0 $t Dissertations Abstracts International $g 85-04B.
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30640635 $z click for full text (PQDT)