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GATA6 : = A Molecular Regulator of Pancreatic Tumour Growth and Phenotype.

紀錄類型:	書目-語言資料,手稿 : Monograph/item
正題名/作者:	GATA6 :/
其他題名:	A Molecular Regulator of Pancreatic Tumour Growth and Phenotype.
作者:	Woo, Tristan.
面頁冊數:	1 online resource (62 pages)
附註:	Source: Masters Abstracts International, Volume: 84-09.
Contained By:	Masters Abstracts International84-09.
標題:	Oncology. -
電子資源:	click for full text (PQDT)
ISBN:	9798377615651

GATA6 : = A Molecular Regulator of Pancreatic Tumour Growth and Phenotype.
Woo, Tristan.

GATA6 :A Molecular Regulator of Pancreatic Tumour Growth and Phenotype. - 1 online resource (62 pages)

Source: Masters Abstracts International, Volume: 84-09.

Thesis (M.Sc.)--University of Toronto (Canada), 2023.

Includes bibliographical references

Pancreatic ductal adenocarcinoma (PDAC) has been classified into two main transcriptional subtypes, Basal-like and Classical. The Classical subtype correlates with GATA6 expression, and ~16% of tumors show amplification in GATA6. The goal of this project is to understand the role of GATA6 as a molecular regulator of the Classical subtype. Competition assays show loss of GATA6 reduced cell fitness. Gene expression analysis showed GATA6 was integral in maintaining Classical gene expression and loss led to shifts towards more Basal-like expression and pathways. Despite a transcriptional shift towards Basal-like expression, phenotypic characteristics of the Basal-like subtype were notably absent (i.e., no EMT, MYC expression, or aggressive growth). This data suggests that loss of GATA6 is not sufficient to cause a full Basal-like phenotype and may lead to a transitional state that does not offer the same growth advantages as being in a full Basal-like state.

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

Mode of access: World Wide Web

ISBN: 9798377615651Subjects--Topical Terms:

593951
Oncology.
Subjects--Index Terms:

Basal-likeIndex Terms--Genre/Form:

554714
Electronic books.

GATA6 : = A Molecular Regulator of Pancreatic Tumour Growth and Phenotype.
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