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Insights Into FHIT Loss-Induced Tumorigenesis

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서명/저자사항Insights Into FHIT Loss-Induced Tumorigenesis.
개인저자Waters, Catherine Elizabeth.
단체저자명The Ohio State University. Biomedical Sciences.
발행사항[S.l.]: The Ohio State University., 2015.
발행사항Ann Arbor: ProQuest Dissertations & Theses, 2015.
형태사항128 p.
기본자료 저록Dissertation Abstracts International 80-01B(E).
Dissertation Abstract International
ISBN9780438310131
학위논문주기Thesis (Ph.D.)--The Ohio State University, 2015.
일반주기 Source: Dissertation Abstracts International, Volume: 80-01(E), Section: B.
Adviser: Kay Huebner.
요약Cancer cells display an elevated rate of genetic mutation at the single nucleotide and chromosome levels, termed genome instability. Genome instability is a facilitating hallmark of cancer in that it raises the probability of generating cancer-p
요약Deletion within fragile site FRA3B, which overlaps exons of the FHIT gene, is a frequent and early genetic alteration in precancerous cells, resulting in reduced or lost Fhit protein expression. Loss of Fhit expression occurs in >50% of human c
요약The cellular processes that can exploit Fhit loss-induced DNA damage and allow increased accumulation of genome alterations and point mutations in Fhit deficient cells and tissues have only recently been examined. APOBEC3B cytidine deaminase act
요약Using data from The Cancer Genome Atlas, we show that FHIT-low/ APOBEC3B-high expressing lung adenocarcinomas display significantly increased numbers of APOBEC signature mutations. Tumor samples in this cohort with normal FHIT expression do not
요약Collectively, these findings support a model where deregulation of the Fhit-TK1 pathway initiates genomic instability in early lesions, providing increased availability of unstable ssDNA regions that can be mutated by enzymes, such as APOBEC3B,
일반주제명Biomedical engineering.
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