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Evaluating sources of intrachromosom...

Bartos, Jeremy David.

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Evaluating sources of intrachromosomal instability in sporadic cancer genomes.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Evaluating sources of intrachromosomal instability in sporadic cancer genomes./
作者:	Bartos, Jeremy David.
面頁冊數:	303 p.
附註:	Adviser: Garth R. Anderson.
Contained By:	Dissertation Abstracts International66-05B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3174305
ISBN:	9780542125430

Evaluating sources of intrachromosomal instability in sporadic cancer genomes.
Bartos, Jeremy David.

Evaluating sources of intrachromosomal instability in sporadic cancer genomes. - 303 p.

Adviser: Garth R. Anderson.

Thesis (Ph.D.)--State University of New York at Buffalo, 2005.

Genomic instability is one of the hallmarks of tumorigenesis, although it is still disputed if this process acts as a progression facilitator, or is a secondary consequence of malignancy. Intrachromosomal genomic instability has been detected in the pre-malignant aberrant crypts of the colon, supporting the model that instability is an early step in the progression to malignancy in sporadic colorectal tumors and is therefore most likely a facilitator of tumorigenesis. Intrachromosomal genomic instability was quantified using Inter-(Simple Sequence Repeat) PCR analysis on paired tumor and normal DNA samples of breast, thyroid, and colorectal cancers, ultimately quantifying similar overall levels of instability. We assessed the correlations between K-ras and GSTM1 mutations and a tumor's level of genomic instability. A significant association was found between tumors with a GSTM1-null status and elevated inter-(simple sequence repeat) FCR instability, while a weak correlation was observed between mutant K-ras and inter-(simple sequence repeat) PCR genomic instability.

ISBN: 9780542125430Subjects--Topical Terms:

1017730
Biology, Genetics.

Evaluating sources of intrachromosomal instability in sporadic cancer genomes.
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245 1 0 $a Evaluating sources of intrachromosomal instability in sporadic cancer genomes.
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500 $a Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2389.
502 $a Thesis (Ph.D.)--State University of New York at Buffalo, 2005.
520 $a Genomic instability is one of the hallmarks of tumorigenesis, although it is still disputed if this process acts as a progression facilitator, or is a secondary consequence of malignancy. Intrachromosomal genomic instability has been detected in the pre-malignant aberrant crypts of the colon, supporting the model that instability is an early step in the progression to malignancy in sporadic colorectal tumors and is therefore most likely a facilitator of tumorigenesis. Intrachromosomal genomic instability was quantified using Inter-(Simple Sequence Repeat) PCR analysis on paired tumor and normal DNA samples of breast, thyroid, and colorectal cancers, ultimately quantifying similar overall levels of instability. We assessed the correlations between K-ras and GSTM1 mutations and a tumor's level of genomic instability. A significant association was found between tumors with a GSTM1-null status and elevated inter-(simple sequence repeat) FCR instability, while a weak correlation was observed between mutant K-ras and inter-(simple sequence repeat) PCR genomic instability.
520 $a Colorectal tumors were analyzed using comparative genomic hybridization BAC microarrays. There is a three BAC-clone region on chromosome 9 that contains the c-ABL gene, where copy number alteration is associated with genome-wide aCGH copy number loss. There is a highly significant interaction between that region of chromosome 9 and chromosome 22q11-13, another region whose loss is associated with genome-wide deletion. Additional regions of interest include the telomeric end of chromosome 14 whose loss is associated with genome-wide copy number losses, and regions on chromosome l, 2, 3, 7, and 13 whose amplification is associated with genome-wide copy number gains.
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