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Frequent copy number variations on c...

Vijayakumar, Sapna.

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Frequent copy number variations on chromosomes 18q and Y, and the functional implications of the Y chromosome loss in prostate cancer.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Frequent copy number variations on chromosomes 18q and Y, and the functional implications of the Y chromosome loss in prostate cancer./
作者:	Vijayakumar, Sapna.
面頁冊數:	194 p.
附註:	Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2431.
Contained By:	Dissertation Abstracts International66-05B.
標題:	Biology, Molecular. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3175317
ISBN:	0542133377

Frequent copy number variations on chromosomes 18q and Y, and the functional implications of the Y chromosome loss in prostate cancer.
Vijayakumar, Sapna.

Frequent copy number variations on chromosomes 18q and Y, and the functional implications of the Y chromosome loss in prostate cancer. - 194 p.

Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2431.

Thesis (Ph.D.)--The University of Texas Health Science Center at San Antonio, 2005.

The loss of Y chromosome is one of the most frequent genetic aberrations observed in prostate cancer. We applied somatic cell genetics technique to test the functional significance of the loss of Y chromosome in prostate cancer. The human Y chromosome was tagged with hisD gene and transferred to PC-3, a human prostate cancer cell line devoid of cytogenetically detectable Y chromosome, by microcell mediated chromosome transfer. Tumorigenicity of these PC-3 hybrids was tested in vivo and in vitro , and the results were correlated to the regions of the Y chromosome contained in the hybrids. Out of 60 mice injected with 12 different PC-3 hybrids (five mice per hybrid) tumor growth was apparent in only one mouse, while tumors grew in all mice injected with the parental PC-3 cells.

ISBN: 0542133377Subjects--Topical Terms:

1017719
Biology, Molecular.

Frequent copy number variations on chromosomes 18q and Y, and the functional implications of the Y chromosome loss in prostate cancer.
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245 1 0 $a Frequent copy number variations on chromosomes 18q and Y, and the functional implications of the Y chromosome loss in prostate cancer.
300 $a 194 p.
500 $a Source: Dissertation Abstracts International, Volume: 66-05, Section: B, page: 2431.
500 $a Supervisor: Susan L. Naylor.
502 $a Thesis (Ph.D.)--The University of Texas Health Science Center at San Antonio, 2005.
520 $a The loss of Y chromosome is one of the most frequent genetic aberrations observed in prostate cancer. We applied somatic cell genetics technique to test the functional significance of the loss of Y chromosome in prostate cancer. The human Y chromosome was tagged with hisD gene and transferred to PC-3, a human prostate cancer cell line devoid of cytogenetically detectable Y chromosome, by microcell mediated chromosome transfer. Tumorigenicity of these PC-3 hybrids was tested in vivo and in vitro , and the results were correlated to the regions of the Y chromosome contained in the hybrids. Out of 60 mice injected with 12 different PC-3 hybrids (five mice per hybrid) tumor growth was apparent in only one mouse, while tumors grew in all mice injected with the parental PC-3 cells.
520 $a Using a high-resolution genomic microarray specific for the human Y chromosome, prostate tumor samples and four prostate cell lines: PC-3, 22Rv1, DU145 and LNCaP, were analyzed by array CGH. The microarray slides also contained 165 BAC clones from chromosome 18q21--q23.
520 $a Out of 37 tumor samples, the deletion at Yp11.2 was observed in 19 (51.4%) samples. In addition, Yp11.2 deletion was present in the tumorigenic PC-3 hybrids, while non-tumorigenic PC-3 hybrids had a near-intact Yp. Within this region, are present a known gene, testis specific protein on Y (TSPY), and a transcript unit cluster, CYorf16, whose exact functions at present are unclear.
520 $a Furthermore, quantitative PCR analyses performed using a probe developed for TSPY, a multi-copy gene cluster present at Yp11.2, gave corroborative results showing copy number variation. We also detected TSPY copy number loss in blood samples, and found a significant association between less copies of TSPY and increased prostate cancer incidence. A novel amplification at 18q22.1 involving cadherin7 was also detected (55%) in the same set of tumors analyzed. Furthermore, overexpression of cadherin 7 was also seen in the tumors that showed amplification at the DNA level.
520 $a More detailed studies will provide insight about the functional significance of the deletion detected at proximal Yp and the gain at 18q22.1 in prostate tumorigenesis.
590 $a School code: 0853.
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650 4 $a Biology, Genetics. $3 1017730
650 4 $a Health Sciences, Oncology. $3 1018566
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710 2 0 $a The University of Texas Health Science Center at San Antonio. $3 1030926
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