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Loss of heterozygosity for chromosomal regions 15q14-21.1, 17q21.31, and 13q12.3-13.1 and its relevance for prostate cancer.

Nowacka-Zawisza M, Forma E, Walczak M, Różański W, Bryś M, Krajewska WM - Med. Oncol. (2015)

Bottom Line: To evaluate the contribution of RAD51 to sporadic prostate cancer, loss of heterozygosity (LOH) for chromosomal region 15q14-21.1 (RAD51 locus) was determined and compared to LOH in 17q21.31 (BRCA1 locus) and 13q12.3-13.1 (BRCA2 region).A significant correlation was found between LOH for studied region and PSAD (prostate-specific antigen density).The findings suggest that RAD51 may be considered as a prostate cancer susceptibility gene.

View Article: PubMed Central - PubMed

Affiliation: Department of Cytobiochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska St. 141/143, 90-236, Lodz, Poland. mnz@biol.uni.lodz.pl.

ABSTRACT
Although prostate cancer is one of the most common cancers in men, the genetic defects underlying its pathogenesis remain poorly understood. DNA damage repair mechanisms have been implicated in human cancer. Accumulating evidence indicates that the fidelity of the response to DNA double-strand breaks is critical for maintaining genome integrity. RAD51 is a central player in double-strand break repair via homologous recombination, and its alterations may confer and increase the risk of cancer. RAD51 functioning depends on the indirect or direct interactions with BRCA1 and BRCA2. To evaluate the contribution of RAD51 to sporadic prostate cancer, loss of heterozygosity (LOH) for chromosomal region 15q14-21.1 (RAD51 locus) was determined and compared to LOH in 17q21.31 (BRCA1 locus) and 13q12.3-13.1 (BRCA2 region). DNA was isolated from prostate biopsies and matched peripheral blood of 50 patients. The regions 15q14-21.1, 17q21.31, and 13q12.3-13.1 were examined using microsatellite markers on chromosome 15 (D15S118, D15S214, D15S1006), chromosome 17 (D17S855, D17S1323), and chromosome 13 (D13S260, D13S290), respectively. The LOH in tumors was analyzed by PCR with fluorescently labeled primers and an ABI PRISM 377 DNA Sequencer. Allele sizing was determined by GeneScan version 3.1.2 and Genotyper version 2.5 software (Applied Biosystems, USA). LOH was identified in 57.5, 23, and 40 % for chromosomal regions 15q14-21.1, 17q21.31, and 13q12.3-13.1, respectively. Twenty-six percent of studied cases manifested LOH for at least one marker in 15q14-21.1 exclusively. A significant correlation was found between LOH for studied region and PSAD (prostate-specific antigen density). The findings suggest that RAD51 may be considered as a prostate cancer susceptibility gene.

No MeSH data available.


Related in: MedlinePlus

Box-and-whisker plot, representing the a mean and b median FAL index values for the PSAD in prostate cancer
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Fig2: Box-and-whisker plot, representing the a mean and b median FAL index values for the PSAD in prostate cancer

Mentions: Mann–Whitney U test revealed statistically significant differences between FAL index levels and PSA density (Fig. 2). There was no statistically significant correlation between FAL index levels and patients’ age, free to total PSA value, prostate volume, Gleason score, and TNM classification (Mann–Whitney U test) as well as total PSA level (Kruskal–Wallis test). Neither correlation between age of patients with LOH and PSA level, free to total PSA value nor PSA density was identified (data not shown).Fig. 2


Loss of heterozygosity for chromosomal regions 15q14-21.1, 17q21.31, and 13q12.3-13.1 and its relevance for prostate cancer.

Nowacka-Zawisza M, Forma E, Walczak M, Różański W, Bryś M, Krajewska WM - Med. Oncol. (2015)

Box-and-whisker plot, representing the a mean and b median FAL index values for the PSAD in prostate cancer
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4592700&req=5

Fig2: Box-and-whisker plot, representing the a mean and b median FAL index values for the PSAD in prostate cancer
Mentions: Mann–Whitney U test revealed statistically significant differences between FAL index levels and PSA density (Fig. 2). There was no statistically significant correlation between FAL index levels and patients’ age, free to total PSA value, prostate volume, Gleason score, and TNM classification (Mann–Whitney U test) as well as total PSA level (Kruskal–Wallis test). Neither correlation between age of patients with LOH and PSA level, free to total PSA value nor PSA density was identified (data not shown).Fig. 2

Bottom Line: To evaluate the contribution of RAD51 to sporadic prostate cancer, loss of heterozygosity (LOH) for chromosomal region 15q14-21.1 (RAD51 locus) was determined and compared to LOH in 17q21.31 (BRCA1 locus) and 13q12.3-13.1 (BRCA2 region).A significant correlation was found between LOH for studied region and PSAD (prostate-specific antigen density).The findings suggest that RAD51 may be considered as a prostate cancer susceptibility gene.

View Article: PubMed Central - PubMed

Affiliation: Department of Cytobiochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska St. 141/143, 90-236, Lodz, Poland. mnz@biol.uni.lodz.pl.

ABSTRACT
Although prostate cancer is one of the most common cancers in men, the genetic defects underlying its pathogenesis remain poorly understood. DNA damage repair mechanisms have been implicated in human cancer. Accumulating evidence indicates that the fidelity of the response to DNA double-strand breaks is critical for maintaining genome integrity. RAD51 is a central player in double-strand break repair via homologous recombination, and its alterations may confer and increase the risk of cancer. RAD51 functioning depends on the indirect or direct interactions with BRCA1 and BRCA2. To evaluate the contribution of RAD51 to sporadic prostate cancer, loss of heterozygosity (LOH) for chromosomal region 15q14-21.1 (RAD51 locus) was determined and compared to LOH in 17q21.31 (BRCA1 locus) and 13q12.3-13.1 (BRCA2 region). DNA was isolated from prostate biopsies and matched peripheral blood of 50 patients. The regions 15q14-21.1, 17q21.31, and 13q12.3-13.1 were examined using microsatellite markers on chromosome 15 (D15S118, D15S214, D15S1006), chromosome 17 (D17S855, D17S1323), and chromosome 13 (D13S260, D13S290), respectively. The LOH in tumors was analyzed by PCR with fluorescently labeled primers and an ABI PRISM 377 DNA Sequencer. Allele sizing was determined by GeneScan version 3.1.2 and Genotyper version 2.5 software (Applied Biosystems, USA). LOH was identified in 57.5, 23, and 40 % for chromosomal regions 15q14-21.1, 17q21.31, and 13q12.3-13.1, respectively. Twenty-six percent of studied cases manifested LOH for at least one marker in 15q14-21.1 exclusively. A significant correlation was found between LOH for studied region and PSAD (prostate-specific antigen density). The findings suggest that RAD51 may be considered as a prostate cancer susceptibility gene.

No MeSH data available.


Related in: MedlinePlus