Discovery of genomic alterations through coregulation analysis of closely linked genes: a frequent gain in 17q25.3 in prostate cancer

Bermudo, Raquel; Abia, David; Benitez, Daniel; Carrió, Ana; Vilella, Ramón; Ortíz, Ángel R.; Thomson, Timothy M.; Fernández, Pedro

doi:10.1111/j.1749-6632.2010.05780.x

Cited by 5 publications

(3 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…16,18 Although there is a known relationship between testosterone levels and prostate cancer, advanced age and genetic factors appear to play a more important role. 19 Finasteride (5 mg) and dutasteride have been reported to exert protective effects against prostate cancer. 20,21 Finasteride, 5-alpha-reductase type 2 inhibitor, does not reduce plasma testosterone and the dose of 1 mg/d is used in patients with AGA; higher doses (5 mg) are used to treat BPH.…”

Section: Discussionmentioning

confidence: 99%

Androgenetic alopecia as an early marker of benign prostatic hyperplasia

Arias‐Santiago

Arrabal-Polo

Buendía‐Eisman

et al. 2012

Journal of the American Academy of Dermatology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Androgenetic alopecia as an early marker of benign prostatic hyperplasia

Arias‐Santiago

Arrabal-Polo

Buendía‐Eisman

et al. 2012

Journal of the American Academy of Dermatology

View full text Add to dashboard Cite

“…Amplification of the 17qter region has been described in several other cancer types, like prostate or ovarian cancers. A highly recurrent gain on chromosome 17q25.3 was reported in prostate cancer [ 39 ]. The region identified overlaps with the same region on chromosome 17q identified in our CGH assay.…”

Section: Discussionmentioning

confidence: 99%

Identification by array comparative genomic hybridization of a new amplicon on chromosome 17q highly recurrent in BRCA1 mutated triple negative breast cancer

et al. 2014

View full text Add to dashboard Cite

IntroductionTriple Negative Breast Cancers (TNBC) represent about 12% to 20% of all breast cancers (BC) and have a worse outcome compared to other BC subtypes. TNBC often show a deficiency in DNA double-strand break repair mechanisms. This is generally related to the inactivation of a repair enzymatic complex involving BRCA1 caused either by genetic mutations, epigenetic modifications or by post-transcriptional regulations.The identification of new molecular biomarkers that would allow the rapid identification of BC presenting a BRCA1 deficiency could be useful to select patients who could benefit from PARP inhibitors, alkylating agents or platinum-based chemotherapy.MethodsGenomic DNA from 131 formalin-fixed paraffin-embedded (FFPE) tumors (luminal A and B, HER2+ and triple negative BC) with known BRCA1 mutation status or unscreened for BRCA1 mutation were analysed by array Comparative Genomic Hybridization (array CGH). One highly significant and recurrent gain in the 17q25.3 genomic region was analysed by fluorescent in situ hybridization (FISH). Expression of the genes of the 17q25.3 amplicon was studied using customized Taqman low density arrays and single Taqman assays (Applied Biosystems).ResultsWe identified by array CGH and confirmed by FISH a gain in the 17q25.3 genomic region in 90% of the BRCA1 mutated tumors. This chromosomal gain was present in only 28.6% of the BRCA1 non-mutated TNBC, 26.7% of the unscreened TNBC, 13.6% of the luminal B, 19.0% of the HER2+ and 0% of the luminal A breast cancers. The 17q25.3 gain was also detected in 50% of the TNBC with BRCA1 promoter methylation. Interestingly, BRCA1 promoter methylation was never detected in BRCA1 mutated BC. Gene expression analyses of the 17q25.3 sub-region showed a significant over-expression of 17 genes in BRCA1 mutated TNBC (n = 15) as compared to the BRCA1 non mutated TNBC (n = 13).ConclusionsIn this study, we have identified by array CGH and confirmed by FISH a recurrent gain in 17q25.3 significantly associated to BRCA1 mutated TNBC. Up-regulated genes in the 17q25.3 amplicon might represent potential therapeutic targets and warrant further investigation.Electronic supplementary materialThe online version of this article (doi:10.1186/s13058-014-0466-y) contains supplementary material, which is available to authorized users.

show abstract

“…Accelerated tumor development has usually been associated with duplication of the mouse subcytoband 11E2 (syntenic to human chromosome 17, cytoband 17q25.3), supporting the importance of this chromosomal region in tumorigenesis ( 12 ). The 17q25 chromosomal region has been reported to be involved in a variety of human cancers including ovary ( 13 , 14 ), prostate ( 15 ), leukemia ( 16 ), neuroblastoma ( 17 , 18 ), esophagus ( 19 - 21 ), sarcoma ( 22 , 23 ), and breast ( 24 ). The frequent observations of allelic gain or loss in this chromosomal region in various types of cancers suggest that oncogenes or tumor suppressor genes, respectively, are located there.…”

Section: Discussionmentioning

confidence: 99%

Copy number gains of chromosome 17 identified by dual in situ hybridization in non-small cell lung cancer tissue correlate with overexpression of c-Myc

Sunpaweravong

Thongwatchara

Sangthong

et al. 2022

Transl Cancer Res TCR

View full text Add to dashboard Cite

Background c-Myc regulates multiple genes involved in cell proliferation in various cancer types including non-small cell lung cancer (NSCLC). Copy number gains of cytoband 17q25.3, along with chromosome 17, have been reported in NSCLC patients, emphasizing the clinical significance as a potential molecular target for therapy. The upregulation of c-Myc has been found to accelerate tumor development associated with duplication of the syntenic human cytoband 17q25.3. This study aimed to explore and compare the correlations of chromosome 17 copy number and c-Myc expression in NSCLC with the paired-normal respiratory epithelium and to examine their role as potential molecular targets for NSCLC therapy. Methods A total of 66 NSCLC tissue samples with paired-normal respiratory epithelium were examined. The copy number of chromosome 17 was determined by human epidermal growth factor receptor 2 ( HER2 )/centromeric enumeration probe of chromosome 17 (CEP17) dual in situ hybridization (DISH). Results Copy number gains of chromosome 17 were identified in 8 of 60 (13.3%) available NSCLC specimens. No copy number gains of chromosome 17 were demonstrated in the paired-normal respiratory epithelium. The mean HER2 (1.2±0.3) and CEP17 (1.4±0.3) copy numbers of the normal respiratory epithelium were significantly lower than those of the NSCLC tissue [1.8±1.0 vs. 2.0±0.8, respectively (P<0.001)]. Twelve of 66 (18.2%) NSCLC patients had overexpression of c-Myc. Five (41.7%) of the patients whose tumors positive for c-Myc had HER2 gene amplification [1] or copy number gain of chromosome 17 [4]. HER2 gene amplification or copy number gain of chromosome 17 and high expression of c-Myc were associated with decreased overall survival. Conclusions Both biomarkers deserve further investigation to identify NSCLC patients with poorer survival outcomes requiring better therapeutic approaches.

show abstract

Discovery of genomic alterations through coregulation analysis of closely linked genes: a frequent gain in 17q25.3 in prostate cancer

Cited by 5 publications

References 33 publications

Androgenetic alopecia as an early marker of benign prostatic hyperplasia

Androgenetic alopecia as an early marker of benign prostatic hyperplasia

Identification by array comparative genomic hybridization of a new amplicon on chromosome 17q highly recurrent in BRCA1 mutated triple negative breast cancer

Copy number gains of chromosome 17 identified by dual in situ hybridization in non-small cell lung cancer tissue correlate with overexpression of c-Myc

Contact Info

Product

Resources

About