Chromosome aberrations in metastatic ovarian cancer: Relationship with abnormalities in primary tumors

Bello, M. Josefa; Rey, Juan A.

doi:10.1002/ijc.2910450111

Cited by 57 publications

(25 citation statements)

References 24 publications

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“…Characterisation of the KLK6 promoter would facilitate future efforts to study the regulation of KLK6, including studying the roles of transcription factors. Lastly, chromosome 19q13 is reportedly rearranged in numerous types of solid tumours (Whang-Peng et al, 1984;Tanaka et al, 1989;Bello and Rey, 1990;Pejovic et al, 1991Pejovic et al, , 1992Jenkins et al, 1993). Potential gene amplification of KLK6 in ovarian cancer has also been suggested (Ni et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Transcriptional upregulation of human tissue kallikrein 6 in ovarian cancer: clinical and mechanistic aspects

et al. 2007

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The human tissue kallikrein family (KLK for protein; KLK for gene) includes 15 members. Twelve kallikreins, including KLK6, are concurrently upregulated in ovarian cancer. However, the mechanism of this phenomenon remains unclear. In this study, we measured KLK6 expression in a large series of ovarian tissue cytosols and examined possible mechanisms of KLK6 up-regulation in ovarian cancer. Using a newly developed enzyme-linked immunosorbent assay (ELISA) with two monoclonal antibodies, we quantified KLK6 expression in ovarian tissue cytosols, and confirmed the upregulation of KLK6 in ovarian cancer and its unfavourable prognostic value. We then examined KLK6 mRNA expression using reverse transcription -polymerase chain reaction and established its good concordance with KLK6 protein expression. This finding suggested that the KLK6 gene is under transcriptional regulation. We then scrutinised a few mechanisms that could explain KLK6 upregulation. The relative abundance of two KLK6 mRNA transcripts was studied; we found the same differential expression pattern in all samples, regardless of KLK6 levels. Genomic mutation screening of all exons and the 5 0 -flanking region of the KLK6 gene identified two linked single-nucleotide polymorphisms in the 5 0 -untranslated region, but neither correlated with KLK6 expression. Ovarian cell lines were separately treated with five steroid hormones. None of the treatments produced significant effects on KLK6 expression. We conclude that KLK6 is transcriptionally upregulated in ovarian cancer, but probably not through alternative mRNA transcript expression, genomic mutation, or steroid hormone induction.

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Section: Discussionmentioning

confidence: 99%

Transcriptional upregulation of human tissue kallikrein 6 in ovarian cancer: clinical and mechanistic aspects

et al. 2007

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“…Previous karyotypic reports of ovarian cancers have revealed complex karyotypes in most cases (Wake et al, 1980;Trent and Salmon, 1981;Whang-Peng et al, 1984;Panani and FertiPassantonopoulou, 1985;Tanaka et al, 1989;Bello and Rey, 1990;Pejovic et al, 1992). In ovarian carcinomas, chromosome arms 1p, 1q, 3p, 3q, 6q, 7p, 9q, 11p, 11q, 17q, 19p, and 19q are preferentially involved in structural rearrangements (reviewed in Heim and Mitelman, 1995).…”

Section: Introductionmentioning

confidence: 93%

Comparative genomic hybridization detects frequent overrepresentation of chromosomal material from 3q26, 8q24, and 20q13 in human ovarian carcinomas

Sonoda

Palazzo

Manoir

et al. 1997

Genes Chromosom. Cancer

171

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“…This site also includes the interferon a genes (Diaz et al, 1988) and the inhibitors of cyclin dependent kinases 4 and 6 (CDK4, CDK6) known as p16 INK4A (CDKN2A) and p15 INK4B (CDKN2B) (Kamb et al, 1994;Nobori et al, 1994;Okamoto et al, 1995;Herman et al, 1997). Loss of heterozygosity (LOH) as well as hemi-and homozygous deletions of the 9p21 region have been described in a variety of primary human tumors and cell lines including acute lymphoblastic leukemia (ALL) (Batova et al, , 1997, melanoma (Cowan et al, 1988;Fountain et al, 1992), ovarian cancer (Bello et al, 1990), glioma (Nobori et al, 1991;Dreyling et al, 1995;Barker et al, 1997), head and neck cancer (van der Riet et al, 1994), bladder cancer (Stadler et al, 1994), chondrosarcoma (Jagasia et al, 1996), small cell (Merlo et al, 1994;Kim et al, 1997) and non-small cell lung cancer (NSCLC) (Nobori et al, 1993;Merlo et al, 1994;Okamoto et al, 1995;Wiest et al, 1997).…”

Section: Ink4amentioning

confidence: 99%

Homozygous deletions of methylthioadenosine phosphorylase (MTAP) are more frequent than p16INK4A (CDKN2) homozygous deletions in primary non-small cell lung cancers (NSCLC)

et al. 1998

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Homozygous deletions of the tumor suppressor gene p16 INK4A and de®ciency of methylthioadenosine phosphorylase (MTAP), both located on chromosome 9p21, have been independently reported in non-small cell lung cancer (NSCLC). To determine the frequency of co-deletion of these two genes, we investigated 50 samples of primary NSCLC using a quantitative PCR-ELISA. All specimens were ®xed in formalin, paran embedded and stored until assayed. Histologic subtypes included 25 adenocarcinomas (50%), 21 squamous cell carcinomas (42%) and four large cell carcinomas (8%). Homozygous deletions of MTAP exon 8 could be detected in 19 of 50 NSCLC samples (38%). Adenocarcinoma (11 of 25, 44%) showed a higher deletion frequency than squamous cell carcinoma (six of 21, 29%). In contrast, homozygous p16INK4A deletions were detected in only nine of 50 (18%) samples using speci®c primers for p16 INK4A exon 1a. No dierence between the histological subtypes and p16INK4A deletion frequency was observed. We further investigated the ten samples with MTAP deletions but intact p16INK4A exon 1a with primers speci®c for p16 INK4Aexon 3, the exon nearest to MTAP exon 8. Interestingly, none of the ten samples had deletion of the p16 INK4A exon 3 coding region. Fine mapping analysis performed in ten samples showed a frequent breakpoint between MTAP exon 4 and exon 5. In addition, p16 protein expression could not be detected in ®ve out of six samples with intact p16 but deleted MTAP locus. These data show a high frequency of homozygous MTAP deletions in NSCLC which is associated with detectable co-deletion of p16INK4A in only half of the cases. This result suggests the existence either of another tumor suppressor gene telomeric of p16

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Chromosome aberrations in metastatic ovarian cancer: Relationship with abnormalities in primary tumors

Cited by 57 publications

References 24 publications

Transcriptional upregulation of human tissue kallikrein 6 in ovarian cancer: clinical and mechanistic aspects

Transcriptional upregulation of human tissue kallikrein 6 in ovarian cancer: clinical and mechanistic aspects

Comparative genomic hybridization detects frequent overrepresentation of chromosomal material from 3q26, 8q24, and 20q13 in human ovarian carcinomas

Homozygous deletions of methylthioadenosine phosphorylase (MTAP) are more frequent than p16INK4A (CDKN2) homozygous deletions in primary non-small cell lung cancers (NSCLC)

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