Significance of chromosome arm 14q loss in nonpapillary renal cell carcinomas

Herbers, Jutta; Schullerus, Dietlinde; Müller, Harald; Kenck, Christiane; Chudek, Jerzy; Weimer, Jörg; Bugert, Peter; Kovács, Gyula

doi:10.1002/(sici)1098-2264(199705)19:1<29::aid-gcc5>3.3.co;2-j

Cited by 14 publications

(18 citation statements)

References 14 publications

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“…In renal cell carcinomas, LOH of 14q is often combined with a higher nuclear grading and staging. 48 In summary, we could demonstrate significant qualitative and quantitative genetic changes associated with clinical stage and morphological phenotype. The broad spectrum of phenotypically heterogeneous DCIS with significantly different aberrations raises the question of multiple pathways for invasive breast cancer with DCIS as a precursor lesion.…”

Section: Discussionmentioning

confidence: 75%

Comparative genomic hybridization of ductal carcinomain situ of the breast?evidence of multiple genetic pathways

et al. 1999

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There is strong evidence that ductal carcinoma in situ (DCIS) represents a precursor lesion of invasive breast cancer. In order to analyse specific chromosomal alterations of DCIS, 38 paraffin‐embedded specimens of DCIS and six associated invasive carcinomas were examined by means of comparative genomic hybridization (CGH). Losses of 16q material were seen almost exclusively in well‐ and intermediately‐differentiated DCIS. These two subgroups differed in the average number of genetic imbalances, 2·5 and 5·5 respectively. Additionally, a higher frequency of gains of 1q and losses of 11q material was seen in intermediately‐differentiated in contrast to well‐differentiated DCIS. Poorly‐differentiated DCIS displayed a higher frequency of amplifications (17q12, 11q13) and a higher average rate of genetic imbalances (7·1). Analysis of adjacent invasive breast carcinoma revealed a genetic pattern almost identical to the one seen in the DCIS counterpart. These data characterize DCIS as a genetically far‐advanced, heterogeneous lesion and as a direct precursor of invasive breast cancer. Copyright © 1999 John Wiley & Sons, Ltd.

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Section: Discussionmentioning

confidence: 75%

Comparative genomic hybridization of ductal carcinomain situ of the breast?evidence of multiple genetic pathways

et al. 1999

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“…(18) Corresponding to this, the frequent occurrence of loss of heterozygosity (LOH) on the long arm of chromosome 14, where Dicer resides, has been reported in lung cancers, (19,20) while a number of studies have also indicated that this chromosomal region is often affected in various other human cancers. (21)(22)(23)(24)(25)(26) It is interesting that LOH on 14q appears to be related to tumor progression of colon cancer, with a higher incidence of this anomaly in metastatic sites than in primary tumors. (27) Accumulating evidence supports the notion that the prognostic impact of reduced Dicer expression observed in our study might have a functional role in the development of lung cancers rather than being a mere surrogate marker.…”

Section: Discussionmentioning

confidence: 99%

Reduced expression of Dicer associated with poor prognosis in lung cancer patients

et al. 2005

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Emerging evidence suggests that microRNA, which are wellconserved, abundant and small regulatory RNA, may be involved in the pathogenesis of human cancers. We recently reported that expression of let-7 was frequently reduced in lung cancers, and that reduced let-7 expression was significantly associated with shorter patient survival. Two members of the double-stranded RNA-specific endonuclease family, Dicer and Drosha, convert precursor forms of microRNA into their mature forms using a stepwise process. In the present study, we examined expression levels of these genes in 67 non-small cell lung cancer cases, and found for the first time that Dicer expression levels were reduced in a fraction of lung cancers with a significant prognostic impact on the survival of surgically treated cases. It should be noted that multivariate COX regression analysis showed that the prognostic impact of Dicer (P = 0.001) appears to be independent of disease stage (P = 0.001), while logistic regression analysis demonstrated that the higher incidence of reduced Dicer expression in poorly differentiated tumors remained significant even after correction for other parameters (P = 0.02).

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“…Interestingly, Schwerdtle et al have found that marker D14S258 also exhibits frequent allelic loss in renal oncocytomas, implicating a locus for a tumour suppressor gene possibly involved in different tumours (Schwerdtle et al, 1997). Furthermore, 14q24-q32 has been found to be the smallest overlapping segment of deletions in both nonpapillary renal cell carcinoma and meningiomas (Simon et al, 1995;Herbers et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Deletions at 14q in malignant mesothelioma detected by microsatellite marker analysis

Wolf

Nordling

et al. 1999

Br J Cancer

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Summary Previous molecular cytogenetic studies by comparative genomic hybridization (CGH) on primary tumours of human malignant mesothelioma have revealed that loss of genetic material at chromosome 14q is one of the most frequently occurring aberrations. Here we further verify the frequency and pattern of deletions at 14q in mesothelioma. A high-resolution deletion mapping analysis of 23 microsatellite markers was performed on 18 primary mesothelioma tumours. Eight of these had previously been analysed by CGH. Loss of heterozygosity or allelic imbalance with at least one marker was detected in ten of 18 tumours (56%). Partial deletions of varying lengths were more common than loss of all informative markers, which occurred in only one tumour. The highest number of tumours with deletions at a specific marker was detected at 14q11.1-q12 with markers D14S283 (five tumours), D14S972 (seven tumours) and D14S64 (five tumours) and at 14q23-q24 with markers D14S258 (five tumours), D14S77 (five tumours) and D14S284 (six tumours). We conclude from these data that genomic deletions at 14q are more common than previously reported in mesothelioma. Furthermore, confirmation of previous CGH results was obtained in all tumours but one. This tumour showed deletions by allelotyping, but did not show any DNA copy number change at 14q by CGH. Although the number of tumours allelotyped was small and the deletion pattern was complex, 14q11.1-q12 and 14q23-q24 were found to be the most involved regions in deletions. These regions provide a good basis for further molecular analyses and may highlight chromosomal locations of tumour suppressor genes that could be important in the tumorigenesis of malignant mesothelioma.

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Significance of chromosome arm 14q loss in nonpapillary renal cell carcinomas

Cited by 14 publications

References 14 publications

Comparative genomic hybridization of ductal carcinomain situ of the breast?evidence of multiple genetic pathways

Comparative genomic hybridization of ductal carcinomain situ of the breast?evidence of multiple genetic pathways

Reduced expression of Dicer associated with poor prognosis in lung cancer patients

Deletions at 14q in malignant mesothelioma detected by microsatellite marker analysis

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