Whole genome scanning identifies genotypes associated with recurrence and metastasis in prostate tumors

Paris, Pamela L.; Andaya, Armann; Fridlyand, Jane; Jain, Ajay N.; Weinberg, Vivian; Kowbel, David; Brebner, John H.; Simko, Jeff; Watson, J. E. V.; Volik, Stas; Albertson, Donna G.; Pinkel, Daniel; Alers, Janneke C.; Kwast, Theodorus H. van der; Vissers, Kees J.; Schröder, Fritz H.; Wildhagen, Mark F.; Febbo, Phillip G.; Chinnaiyan, Arul M.; Pienta, Kenneth J.; Carroll, Peter R.; Rubin, Mark A.; Collins, Colin C.; Dekken, Herman van

doi:10.1093/hmg/ddh155

Cited by 168 publications

(156 citation statements)

References 52 publications

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“…The region at 5p13 showing copy gain harbours the F-box protein SKP2, which is upregulated in advanced PCa (Dhanasekaran et al, 2001) and was found to induce PCa in a transgenic mouse model (Shim et al, 2003). Copy gain at chromosome 11q13 was shown to predict postoperative recurrence independent of stage and grade, but a specific biomarker has not been identified at this region (Paris et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Genome-wide analysis of allelic imbalance in prostate cancer using the Affymetrix 50K SNP mapping array

et al. 2007

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Prostate cancer (PCa) is the most commonly diagnosed non-cutaneous cancer in male subjects in Western countries. The widespread use of prostate-specific antigen (PSA) has increased the detection of this cancer form in earlier stages. Moreover, it has increased the need for new diagnostic procedures to be developed for patient stratification based on risk of progression. We analysed laser-microdissected prostate tumour tissue from 43 patients with histologically verified PCa, using the new high-resolution Affymetrix Mapping 50K single-nucleotide polymorphism array. The results showed six major loss of heterozygosity regions at chromosomes 6q14 -16, 8p23 -11, 10q23, 13q13 -21 and 16q21 -24 and a novel region at chromosome 21q22.2, all of which reveal concomitant copy number loss. Tumour development was further characterised by numerous novel genomic regions almost exclusively showing copy number loss. However, tumour progression towards a metastatic stage, as well as poor differentiation, was identified by specific patterns of copy number gains of genomic regions located at chromosomes 8q, 1q, 3q and 7q. Androgen ablation therapy was further characterised by copy gain at chromosomes 2p and 10q. In conclusion, patterns of allelic imbalance were discovered in PCa, consisting allelic loss as an early event in tumour development, and distinct patterns of allelic amplification related to tumour progression and poor differentiation.

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Section: Discussionmentioning

confidence: 99%

Genome-wide analysis of allelic imbalance in prostate cancer using the Affymetrix 50K SNP mapping array

et al. 2007

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“…All data transformation and statistical analysis were carried out in R 2.0.1 (http://www.r-project.org/), BioConductor 1.5 (http:// www.bioconductor.org/), making extensive use of modified versions of the package aCGH in particular (Paris et al, 2004;Natrajan et al, 2006) and S-Plus (version 6.2.1). The log 2 ratio of each BAC clone in each tumour sample was centred by the median of each case.…”

Section: Discussionmentioning

confidence: 99%

Microarray-based comparative genomic hybridisation of breast cancer patients receiving neoadjuvant chemotherapy

et al. 2006

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We analysed the molecular genetic profiles of breast cancer samples before and after neoadjuvant chemotherapy with combination doxorubicin and cyclophosphamide (AC). DNA was obtained from microdissected frozen breast core biopsies from 44 patients before chemotherapy. Additional samples were obtained before the second course of chemotherapy (D21) and after the completion of the treatment (surgical specimens) in 17 and 21 patients, respectively. Microarray-based comparative genome hybridisation was performed using a platform containing B5800 bacterial artificial chromosome clones (genome-wide resolution: 0.9 Mb). Analysis of the 44 pretreatment biopsies revealed that losses of 4p, 4q, 5q, 12q13.11 -12q13.12, 17p11.2 and 17q11.2; and gains of 1p, 2p, 7q, 9p, 11q, 19p and 19q were significantly associated with oestrogen receptor negativity. 16q21 -q22.1 losses were associated with lobular and 8q24 gains with ductal types. Losses of 5q33.3 -q4 and 18p11.31 and gains of 6p25.1 -p25.2 and Xp11.4 were associated with HER2 amplification. No correlations between DNA copy number changes and clinical response to AC were found. Microarray-based comparative genome hybridisation analysis of matched pretreatment and D21 biopsies failed to identify statistically significant differences, whereas a comparison between matched pretreatment and surgical samples revealed a statistically significant acquired copy number gain on 11p15.2 -11p15.5. The modest chemotherapy-driven genomic changes, despite profound loss of cell numbers, suggest that there is little therapeutic selection of resistant non-modal cell lineages.

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“…Vol. 63,2006 Review Article 455 pressor genes) are sufficient for certain tumor cells to spread [125,126]. For instance, gene microarray analysis has identified specific expression profiles in metastatic versus non-metastatic primary human carcinomas [127][128][129][130].…”

Section: Genes Mediating Metastasismentioning

confidence: 99%

Metastasis: cell-autonomous mechanisms versus contributions by the tumor microenvironment

Kopfstein

Christofori

2006

Cell. Mol. Life Sci.

207

160

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Abstract. The fatality of cancer predominantly results from the dissemination of primary tumor cells to distant sites and the subsequent formation of metastases. During tumor progression, some of the primary tumor cells as well as the tumor microenvironment undergo characteristic molecular changes, which are essential for the metastatic dissemination of tumor cells. In this review, we will discuss recent insights into pro-metastatic events occurring in tumor cells themselves and in the tumor stroma. Tumor cell-intrinsic alterations include the loss of cell polarity and alterations in cell-cell and cell-matrix Cell. Mol. Life Sci. 63 (2006) 449-468 1420-682X/06/040449-20 DOI 10.1007/s00018-005-5296-8 © Birkhäuser Verlag, Basel, 2006 adhesion as well as deregulated receptor kinase signaling, which together support detachment, migration and invasion of tumor cells. On the other hand, the tumor stroma, including endothelial cells, fibroblasts and cells of the immune system, is engaged in an active molecular crosstalk within the tumor microenvironment. Subsequent activation of blood vessel and lymph vessel angiogenesis together with inflammatory and immune-suppressive responses further promotes cancer cell migration and invasion, as well as initiation of the metastatic process.

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Whole genome scanning identifies genotypes associated with recurrence and metastasis in prostate tumors

Cited by 168 publications

References 52 publications

Genome-wide analysis of allelic imbalance in prostate cancer using the Affymetrix 50K SNP mapping array

Genome-wide analysis of allelic imbalance in prostate cancer using the Affymetrix 50K SNP mapping array

Microarray-based comparative genomic hybridisation of breast cancer patients receiving neoadjuvant chemotherapy

Metastasis: cell-autonomous mechanisms versus contributions by the tumor microenvironment

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