Allelic loss on chromosome band 18p11.3 occurs early and reveals heterogeneity in breast cancer progression

Kittiniyom, Kanokwan; Gorse, Karen; Dalbègue, Fabienne; Lichy, Jack H.; Taubenberger, Jeffery K.; Newsham, Irene

doi:10.1186/bcr294

Cited by 33 publications

(34 citation statements)

References 19 publications

(28 reference statements)

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“…Loss of the 18p chromosomal region has been shown as an early event in breast cancer progression [35] and has been associated with a poor outcome [7]. Addou-Klouche et al…”

Section: Discussionmentioning

confidence: 99%

Loss of protein tyrosine phosphatase, non-receptor type 2 is associated with activation of AKT and tamoxifen resistance in breast cancer

Karlsson

Veenstra

Emin

et al. 2015

Breast Cancer Res Treat

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Gene copy loss of PTPN2 was detected in 16% (34/215) of the tumours and this was significantly correlated with lower levels of PTPN2 mRNA. PTPN2 gene loss and lower mRNA levels were associated with activation of AKT and a poor prognosis. Furthermore, PTPN2 gene loss was a significant predictive marker of poor benefit from tamoxifen treatment.In conclusion, genomic loss of PTPN2 may be a previously unknown mechanism of PI3K/AKT upregulation in breast cancer. PTPN2 status is a potential new clinical marker of endocrine treatment benefit which could guide further individualised therapies in breast cancer.

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“…Loss of the 18p chromosomal region has been shown as an early event in breast cancer progression [35] and has been associated with a poor outcome [7]. Addou-Klouche et al…”

Section: Discussionmentioning

confidence: 99%

Loss of protein tyrosine phosphatase, non-receptor type 2 is associated with activation of AKT and tamoxifen resistance in breast cancer

Karlsson

Veenstra

Emin

et al. 2015

Breast Cancer Res Treat

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“…Loss of heterozygosity at multiple loci has been reported to occur early in tumorigenesis in a number of cancers (Watson et al 1998;Lakhani et al 1999;Kittiniyom et al 2001). Assessment of metastatic potential will be another exciting application, as demonstrated by the recent findings that gene-dosage increases for PRL3 at 8q24.3 correlate with metastasis in colon cancer (Saha et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Whole Genome Analysis of Genetic Alterations in Small DNA Samples Using Hyperbranched Strand Displacement Amplification and Array–CGH

Lage¹,

Leamon²,

Pejović³

et al. 2003

Genome Res.

233

210

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Structural genetic alterations in cancer often involve gene loss or gene amplification. With the advent of microarray approaches for the analysis of the genome, as exemplified by array–CGH (Comparative GenomicHybridization), scanning for gene-dosage alterations is limited only by issues of DNA microarray density. However, samples of interest to the pathologist often comprise small clusters of just a few hundred cells, which do not provide sufficient DNA for array–CGH analysis. We sought to develop a simple method that would permit amplification of the whole genome without the use of thermocycling or ligation of DNA adaptors, because such a method would lend itself to the automated processing of a large number of tissue samples. We describe a method that permits the isothermal amplification of genomic DNA with high fidelity and limited sequence representation bias. The method is based on strand displacement reactions that propagate by a hyperbranching mechanism, and generate hundreds, or even thousands, of copies of the genome in a few hours. Using whole genome isothermal amplification, in combination with comparative genomic hybridization on cDNA microarrays, we demonstrate the ability to detect gene losses in yeast and gene dosage imbalances in human breast tumor cell lines. Although sequence representation bias in the amplified DNA presents potential problems for CGH analysis, these problems have been overcome by using amplified DNA in both control and tester samples. Gene-dosage alterations of threefold or more can be observed with high reproducibility with as few as 1000 cells of starting material.

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“…Previous reports have suggested that protein 4.1B may function as a tumor suppressor protein whose expression is lost in breast cancers (Tran et al, 1998;Kittiniyom et al, 2001;Charboneau et al, 2002). However, the role of 4.1B in normal mammary epithelium had not been previously tested.…”

Section: Protein 41b Expression Is Induced In Mammary Epithelia Durimentioning

confidence: 99%

“…Because loss of this region occurs with relatively high frequency in ductal carcinomas in situ (56%), it has been proposed to be an early event in tumor progression in the breast (Kittiniyom et al, 2001). Furthermore, re-introduction of the minimal growth inhibitory domain of 4.1B, called DAL-1 (differentially expressed in adenocarcinoma of the lung), results in growth suppression in a number of mammary carcinoma cell lines (Charboneau et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Protein 4.1B expression is induced in mammary epithelial cells during pregnancy and regulates their proliferation

et al. 2005

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4.1B is a member of the protein 4.1 superfamily of proteins that link transmembrane proteins to the actin cytoskeleton. The 4.1B gene localizes to chromosome 18p11.3, which undergoes loss of heterozygosity in mammary tumors. Here, we examine the expression of 4.1B in murine mammary epithelium and find that 4.1B is dramatically upregulated in mammary epithelial cells during pregnancy when there is extensive cell proliferation. In contrast, 4.1B is not expressed in virgin, lactating, or involuting mammary epithelium. To examine the consequence of 4.1B loss on mammary epithelial cell proliferation, we analysed mammary glands in 4.1B-null mice. 4.1B loss results in a significant increase in mammary epithelial cell proliferation during pregnancy, but has no effect on mammary epithelial cell proliferation, in virgin or involuting mice. Furthermore, we show that 4.1B inhibits the proliferation of mammary epithelial cell lines by inducing a G 1 cell cycle arrest, characterized by decreased cyclin A expression and reduced Rb phosphorylation, and accompanied by reduced erbB2 phosphorylation. This cell cycle arrest does not involve alterations in the activities of MAPK, JNK, or Akt. Collectively, our findings demonstrate that 4.1B regulates mammary epithelial cell proliferation during pregnancy and suggest that its loss may influence mammary carcinoma pathogenesis in multiparous women.

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Allelic loss on chromosome band 18p11.3 occurs early and reveals heterogeneity in breast cancer progression

Cited by 33 publications

References 19 publications

Loss of protein tyrosine phosphatase, non-receptor type 2 is associated with activation of AKT and tamoxifen resistance in breast cancer

Loss of protein tyrosine phosphatase, non-receptor type 2 is associated with activation of AKT and tamoxifen resistance in breast cancer

Whole Genome Analysis of Genetic Alterations in Small DNA Samples Using Hyperbranched Strand Displacement Amplification and Array–CGH

Protein 4.1B expression is induced in mammary epithelial cells during pregnancy and regulates their proliferation

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