HIC1 promoter methylation and 17p13.3 allelic loss in invasive ductal carcinoma of the breast

Paola Parrella; Marina Scintu; Maria Prencipe; Maria Luana Poeta; Antonietta Pia Gallo; Carla Rabitti; Monica Rinaldi; Stefania Tommasi; Angelo Paradiso; Francesco Schittulli; Vanna Maria Valori; Salvatore Toma; Vittorio Altomare; Vito Michele Fazio

doi:10.1016/j.canlet.2004.08.026

HIC1 promoter methylation and 17p13.3 allelic loss in invasive ductal carcinoma of the breast

Paola Parrella, Marina Scintu, Maria Prencipe, Maria Luana Poeta, Antonietta Pia Gallo, Carla Rabitti, Monica Rinaldi, Stefania Tommasi, Angelo Paradiso, Francesco Schittulli, Vanna Maria Valori, Salvatore Toma, Vittorio Altomare, Vito Michele Fazio

Research output: Contribution to journal › Article › peer-review

Abstract

The HIC1 gene is a transcriptional regulator commonly methylated in a variety of human cancer. Thirty-three invasive ductal carcinomas of the breast and 21 matched normal breast tissues were analysed for HIC1 promoter methylation, and allelic loss of a 700 kb region spanning the gene locus. At least one genetic or epigenetic abnormality was found in 27 of the carcinomas tested (82%). Promoter methylation was demonstrated in 21 carcinomas (64%), and nine normal tissues (43%), whereas 18 malignant tumors (54%) showed allelic loss. Concomitant loss of heterozigosity and promoter hypermethylation in the region spanning HIC1 was detected in eight carcinomas (24%) suggesting that in this subset of tumors both copies of the gene are functionally lost. These observations support a role for the HIC1 gene in the pathogenesis of breast ductal carcinomas.

Original language	English
Pages (from-to)	75-81
Number of pages	7
Journal	Cancer Letters
Volume	222
Issue number	1
DOIs	https://doi.org/10.1016/j.canlet.2004.08.026
Publication status	Published - May 10 2005

Keywords

Breast cancer
Chromosome 17p13
DNA methylation
HIC1
LOH
Tumor suppressor genes

ASJC Scopus subject areas

Cancer Research
Molecular Biology
Oncology

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HIC1 promoter methylation and 17p13.3 allelic loss in invasive ductal carcinoma of the breast. / Parrella, Paola; Scintu, Marina; Prencipe, Maria; Poeta, Maria Luana; Gallo, Antonietta Pia; Rabitti, Carla; Rinaldi, Monica; Tommasi, Stefania ; Paradiso, Angelo; Schittulli, Francesco; Valori, Vanna Maria; Toma, Salvatore; Altomare, Vittorio; Fazio, Vito Michele.

In: Cancer Letters, Vol. 222, No. 1, 10.05.2005, p. 75-81.

Research output: Contribution to journal › Article › peer-review

Parrella, Paola ; Scintu, Marina ; Prencipe, Maria ; Poeta, Maria Luana ; Gallo, Antonietta Pia ; Rabitti, Carla ; Rinaldi, Monica ; Tommasi, Stefania ; Paradiso, Angelo ; Schittulli, Francesco ; Valori, Vanna Maria ; Toma, Salvatore ; Altomare, Vittorio ; Fazio, Vito Michele. / HIC1 promoter methylation and 17p13.3 allelic loss in invasive ductal carcinoma of the breast. In: Cancer Letters. 2005 ; Vol. 222, No. 1. pp. 75-81.

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title = "HIC1 promoter methylation and 17p13.3 allelic loss in invasive ductal carcinoma of the breast",

abstract = "The HIC1 gene is a transcriptional regulator commonly methylated in a variety of human cancer. Thirty-three invasive ductal carcinomas of the breast and 21 matched normal breast tissues were analysed for HIC1 promoter methylation, and allelic loss of a 700 kb region spanning the gene locus. At least one genetic or epigenetic abnormality was found in 27 of the carcinomas tested (82%). Promoter methylation was demonstrated in 21 carcinomas (64%), and nine normal tissues (43%), whereas 18 malignant tumors (54%) showed allelic loss. Concomitant loss of heterozigosity and promoter hypermethylation in the region spanning HIC1 was detected in eight carcinomas (24%) suggesting that in this subset of tumors both copies of the gene are functionally lost. These observations support a role for the HIC1 gene in the pathogenesis of breast ductal carcinomas.",

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AU - Prencipe, Maria

AU - Poeta, Maria Luana

AU - Gallo, Antonietta Pia

AU - Rabitti, Carla

AU - Rinaldi, Monica

AU - Tommasi, Stefania

AU - Paradiso, Angelo

AU - Schittulli, Francesco

AU - Valori, Vanna Maria

AU - Toma, Salvatore

AU - Altomare, Vittorio

AU - Fazio, Vito Michele

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N2 - The HIC1 gene is a transcriptional regulator commonly methylated in a variety of human cancer. Thirty-three invasive ductal carcinomas of the breast and 21 matched normal breast tissues were analysed for HIC1 promoter methylation, and allelic loss of a 700 kb region spanning the gene locus. At least one genetic or epigenetic abnormality was found in 27 of the carcinomas tested (82%). Promoter methylation was demonstrated in 21 carcinomas (64%), and nine normal tissues (43%), whereas 18 malignant tumors (54%) showed allelic loss. Concomitant loss of heterozigosity and promoter hypermethylation in the region spanning HIC1 was detected in eight carcinomas (24%) suggesting that in this subset of tumors both copies of the gene are functionally lost. These observations support a role for the HIC1 gene in the pathogenesis of breast ductal carcinomas.

AB - The HIC1 gene is a transcriptional regulator commonly methylated in a variety of human cancer. Thirty-three invasive ductal carcinomas of the breast and 21 matched normal breast tissues were analysed for HIC1 promoter methylation, and allelic loss of a 700 kb region spanning the gene locus. At least one genetic or epigenetic abnormality was found in 27 of the carcinomas tested (82%). Promoter methylation was demonstrated in 21 carcinomas (64%), and nine normal tissues (43%), whereas 18 malignant tumors (54%) showed allelic loss. Concomitant loss of heterozigosity and promoter hypermethylation in the region spanning HIC1 was detected in eight carcinomas (24%) suggesting that in this subset of tumors both copies of the gene are functionally lost. These observations support a role for the HIC1 gene in the pathogenesis of breast ductal carcinomas.

KW - Breast cancer

KW - Chromosome 17p13

KW - DNA methylation

KW - HIC1

KW - LOH

KW - Tumor suppressor genes

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HIC1 promoter methylation and 17p13.3 allelic loss in invasive ductal carcinoma of the breast

Abstract

Keywords

ASJC Scopus subject areas

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