Methylation of CpG islands of p16INK4a and cyclinD1 overexpression associated with progression of intraductal proliferative lesions of the breast

Liu, Tieju; Niu, Yun; Yang, Feng; Niu, Ruifang; Yu, Yonghao; Lv, Ajuan; Yang, Yi

doi:10.1016/j.humpath.2008.04.001

Cited by 25 publications

(21 citation statements)

References 32 publications

(34 reference statements)

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“…[21][22][23] Cyclin D1, CDK4 and E2F1 are important proteins promoting transition of G 1 to S phase. [24][25][26][27] On the other hand, p27 acts as the inhibitor of transition of G 1 to S phase.…”

Section: Discussionmentioning

confidence: 99%

Secalonic Acid D induced leukemia cell apoptosis and cell cycle arrest of G1 with involvement of GSK-3β/β-catenin/c-Myc pathway

Zhang¹,

Tao²,

Liang³

et al. 2009

Cell Cycle

100

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Section: Discussionmentioning

confidence: 99%

Secalonic Acid D induced leukemia cell apoptosis and cell cycle arrest of G1 with involvement of GSK-3β/β-catenin/c-Myc pathway

Zhang¹,

Tao²,

Liang³

et al. 2009

Cell Cycle

100

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“…Promoter methylation of 14-3-3 sigma [8,9], RASSF1A [9][10][11], GSTP1 [10,12], APC1 [11], HIN-1 [11], and p16 (INK4a) [13] has been reported in ductal hyperplasia. However, some studies have reported an increase of methylation levels or frequencies with progression to DCIS, while other analyses of the same tumor-related genes detected no difference between ductal hyperplasia and DCIS.…”

Section: Introductionmentioning

confidence: 99%

“…However, some studies have reported an increase of methylation levels or frequencies with progression to DCIS, while other analyses of the same tumor-related genes detected no difference between ductal hyperplasia and DCIS. Methylation studies of FEA was even rare, and only p16 (INK4a) promoter methylation has been reported in FEA [13]. Moreover, most of the studies focused on a single specific gene, or at most a few genes.…”

Section: Introductionmentioning

confidence: 99%

Promoter CpG island hypermethylation during breast cancer progression

et al. 2010

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This study was designed to evaluate the changes in promoter CpG islands hypermethylation during breast cancer progression from pre-invasive lesions [flat epithelial atypia (FEA), atypical ductal hyperplasia (ADH), and ductal carcinoma in situ (DCIS)] to invasive ductal carcinoma (IDC). We performed MethyLight analysis for the methylation status of 57 promoter CpG island loci in 20 IDCs and their paired normal breast tissues. After selecting 15 CpG island loci showing breast cancer-specific DNA methylation, another set of normal breast tissue (n = 10), ADH/FEA (n = 30), DCIS (n = 35), and IDC (n = 30) of the breast were analyzed for these loci. We found six new methylation markers of breast cancer, namely DLEC1, GRIN2B, HOXA1, MT1G, SFRP4, and TMEFF2, in addition to APC, GSTP1, HOXA10, IGF2, RARB, RASSF1A, RUNX3, SCGB3A1 (HIN-1), and SFRP1. The number of methylated genes increased stepwise from normal breast to ADH/FEA and DCIS, while IDC did not differ from DCIS. Methylation levels and frequencies of APC, DLEC1, HOXA1, and RASSF1A promoter CpG islands were significantly higher in ADH/FEA than in normal breast tissue. GRIN2B, GSTP1, HOXA1, RARB, RUNX3, SFRP1, and TMEFF2 showed higher methylation levels and frequencies in DCIS than in ADH/FEA. DICS and IDC did not differ in the methylation levels or frequencies for most CpG island loci except SFRP1 and HOXA10. Our findings showed that promoter CpG island methylation changed significantly in pre-invasive lesions, and was similar in IDC and DCIS, suggesting that CpG island methylation of tumor-related genes is an early event in breast cancer progression.

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“…The overexpression of cyclinD1 has been documented in several carcinomas, including GC [16-18, 21, 22]. Studies have also shown a positive association between CCND1 overexpression and CIHM status of certain genes in gastric cancer [30], colon cancer [31], and intraductal proliferative lesions [32] in the breast. The common G-to-A polymorphism, located at nucleotide 870 in codon 242 in exon 4, leads not to an amino acid change, but to an alternate splicing event, resulting in an altered protein.…”

Section: Discussionmentioning

confidence: 99%

“…Reports have shown a positive association between CCND1 overexpression and CIHM status of certain genes in gastric cancer [30], colon cancer [31], and intraductal proliferative lesions [32] in the breast. However, there have been no reports concerning the association between the CCND1 G870A polymorphism and CIHM in cancer.…”

Section: Introductionmentioning

confidence: 99%

Association Between Cyclin D1 Polymorphism with CpG Island Promoter Methylation Status of Tumor Suppressor Genes in Gastric Cancer

et al. 2010

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Methylation of CpG islands of p16INK4a and cyclinD1 overexpression associated with progression of intraductal proliferative lesions of the breast

Cited by 25 publications

References 32 publications

Secalonic Acid D induced leukemia cell apoptosis and cell cycle arrest of G1 with involvement of GSK-3β/β-catenin/c-Myc pathway

Secalonic Acid D induced leukemia cell apoptosis and cell cycle arrest of G1 with involvement of GSK-3β/β-catenin/c-Myc pathway

Promoter CpG island hypermethylation during breast cancer progression

Association Between Cyclin D1 Polymorphism with CpG Island Promoter Methylation Status of Tumor Suppressor Genes in Gastric Cancer

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