We investigated the clinical relevance of β-arrestin-1 in breast cancer and elucidated a potential link between β-arrestin-1 expression and CCND1 amplification.
Here, we investigate the prognostic significance of CCND1 and EMSY amplification in a large series of breast carcinomas and in BRCA1 and BRCA2 mutation positive breast cancers.
<b>Conclusion</b>: This study demonstrated that the low LPP1 expression in breast cancer cells is associated with high levels of cyclin D1/D3 and MMPs as a result of increased transcription by cFOS and cJUN.
Here, we utilized 6 for preparation of labeled oligodeoxynucleotide (ODN) probes based on MS2 and cyclin D1 (a known breast cancer mRNA marker) sequences.
Progestin and antiprogestin responsiveness in breast cancer is driven by the PRA/PRB ratio via AIB1 or SMRT recruitment to the CCND1 and MYC promoters.
Homozygosity for CCND1 A allele was associated with ALL patients and was a risk factor for ALL development, while the presence of the A allele, whether in homozygous or heterozygous state was associated with breast cancer cases and was a risk for breast cancer .Homozygosity for CCND1 G allele was associated with the control group.
The protein synthesis inhibitor silvestrol has potent activity in B-cell leukemias via the mitochondrial pathway of apoptosis, and also reduces cyclin D1 expression in breast cancer and lymphoma cell lines.
Amplification of chromosomal region 11q13, containing the cell cycle regulatory gene CCND1, is frequently found in breast cancer and other malignancies.
The risk of breast cancer development and prognosis may be associated with genetic variation in the CCND1 genotype, which may be used as a biomarker for further studies.
Four antibodies were reactive with both PRAD1 fusion products and cell lysates of B-cell tumor cell lines with t(11;14)(q13;q32) and a breast cancer cell line with 11q13 amplification, on immunoblotting.
These results suggest that arachidonic acid may exert a stimulatory effect on breast cancer cell growth and that this effect possibly involves the induction of cyclin D1 gene expression leading to cell cycle progression.
Histone deacetylase inhibitor trichostatin A represses estrogen receptor alpha-dependent transcription and promotes proteasomal degradation of cyclin D1 in human breast carcinoma cell lines.