scholarly journals O-13 D-glucuronyl C5-epimerase inhibits breast cancer cells proliferation through the tumour suppressor genes activation

2010 ◽  
Vol 8 (6) ◽  
pp. 5
Author(s):  
T.Y. Prudnikova ◽  
N.V. Domanitskaya ◽  
L.A. Mostovich ◽  
T.V. Pavlova ◽  
V.I. Kashuba ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Suppressor Genes

Clofarabine, a novel adenosine analogue, reactivates DNA methylation-silenced tumour suppressor genes and inhibits cell growth in breast cancer cells

2014 ◽  
Vol 723 ◽  
pp. 276-287 ◽  
Author(s):  
Katarzyna Lubecka-Pietruszewska ◽  
Agnieszka Kaufman-Szymczyk ◽  
Barbara Stefanska ◽  
Barbara Cebula-Obrzut ◽  
Piotr Smolewski ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Cell Growth ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Suppressor Genes ◽  
Adenosine Analogue

scholarly journals Anti-proliferative effect of estrogen in breast cancer cells that re-express ERα is mediated by aberrant regulation of cell cycle genes

2005 ◽  
Vol 34 (2) ◽  
pp. 535-551 ◽  
Author(s):  
J G Moggs ◽  
T C Murphy ◽  
F L Lim ◽  
D J Moore ◽  
R Stuckey ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cyclin B1 ◽  
Tumour Suppressor Genes ◽  
Cell Cycle Regulators ◽  
Adenoviral Infection ◽  
Promote Cell Proliferation ◽  
Er Positive

Estrogen receptor (ER)-negative breast carcinomas do not respond to hormone therapy, making their effective treatment very difficult. The re-expression of ERα in ER-negative MDA-MB-231 breast cancer cells has been used as a model system, in which hormone-dependent responses can be restored. Paradoxically, in contrast to the mitogenic activity of 17β-estradiol (E2) in ER-positive breast cancer cells, E2 suppresses proliferation in ER-negative breast cancer cells in which ERα has been re-expressed. We have used global gene expression profiling to investigate the mechanism by which E2 suppresses proliferation in MDA-MB-231 cells that express ERα through adenoviral infection. We show that a number of genes known to promote cell proliferation and survival are repressed by E2 in these cells. These include genes encoding the anti-apoptosis factor SURVIVIN, positive cell cycle regulators (CDC2, CYCLIN B1, CYCLIN B2, CYCLIN G1, CHK1, BUB3, STK6, SKB1, CSE1 L) and chromosome replication proteins (MCM2, MCM3, FEN1, RRM2, TOP2A, RFC1). In parallel, E2-induced the expression of the negative cell cycle regulators KIP2 and QUIESCIN Q6, and the tumour-suppressor genes E-CADHERIN and NBL1. Strikingly, the expression of several of these genes is regulated in the opposite direction by E2 compared with their regulation in ER-positive MCF-7 cells. Together, these data suggest a mechanism for the E2-dependent suppression of proliferation in ER-negative breast cancer cells into which ERα has been reintroduced.

Use of Monozygotic Twins in Search for Breast Cancer Susceptibility Loci

Twin Research ◽  
2001 ◽  
Vol 4 (4) ◽  
pp. 251-259 ◽  
Author(s):  
Asta Försti ◽  
Qianren Jin ◽  
Lena Sundqvist ◽  
Magnus Söderberg ◽  
Kari Hemminki
Keyword(s):  
Breast Cancer ◽  
Cancer Susceptibility ◽  
Monozygotic Twins ◽  
Monozygotic Twin ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Suppressor Genes ◽  
Twin Model

AbstractWe have used Swedish monozygotic twins concordant for breast cancer to study genetic changes associated with the development of breast cancer. Because loss of heterozygosity (LOH) at a specific genomic region may reflect the presence of a tumour suppressor gene, loss of the same allele in both of the twins concordant for breast cancer may pinpoint a tumour suppressor gene that confers a strong predisposition to breast cancer. DNA samples extracted from the matched tumour and normal tissues of nine twin pairs were analysed for allelic imbalance using a set of microsatellite markers on chromosomes 1, 13, 16 and 17, containing loci with known tumour suppressor genes. The two main regions, where more twin pairs than expected had lost the same allele, were located at 16qtel, including markers D16S393, D16S305 and D16S413, and at 17p13, distal to the p53 locus. Our results show that the monozygotic twin model can be used to suggest candidate regions of potential tumour suppressor genes, even with a limited number of twin pairs.

scholarly journals REVERSAL OF HYPERMETHYLATION AND REACTIVATION OF TUMOR SUPPRESSOR GENES DUE TO NATURAL COMPOUNDS IN BREAST CANCER CELLS

2020 ◽  
Vol 02 (01) ◽  
pp. 63-75
Author(s):  
Debasray Saha ◽  
Neeraj Vaishnav ◽  
Zubiya Ahsan ◽  
Nisha Rani ◽  
Runjhun Mathur ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Genes ◽  
Breast Cancer Cells ◽  
Natural Compounds ◽  
Suppressor Genes

scholarly journals Synthetic lethality: the road to novel therapies for breast cancer

2016 ◽  
Vol 23 (10) ◽  
pp. T39-T55 ◽  
Author(s):  
Kiranjit K Dhillon ◽  
Ilirjana Bajrami ◽  
Toshiyasu Taniguchi ◽  
Christopher J Lord
Keyword(s):  
Breast Cancer ◽  
Synthetic Lethality ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Novel Therapies ◽  
Loss Of Function ◽  
Molecular Processes ◽  
Suppressor Genes ◽  
The Road ◽  
Over Time

When theBRCA1andBRCA2tumour suppressor genes were identified in the early 1990s, the immediate implications of mapping, cloning and delineating the sequence of these genes were that individuals in families with aBRCAgene mutation could be tested for the presence of a mutation and their risk of developing cancer could be predicted. Over time though, the discovery ofBRCA1andBRCA2has had a much greater influence than many might have imagined. In this review, we discuss how the discovery ofBRCA1andBRCA2has not only provided an understanding of the molecular processes that drive tumourigenesis but also reignited an interest in therapeutically exploiting loss-of-function alterations in tumour suppressor genes.

scholarly journals Is DNA methylation of tumour suppressor genes epigenetic?

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Kevin Struhl
Keyword(s):  
Colorectal Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Suppressor Genes ◽  
Colorectal Cancer Cells ◽  
Transcriptional Pathway

In colorectal cancer cells, a non-epigenetic transcriptional pathway that is mediated by an oncogene maintains DNA methylation of tumour suppressor genes

scholarly journals CRISPR–Cas9/long-read sequencing approach to identify cryptic mutations in BRCA1 and other tumour suppressor genes

2020 ◽  
pp. jmedgenet-2020-107320 ◽  
Author(s):  
Tom Walsh ◽  
Silvia Casadei ◽  
Katherine M Munson ◽  
Mary Eng ◽  
Jessica B Mandell ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Bilateral Breast Cancer ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Single Nucleotide Variants ◽  
Suppressor Genes ◽  
Small Indels ◽  
Long Reads ◽  
Long Read ◽  
Genomic Regions

AbstractCurrent clinical approaches for mutation discovery are based on short sequence reads (100–300 bp) of exons and flanking splice sites targeted by multigene panels or whole exomes. Short-read sequencing is highly accurate for detection of single nucleotide variants, small indels and simple copy number differences but is of limited use for identifying complex insertions and deletions and other structural rearrangements. We used CRISPR-Cas9 to excise complete BRCA1 and BRCA2 genomic regions from lymphoblast cells of patients with breast cancer, then sequenced these regions with long reads (>10 000 bp) to fully characterise all non-coding regions for structural variation. In a family severely affected with early-onset bilateral breast cancer and with negative (normal) results by gene panel and exome sequencing, we identified an intronic SINE-VNTR-Alu retrotransposon insertion that led to the creation of a pseudoexon in the BRCA1 message and introduced a premature truncation. This combination of CRISPR–Cas9 excision and long-read sequencing reveals a class of complex, damaging and otherwise cryptic mutations that may be particularly frequent in tumour suppressor genes replete with intronic repeats.

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