What The Experts Are Saying
Epigenetics is the foundation of our research. See what leading research has to say about this exciting and upcoming field.
“The current study reveals the importance of gene regulation by epigenetic rather than genetic mechanisms enabling the cancer cells to readily adapt to new microenvironments of the various organs of the human body at sites away from the initial sites at which the cancer cells formed.”
BOSTON UNIVERSITY
MEDICAL CENTER
Epigenetic regulation of metastatic breast cancer
progression may guide prognosis, future therapy
Evidence of Epigenetic Role in Breast Cancer
“Now that we have identified a new mechanism directly connecting an oncogenic signaling pathway with epigenetic regulation in ER-positive breast cancer, we can explore the possibility of targeted and personalized therapies with a more limited chance of resistance in this setting.”
Epigenetic Research
Epigenetics in Breast Cancer: What’s New?
“While an understanding of epigenetic changes in breast cancer has yet to be translated into clinical care, we should expect major steps forward over the next few years. Fundamental discoveries in the understanding of basic epigenetic regulatory mechanisms and dramatic advances in powerful technologies, together with large national and international epigenome projects, will enable identification of breast cancer-specific alterations, and thus potential predictive markers and treatment targets. We firmly believe we have entered an era of epigenomics that will bring benefits for breast cancer patients.”
Epigenetic Targeting In Breast Cancer: Therapeutic Impact and Future Direction
“Since epigenetic changes are potentially reversible processes, much effort has been directed toward understanding this mechanism with the goal of finding novel therapies as well as more refined diagnostic and prognostic tools in breast cancer.”
The increasing roles of epigenetics in breast cancer: Implications for pathogenicity, biomarkers, prevention and treatment.
“Nowadays, the mechanisms governing the occurrence of cancer are thought to be the consequence not only of genetic defects but also of epigenetic modifications. Therefore, epigenetic has become a very attractive and increasingly investigated field of research in order to find new ways of prevention and treatment of neoplasia, and this is particularly the case for breast cancer (BC).”
Therapeutic Implications of Epigenetic Signaling in Breast Cancer
“This rapidly emerging discipline provides the promise of improved clinical outcomes and real changes to survival rates that decrease the probability of tumor relapse and metastasis. In conclusion, emerging studies and further investigation of epigenetic signaling coupled with the development of therapeutic compounds will lead to crucial advances in pharmacological treatment of breast cancer.”
The Epigenetics of Breast Cancer
“Currently three breast cancer projects within the framework of the ICGC have been announced that will analyze together at least 1500 breast tumors at the genetic, transcriptomic and epigenetic (DNA methylation) level… The results will yield an immense amount of data to decipher the epigenetic (and other molecular) alterations implicated in breast carcinogenesis and will permit to identify correlations between tumor-specific epigenetic changes with clinical and histopathological data including prognosis, prediction of therapy response and tumor classification schemes for diagnosis and might eventually lead to the development of novel specific therapies.”
Epigenetic Events Associated with Breast Cancer and Their Prevention by Dietary Components Targeting the Epigenome
“…bioactive components are able to modulate epigenetic events, and their epigenetic targets are known to be associated with breast cancer prevention and therapy. This approach could facilitate the discovery and development of novel drugs for the treatment of breast cancer. In this brief review, we will summarize the epigenetic events associated with breast cancer and the potential of some of these bioactive dietary components to modulate these events and thus afford new therapeutic or preventive approaches.”
TIMP3 Promoter Methylation Represents an Epigenetic Marker of BRCA1ness Breast Cancer Tumours.
“In our study, we analyzed the frequency of methylation changes of 24 tumour suppressor genes and explored their association with BRCAness profile…we confirmed that TIMP3 methylation is a marker for TN tumours and furthermore we showed for the first time that TIMP3 promoter methylation is an epigenetic marker of BRCA1ness tumours.”
Candidate gene DNA methylation associations with breast cancer characteristics and tumor progression.
“GSTM2 promoter hypermethylation may serve as a potential biomarker of aggressive tumor development and a mechanism for ER/PR-negative tumor progression.”
ATF-3/miR-590/GOLPH3 signaling pathway regulates proliferation of breast cancer.
“This study not only suggests that the ATF-3/miR-590/GOLPH3 signaling pathway is critically involved in the proliferation of breast cancer cells, but provides a novel therapeutic target and new insight base on epigenetic regulation for future breast cancer diagnosis and clinical treatment.”
MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state.
“Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways.”
Frequent downregulation of LRRC26 by epigenetic alterations is involved in the malignant progression of triple-negative breast cancer.
“Triple-negative breast cancer (TNBC), defined as breast cancer lacking estrogen- and progesterone‑receptor expression and human epidermal growth factor receptor 2 (HER2) amplification, is a heterogeneous disease… findings demonstrate that LRRC26 is frequently downregulated in TNBC due to DNA methylation and that it suppresses the TNF-α-independent anchorage-independent growth, invasion and migration of TNBC cells. Loss of LRRC26 function may be a critical event in the aggressiveness of TNBC cells through a TNF-α/NF-κB-independent mechanism.”