![]() Evidence suggests that the malignant potential is already present in the non invasive period. Herein we will review the epigenetic interactions that have been uncovered in early stage lesions that impact breast cancer progression, and how these players may be utilized as biomarkers to mitigate overdiagnosis and overtreatment.ĭuctal Carcinoma in Situ is an entity which bears the risk of progression into Invasive Breast Carcinoma of No Special Type (IBC of NST). In addition to DNA methylation, histone modifications, and chromatin remodeling, we must also consider enhancers as well as the growing field of noncoding RNAs. The types of epigenetic changes, as well as the molecular players, are expanding. Epigenetic signaling pathways, and the molecular players that interpret and sustain their signals, are critical to understanding the underlying pathology of breast cancer progression. Epigenetic changes, critical for imprinting and tissue specific development, in the incorrect context can lead to global signaling rewiring driving pathological phenotypes. Interrogating the transcriptome alone has yet to define clear functional determinants of progression from DCIS to IDC. This has led to a current state of overdiagnosis and overtreatment. ![]() ![]() Thus, patients diagnosed with DCIS will undergo surgery with the potential for radiation and hormone therapy. Although only a small subset of DCIS lesions are predicted to progress into a breast cancer, distinguishing innocuous from minacious DCIS lesions remains a clinical challenge. ![]() Ductal Carcinoma in Situ (DCIS) is an early breast cancer lesion that is considered a nonobligate precursor to development of invasive ductal carcinoma (IDC). ![]()
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