| Autor: |
Ferrer AI; Department of Medicine, Rutgers New Jersey Medical School, Newark, NJ, 07103, USA., Trinidad JR; Department of Biological Sciences, Rutgers University, Newark, NJ, 07102, USA., Sandiford O; Department of Medicine, Rutgers New Jersey Medical School, Newark, NJ, 07103, USA., Etchegaray JP; Department of Biological Sciences, Rutgers University, Newark, NJ, 07102, USA. etchegje@newark.rutgers.edu., Rameshwar P; Department of Medicine, Rutgers New Jersey Medical School, Newark, NJ, 07103, USA. rameshwa@njms.rutgers.edu. |
| Abstrakt: |
Cancer remains one of the most challenging diseases despite significant advances of early diagnosis and therapeutic treatments. Cancerous tumors are composed of various cell types including cancer stem cells capable of self-renewal, proliferation, differentiation, and invasion of distal tumor sites. Most notably, these cells can enter a dormant cellular state that is resistant to conventional therapies. Thereby, cancer stem cells have the intrinsic potential for tumor initiation, tumor growth, metastasis, and tumor relapse after therapy. Both genetic and epigenetic alterations are attributed to the formation of multiple tumor types. This review is focused on how epigenetic dynamics involving DNA methylation and DNA oxidations are implicated in breast cancer and glioblastoma multiforme. The emergence and progression of these cancer types rely on cancer stem cells with the capacity to enter quiescence also known as a dormant cellular state, which dictates the distinct tumorigenic aggressiveness between breast cancer and glioblastomas. |
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