In the last few years, many studies have demonstrated a link between the trancriptional networks that
maintain stem cell cell self-renewal and cancer initiation. For example, expression of pluripotency
transcription factors has been described in many tumor models such as breast, ovarian, lung and brain
tumors. However, very little is known about the regulation of these transcriptional networks in cancer, and
whether their activation results in a disrupted epigenome. The objective of this research topic is to bring
together the scientific community that actively investigates the molecular basis of cancer initiation, with focus
on the role of pluripotency genes, and how the disrupted transcriptional and epigenomic network might lead
to tumorigenesis and tumor progression. Further, novel molecular tools designed to reprogram this aberrant
epigenetic and transcriptomal state in cancer are anticipated to "correct" the cancer epigenome.
In the last few years, many studies have demonstrated a link between the trancriptional networks that
maintain stem cell cell self-renewal and cancer initiation. For example, expression of pluripotency
transcription factors has been described in many tumor models such as breast, ovarian, lung and brain
tumors. However, very little is known about the regulation of these transcriptional networks in cancer, and
whether their activation results in a disrupted epigenome. The objective of this research topic is to bring
together the scientific community that actively investigates the molecular basis of cancer initiation, with focus
on the role of pluripotency genes, and how the disrupted transcriptional and epigenomic network might lead
to tumorigenesis and tumor progression. Further, novel molecular tools designed to reprogram this aberrant
epigenetic and transcriptomal state in cancer are anticipated to "correct" the cancer epigenome.