The article "Stem Cells and Cancer: Two Faces of Eve" by Michael F. Clarke and Margaret Fuller explores the role of stem cells in cancer development and progression. It highlights that a subset of cancer cells, known as cancer stem cells (CSCs), may drive tumor growth and metastasis. These CSCs have the ability to self-renew and differentiate, unlike the majority of cancer cells which have limited proliferation potential. The presence of CSCs in tumors suggests that targeting these cells is crucial for effective treatment. The authors discuss the evolutionary advantage of stem cells in maintaining tissue homeostasis and preventing cancer. They argue that long-lived multicellular organisms have evolved mechanisms to limit the number of long-lived cells with self-renewal capacity, reducing the risk of cancer. This is achieved through the regulation of stem cell expansion by the stem cell niche, a specialized microenvironment that controls stem cell maintenance and differentiation. The article also delves into the molecular pathways involved in stem cell self-renewal and differentiation, such as the role of Bmi1 in maintaining stem cell identity. It suggests that oncogenic mutations can disrupt these pathways, leading to the emergence of CSCs. These mutations can either inactivate normal stem cell expansion constraints or allow transit-amplifying cells to continue proliferating without differentiating, ultimately giving rise to CSCs. Finally, the authors emphasize the importance of understanding the differences between normal and cancer stem cells to develop more effective therapeutic strategies. They propose that targeting the signals transmitted by the niche to CSCs and disrupting the pathways that regulate the programmed decline in replication potential of transit-amplifying progenitor cells could be key to developing more effective cancer treatments.The article "Stem Cells and Cancer: Two Faces of Eve" by Michael F. Clarke and Margaret Fuller explores the role of stem cells in cancer development and progression. It highlights that a subset of cancer cells, known as cancer stem cells (CSCs), may drive tumor growth and metastasis. These CSCs have the ability to self-renew and differentiate, unlike the majority of cancer cells which have limited proliferation potential. The presence of CSCs in tumors suggests that targeting these cells is crucial for effective treatment. The authors discuss the evolutionary advantage of stem cells in maintaining tissue homeostasis and preventing cancer. They argue that long-lived multicellular organisms have evolved mechanisms to limit the number of long-lived cells with self-renewal capacity, reducing the risk of cancer. This is achieved through the regulation of stem cell expansion by the stem cell niche, a specialized microenvironment that controls stem cell maintenance and differentiation. The article also delves into the molecular pathways involved in stem cell self-renewal and differentiation, such as the role of Bmi1 in maintaining stem cell identity. It suggests that oncogenic mutations can disrupt these pathways, leading to the emergence of CSCs. These mutations can either inactivate normal stem cell expansion constraints or allow transit-amplifying cells to continue proliferating without differentiating, ultimately giving rise to CSCs. Finally, the authors emphasize the importance of understanding the differences between normal and cancer stem cells to develop more effective therapeutic strategies. They propose that targeting the signals transmitted by the niche to CSCs and disrupting the pathways that regulate the programmed decline in replication potential of transit-amplifying progenitor cells could be key to developing more effective cancer treatments.