Editorial

Self-renewal and pluripotency have been initially attributed to normal stem cells that posses the ability to give rise to all cell types in the adult organism. Seminal findings by John Dick in acute myeloid leukemia in the late 1990s led to the identification of cancer stem cells (CSCs). Since then, they have been an intense focus of cancer research. CSCs have been identified in most if not all the hematological malignancies as well as the solid tumors. CSCs may generate tumors through the stem cell processes of self-renewal and differentiation into multiple cell types. These cells are proposed to resist various forms of chemotherapy and radiotherapy and cause relapse and metastasis by giving rise to new tumors. Here, in the series of the review articles, we aim to draw parallels between epigenetics, molecular circuits and phenotype between normal pluripotent stem cells and cells with the stem cell like phenotype that propel tumor growth.
Development of specific therapies targeted at CSCs holds hope for improvement of survival and quality of life of cancer patients, especially for patients with metastatic disease. Stem cell paradigm in hematopoietic malignancies has been thoroughly described by Zagożdżon and Gołąb. The authors describe in detail the phenotype and molecular features of CSCs as well as their oncogenic pathways that can be targeted by novel therapies.
Next, focusing on the regulation of breast cancer stem cell features (also named tumor-initiating cells), the review by Czerwińska and Kamińska provides a comprehensive overview of the pathway dependencies (Wnt/-catenin, sonic hedgehog (Shh), Notch and BMP/TGF signaling) that contribute to the self-renewal properties of stem and/or progenitor cells. Adding to this complexity are emerging epigenetic and MicroRNA-based mechanisms that control pluripotency and stemness through regulating transcriptions factors such as Oct3/4, Nanog or Sox2. As discussed by these authors, this cross-talk between epigenetics and canonical signaling pathways opens up for exciting therapeutic opportunities as inhibition of DNA methylation, histone methyltransferases and histone deacetylases may directly impact some of the cell signaling pathways that controls stemness, tumorigenesis and metastatic potential. Therapeutic approaches to cancer have traditionally focused on ‘chemotherapy’ and on targeting oncogenic signaling and mechanisms intrinsic to cancer cell proliferation and survival. Along these...


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