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The theory of cancer stem cells states that a subset of cancer cells within a tumor has the ability to self-renew and differentiate. Only those cells within a tumor that have these two properties are called cancer stem cells. This concept was first demonstrated in the study of leukemia where only cells with specific surface antigen profiles were able to cause leukemia when engrafted into immunodeficient mice. In recent years solid tumors were studied utilizing similar techniques in mice. Human tumors where evidence of cancer stem cells has been published include tumors of the breast, brain, pancreas, head and neck, and colon. If this difference in tumorigenicity of cancer cells also occurs in patients, then the ability to enrich for cancer stem cells lays an important groundwork for future studies where mechanisms involved in cancer stem cells can now be investigated. [Copyright &y& Elsevier]

• Not all cancer cells are created equal. There are intrinsic differences among cancer cells from the same patient in terms of their ability to proliferate and form tumors in vivo. • A subset of cancer cells have the properties of cancer stem cells, which self-renew to generate additional cancer stem cells and differentiate to generate phenotypically diverse cancer cells with limited proliferative potential. Cancer stem cells are highly enriched for the ability to form tumors following transplantation relative to bulk tumor cells or non-tumorigenic cancer cells. • Cancer stem cells have been characterized in the context of human acute myeloid leukemia, breast cancer and glioblastoma. In each case, surface markers have been identified that distinguish cancer stem cells from cancer cells with more limited proliferative potential, allowing the prospective identification of cancer stem cells. • In some cases, cancer stem cells might arise from the mutational transformation of normal stem cells, whereas in other cases mutations might cause restricted progenitors or differentiated cells to acquire properties of cancer stem cells such as self-renewal potential. • The neoplastic proliferation of cancer stem cells is likely to be driven by mutations that inappropriately activate pathways that promote the self-renewal of normal stem cells. Examples of these pathways include the WNT, and BMIl-dependent pathways that regulate the self-renewal of haematopoietic stem cells and neural stem cells. • Further characterization of cancer stem cells might lead to improved diagnostics and therapies by allowing us to better identify and target cancer stem cells. To cure cancer it is necessary to kill, differentiate or prevent the metastasis of cancer stem cells. INSETS: Summary;Targeting cancer-stem-cel self-renewal. [ABSTRACT FROM AUTHOR]

The article presents an editorial regarding chronic myelogenous leukemia (CML). Untreated, CML progresses to an accelerated phase and finally to a blast crisis, in which blast cells appear in the bone marrow and blood. The blasts in most patients with blast crisis regenerate after initially regressing in response to the drug imatinib. A study in this issue of the journal by Jamieson and colleagues is mentioned that reports the identification of self-renewing leukemic stem cells.