Italian scientists R. M. R. Gangemi et al. from the University of Genova published their study results in the October 23rd online edition of Stem Cells on the role of the pluripotent gene Sox2 in regulating the proliferation of tumor initiating cells (TICs). With fresh tissue biopsy from patients with glioblastoma, the investigators found that the TICs (cancer stem cells) expressed Sox2. With siRNA to silence the glioblastoma TLCs, the cells lost their ability to proliferate and their tumorigenicity in immunodeficient mice. The authors concluded that Sox2 is required for maintenance and self-renewal for not only neural stem cells but also "when they have acquired cancer properties. Sox2, or its immediate downstream effectors, would then be an ideal target for glioblastoma therapy."

There is mounting evidence that adult stem cells undergoing uncontrolled cell division may lead to cancer. Conversely, there is a link between a loss in adult stem cell function and aging. Discovering how stem cells regulate errors during cell division in order to prevent runaway proliferation and tumor formation may prove pivotal in understanding tumorigenesis. In the October 15th online edition of Nature, Univ. of Michigan's J. Cheng et al., reported the results of their study on the mechanism of asymmetric cell division in the Drosophila's male germline stem cells during aging. Investigators presented data showing that orientation of the centrosome to the stem niche (hub) during cell division of the germline stem cells (GSCs) determines whether the cell proceed with asymmetric cell division. It was found that misorientation of the centrosomes in GSCs results in a decline in spermatogenesis and cell cycle arrest. Cell cycle arrest appears to be transient which can be mitigated by correction of centrosome orientation. The authors concluded that misorientation of the centrosomes functions as " a mechanism to ensure asymmetric stem cell division, and that the inability of stem cells to maintain correct orientation during aging contributes to the decline in spermatogenesis."

Chronic inflammation in certain tissues and organs has been associated with a pre-cancerous condition. It is believed that this inflammatory microevironnment leads to constant activation and proliferation of stem cells, which could give rise to cells undergoing somatic mutations. Scientists from Rockefeller University, M. Perez-Moreno et al., reported their experimental results in the October 7th issue of PNAS their experimental results which revealed the loss of p120 catenin in mice give rise to progressive development of skin neoplasias. With the loss of p120, the investigators found there was an intrinsic activation of NF-kB that appeared to impact the epidermal micrcoenvironment. In vitro data of p120-null keratinocytes demonstrated that the cells displayed a growth-arrested phenotype in culture. The researchers traced this behaviour to a mitotic defect leading to unstable binucleated cells both in vitro and in vivo. Inhibiting RhoA expression appeared to abrogate abnormal mitoses. Conversely, elevating the level of RhoA increased the frequency of abnormal mitoses in cultivated keratinocytes. The authors concluded that p120 deficiency and subsequent chronic inflammation "facilitate the development of genetic instability in vivo...which may eventually result in skin cancer progression."

In the October 2nd online edition of Stem Cells, B. Moshaver et al. from VU University Medical Center in Amsterdam reported their results in isolatiing and characterizing leukemic stem cells in patients with acute myeloid leukemia (AML). With FACS analysis of bone marrow tissues and peripheral blood samples, the investigators found that CD34+CD38- leukemic stem cells were found in a side population (SP) fraction with the surface marker CLL-1 and the lineage markers CD7, CD19 and CD56. Further FACS analysis revealed three distinct subpopulations of cells within the SP fraction. The authors concluded from their experimental results that the AML SP cells contained a SP of leukemia-initiating stem cells expressing the CLL-1 marker as well as the lineage markers described above. The leukemic stem cells within the SP fraction were present in a low frequency (median 0.0016%) and where "the likely candidate to be enriched for leukemia stem cells."