Thus, lsy-2 and the LIN-35/Rb-containing DRM complex function in parallel to repress the expression of germ cell traits in somatic cells.
Currently, it is known that sub-populations of chemoresistant cells share biological properties with cancer stem cells (CSC), which are believed to be responsible for tumor relapse, invasion and ultimately disease dissemination through acquisition of mesenchymal cell traits.
In concurrent BCX analyses, there was overlap of platelet-associated variants with red (MAP1A, TMPRSS6, ZMIZ2) and white (PEAR1, ZMIZ2, LY75) blood cell traits, suggesting common regulatory pathways with shared genetic architecture among these hematopoietic lineages.
We show that stem cell traits normally present in NSCs are aberrantly co-expressed with pluripotent stem cell markers in high grade gliomas.
Random integration and amplification may also disrupt or dysregulate endogenous genes [11] [13] creating the potential for variation in other cell traits [14], [15].
Regardless, the association of stem cell traits with cancer pathogenesis motivates a further characterization of stem cell related signatures in tumors and a better description of molecular similarities and differences in comparison with non-transformed stem cells.
Together these results demonstrate a general deregulated expression of neural and pluripotent stem cell traits in malignant human gliomas, and indicate that stem cell regulatory factors may provide significant targets for therapeutic strategies.
However, not all cancer cell traits (e.g. migration, invasiveness, stimulation of angiogenesis, resistance to cytotoxic agents) can be directly related to their ability to proliferate in the absence of growth factors.
Persistent presence of pluripotent stem cell traits could only be detected in solid tumors, and observations based on in vitro studies and xenograft transplantations in mice imply that this presence is dependent on the combined activity of intrinsic and extrinsic regulatory cues.
These TFs suppress critical epithelial cell traits, permitting the transformation to mesenchymal cells to occur.
Another QTL for fat cell traits was found at position 53-55 cM (W × P cross).
