Although several ALCL cases have been reported to express antigens of T-cell or B-cell lineage, many cases may lack lymphoid antigens (null type), and rare cases may express both markers [2].
These data suggest that G-CSF may not only expand the numbers of hematopoietic stem cells, but also cells that express markers that may indicate stem-like characteristics.
However, most BrdU cells in the SN failed to express markers for microglia, astroglia, oligodendroglia, or neurons, suggesting that they may remain as uncommitted progenitors.
Thus, it is possible that the drug-resistant cell lines used in our study may express the aforementioned markers and confer resistance to cabazitaxel.
Thus, human endothelial cell precursors may express both progenitor cell markers (CD34, CD133), monocyte markers (CD14 and or CD11b) and endothelial markers (VEGFR2).
Human MDSCs may express the common myeloid marker CD15 or CD33 but lack the expression of markers of mature myeloid and lymphoid cells and the MHC-class-II molecule HLA-DR [ 28– 30].
As noted above, carcinoma cells may not completely lose their epithelial phenotype during an oncogenic EMT and may express epithelial and mesenchymal markers simultaneously [ 3].
Patients may express different serum levels of markers when exposed to bacterial toxins, and this stimulation may be multifactorial.
There is also evidence that adipose tissue isolated from specific fat depots, such as visceral fat, may express higher levels of inflammatory markers such as IL-6 (7), MCP-1 (8), and plasminogen activator inhibitor type 1 (PAI-1) (9).
These preliminary results suggest that although human Treg subsets may express many of the same surface markers or receptors and produce the same cytokines as conventional CD4+CD25− or CD4+CD25low T cells, proliferation of these T cell subsets in response to TCR-mediated signals and IL-2 might be differentially regulated.
