Phenotypic and Functional Analysis of Dendritic Cells and Clinical Outcome in Patients With High-Risk Melanoma Treated With Adjuvant Granulocyte Macrophage Colony-Stimulating Factor

Abstract

GM-CSF treatment was associated with a transient increase in mature DCs, but not MDSCs. Greater increase of DCs was associated with remission or delayed recurrence. The prolonged overall survival observed warrants further exploration.

T cytotoxic 17 cells suppress the inflammatory reaction by regulating chemokines in colonic cancer

“…larly with previous studies about CCL2 [14,18], CXCL12 [19] and GM-CSF [20], our results demonstrated higher CCL2, CXCL12 and GM-CSF expressions in SW620 cells. Therefore, the result suggested that Tc17 cells could induce the immunosuppression status by promoting the expression of immunosuppression chemokines.…”

Involvement of a Rac1-Dependent Macropinocytosis Pathway in Plasmid DNA Delivery by Electrotransfection

“…The technique relies on delivery of a sequence of electric pulses to target cells or tissues placed between electrodes, which leads to the entry of cell-impermeable molecules, including plasmid DNA (pDNA). 22,23 Although electrotransfection has been implemented as a powerful tool in both basic research and clinical applications, [24][25][26][27][28][29][30][31][32] the exact mechanism of electro-gene transfer is still largely unknown. [33][34][35][36] One of the most popular mechanisms, known as the "pore theory," states that, when electric-field-induced transmembrane potential exceeds a certain threshold, transient pores will form in the plasma membrane, [37][38][39][40][41][42] allowing extracellular molecules to enter cytoplasm through diffusion, electrophoresis, and/or electro-osmosis.…”

Horizontal gene transfers and cell fusions in microbiology, immunology and oncology (Review)

“…Interestingly, GM-CSF is included in certain melanoma treatment protocols as a stimulator of DCs. It may increase response rates and delay relapses (205,206), but these additional benefits are not unequivocally confirmed (207). Single melanoma cells may be killed by a host immune attack thus induced, while subclones of melanoma cell-macrophage hybrids may be stimulated by GM-CSF and cause a relapse.…”

“…Overexpression of all the above listed receptors in metastatic melanoma cells strongly suggests that these tumor cells have hybridized with macrophages and are driven by an excessive gene load to grow by capturing their ligands MC, MSH and HGF/SF. These systems work in both paracrine and autocrine circuitries (204)(205)(206). , that retinoblastomas arise due to germ cell and somatic cell mutations (240) lead to the discovery of the human retinoblastoma gene (mapped to 13q14.2) and its gene product protein acting as a brake of the cell cycle.…”

“…Oncolytic adenoviral vectors induce autophagy in malignant glioblastoma cells (227,228). Autophagic tumor cells are not necessarily so due to fusion with a macrophage (204)(205)(206): autophagy may be a sign of viral infection, attack by cytotoxic lymphocytes (49), or a survival strategy of a chemotherapy-damaged tumor cell (229).…”