Project description:To further determine the candidate genes which expressed in four melanoma cells and melanocyte after treatment with IFN-β, total RNA was extracted from melanoma cells, which have different sensitivities to IFN-β, and melanocyte after treatment with or without IFN-β at a concentration of 1,000 IU/ml for 48 h. For expression profiling, oligonucleotide microarray analysis was performed at Hokkaido System Science (Sapporo, Japan) using an Agilent Human Genomic microarray 8 × 60 K version 2.0 (Agilent Technologies, Santa Clara, CA). Then, we focused on two candidate genes, CXCL-10 and IL-24, which are associated with the sensistibity of melanoma cells to IFN-β. We examined whether CXCL10 and IL-24 directly or indirectly cause sensitivitiy of melanoma to IFN-β.
Project description:Time course experiment for treatment of B16 mouse melanoma cells with all-trans retinoic acid Keywords: Time couse Time-course experiment with treatment at 4hr, 10hr, 24hr, and 48hr. Six biological replicates per time point; one biological replicate per array. Dye swap.
Project description:4 replicates were prepared from A2058 melanoma cells [transfected with 10ng of empty vector (pcDNA3.1+)] and treated with 5ng/ml TGFβ1 or vehicle control for 24hrs This is the control arm of a larger experiment where cells transfected with a particular expression plasmid were treated with TGFβ1 or control vehicle. The transfection with the expresion plasmid was unsucessful so this empty vector data has been used alone to simply examine the effect of TGFβ1 treatment on A2058 cells.
Project description:A previous case study described an adrenal incidentaloma initially misdiagnosed as adrenocortical carcinoma (ACC) and treated with mitotane. The final diagnosis was metastatic melanoma of unknown primary origin. However, the patient developed rapid disease progression after mitotane withdrawal, suggesting a protective role for mitotane in a non-adrenal derived tumour. The aim of the present study was to determine the biological response of primary melanoma cells obtained from that patient and in two other established melanoma and ACC cell lines treated with mitotane. Although mitotane inhibited proliferation of both ACC and melanoma cells, its role in melanoma treatment appears to be limited. Flow cytometry analysis and transcriptomic studies indicated that the ACC cell line was highly responsive to mitotane treatment, although the primary melanoma cell line showed a moderate response in vitro. Mitotane modified activity in several key biological processes, including “mitotic nuclear division”, “DNA repair”, “angiogenesis”, and “negative regulation of ERK1 and ERK2 cascade”.
