Smoking is the leading cause of lung cancer death, although only a small percentage of smokers develop the disease. Cigarette smoke exposure is known to cause a field of injury in cells throughout the respiratory tract, and while these airway epithelial cells are morphologically normal, they can undergo genetic alterations in response to cigarette smoke exposure.
Smoking-induced gene expression changes in the bronchial airway are reflected in nasal and buccal epithelium.
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View SamplesGlatiramer Acetate (GA) has provided safe and effective treatment for multiple sclerosis (MS) patients for two decades. It acts as an antigen, yet the precise mechanism of action remains to be fully elucidated, and no validated pharmacokinetic or pharmacodynamic biomarkers exist. In order to better characterize GAs biological impact, genome-wide expression studies were conducted with a human monocyte (THP-1) cell line. Consistent with previous literature, branded GA upregulated antiinflammatory markers (e.g. IL10), and modulated multiple immune-related pathways. Despite some similarities, significant differences were observed between expression profiles induced by branded GA and Probioglat, a differently-manufactured glatiramoid purported to be a generic GA.
Gene expression studies of a human monocyte cell line identify dissimilarities between differently manufactured glatiramoids.
Cell line, Treatment, Time
View SamplesThe ability to dissect heterogeneity in colorectal cancer (CRC) is a critical step in developing predictive biomarkers. The goal of this study was to develop a gene expression based molecular subgrouping model, which predicts the likelihood that patients will respond to specific therapies.
Activation of the mTOR Pathway by Oxaliplatin in the Treatment of Colorectal Cancer Liver Metastasis.
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View SamplesAnalysis of T-cells isolated from CD3+ T-cells of patients with B-cell chronic lymphocytic leukemia (B-CLL). In contrast to other types of cancers, the non-malignant T-cell compartment of B CLL patients is expanded. Results provide insights into the role of T-cells in B-CLL.
Expanded CD8+ T cells of murine and human CLL are driven into a senescent KLRG1+ effector memory phenotype.
Specimen part
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