Project description:Gobal expression analysis in four somatic tissues (brain, liver, kidney and muscle) of adult 40,XX and 39,XO mice with the aim of identifying which genes are expressed from both X chromosomes as well as those genes deregulated in X chromosome monosomy. Keywords: Expression profiling by array
Project description:Primary Objective:
Correlation of the skin and/or eye toxicity grade secondary to Cetuximab or Panitumumab and the SNP profile of the Epidermal Growth Factor Receptor (EGFR) domain III region.
Secondary Objectives:
Correlation of SNP profile with indicators of tumour response parameters, such as radiological response, duration of response, time to progression (TTP), overall survival (OS) time, incidence of non-dermatological adverse events.
Project description:Gobal expression analysis in four somatic tissues (brain, liver, kidney and muscle) of adult 40,XX and 39,XO mice with the aim of identifying which genes are expressed from both X chromosomes as well as those genes deregulated in X chromosome monosomy. Keywords: Expression profiling by array For each tissue, the RNA samples of seven 40,XX, eight 39,XpO and eight 39,XmO mice were pooled by genotype into 9 groups, representing 3 biological replicates per genotype, as follows: 39,XpO-1 and 39,XpO-2 (3 pooled individuals each), 39,XpO-3 (2 pooled individuals); 39,XmO-1 and 39,XmO-2 (3 pooled individuals each), 39,XmO-3 (2 pooled individuals); 40,XX-1 and 40,XX-2 (3 pooled individuals each) 40,XX-3 (2 pooled individuals)
Project description:Long noncoding RNAs (lncRNAs) play an important role in lung adenocarcinoma (LUAD) metastasis. Here, we found that lncRNA chromatin-associated RNA 10 (CAR10) was upregulated in the tumor tissue of patients with LUAD and enhanced tumor metastasis in vitro and in vivo. Mechanistically, CAR10 induced epithelial-to-mesenchymal transition (EMT) by directly binding with miR-30 and miR-203 and then regulating the expression of SNAI1 and SNAI2. CAR10 overexpression was positively correlated with a poor prognosis in LUAD patients, whereas overexpression of both CAR10 and SNAI was correlated with even worse clinical outcomes. In conclusion, the CAR10/miR-30/203/SNAI axis is a novel and potential therapeutic target for LUAD.