# _embedded.samples[].organization[].Name
University of Medicine and Dentistry of New Jersey

# _embedded.samples[].organization[].Name
University of Medicine and Dentistry of New Jersey

# _embedded.samples[].characteristics.description[].text
Gene expression data from parental-adherent considered as cells commited to differentiation

# _embedded.samples[].characteristics.sample source name[].text
PCSC-2 parental cultures in PCSCs medium

# _embedded.samples[].organization[].Name
University of Medicine and Dentistry of New Jersey

# _embedded.samples[].characteristics.submission description[].text
CDC1551 induced more vigorous immune response in murine bone marrow derived macrophage (BMM). In contrast, in HN878-infected cells, host transcriptional response was delayed but lasted longer. HN878 induced more genes involved in host lipid metabolism than CDC1551 did. Murine bone marrow derived macrophages were infected with M. tuberculosis CDC1551 or HN878 up to 24 h. Total RNA was processed for microarray and global gene expression was read.

# _embedded.samples[].characteristics.submission title[].text
Mtb-mediated host transcriptional reponse is strain-specific

# _embedded.samples[].organization[].Name
University of Medicine and Dentistry of New Jersey

# _embedded.samples[].organization[].Name
University of Illinois at Champaign-Urbana

# _embedded.samples[].organization[].Name
University of Medicine and Dentistry of New Jersey

# _embedded.samples[].characteristics.description[].text
Human pretherapeutic rectal cancer patient biopsy sample P049M

# _embedded.samples[].characteristics.sample source name[].text
Pretherapeutic rectal cancer patient biopsy

# _embedded.samples[].characteristics.description[].text
Gene expression data from parental-adherent considered as cells commited to differentiation

# _embedded.samples[].characteristics.description[].text
Gene expression data from parental-adherent considered as cells commited to differentiation

# _embedded.samples[].characteristics.sample source name[].text
PCSC-1 parental cultures in PCSCs medium

# _embedded.samples[].characteristics.submission description[].text
In this study, we shought to identify the cytokines produced by skin-resident T cells in normal skin, localize the receptors for these cytokines, and examine how these cytokines alter gene expression profiles of the cells bearing cognate receptors. Experiment Overall Design: In this study, primary keratinocytes were treated with either IL-17, IL-22 or IFNg for 24 hours then harvested for RNA extraction and subsequent gene array analysis

# _embedded.samples[].characteristics.submission title[].text
Transcription profiling of human primary keratinocytes treated with either IL-17, IL-22 or IFNg

# _embedded.samples[].organization[].Name
University of Medicine and Dentistry of New Jersey

# _embedded.samples[].organization[].Name
University of Illinois at Champaign-Urbana

# _embedded.samples[].characteristics.submission description[].text
Mutations of the KRAS oncogene are predictive for resistance to treatment with antibodies against the epithelial growth factor receptor in patients with colorectal cancer. Overcoming this therapeutic dilemma could potentially be achieved by the introduction of drugs that inhibit signaling pathways that are activated by KRAS mutations. To comprehensively identify such signaling pathways we profiled pretreatment biopsies from 65 patients with locally advanced rectal cancer - 30 of which carried mutated KRAS - using global gene expression microarrays. By comparing all tumor tissues exclusively to matched normal mucosa, we could improve assay sensitivity, and identified a total of 22,297 features that were differentially expressed (adjusted p-value p<0.05) between normal mucosa and cancer, including several novel potential rectal cancer genes. We then used this comprehensive description of the rectal cancer transcriptome as the baseline for identifying KRAS-dependent alterations. The presence of activating KRAS mutations resulted in significant upregulation of 13 genes (adjusted p-value < 0.05), among them DUSP4, a MAP-kinase phosphatase, and SMYD3, a histone methyltransferase. Inhibition of the expression of both genes has been achieved therapeutically with the MEK1-inhibitor PD98059 and the antibacterial compound Novobiocin, respectively, suggesting a potential approach to overcome resistance to treatment with antibodies against the epithelial growth factor receptor in patients with KRAS-mutant rectal carcinomas. Paired samples of tumor and mucosa from a total of 65 patients, i.e. 130 arrays

# _embedded.samples[].characteristics.submission title[].text
Mutated KRAS induces overexpression of DUSP4, a MAP-kinase phosphatase, and SMYD3, a histone methyltransferase, in rectal carcinomas