The spinal cords of mice submitted to aortic cross-clamping for 7.5 minutes present with gray matter damage and central cord edema. 60% of mice subsequently experience hindlimb and tail paralysis.
No associated publication
Specimen part
View SamplesEGFR tyrosine kinase inhibitors cause dramatic responses in EGFR-mutant lung cancer, but resistance universally develops. The involvement of -catenin in EGFR TKI resistance has been previously reported however the precise mechanism by which -catenin activation contributes to EGFR TKI resistance is not clear. Here, we show that EGFR inhibition results in the activation of -catenin signaling in a Notch3-dependent manner, which facilitates the survival of a subset of cells that we call adaptive persisters. We previously reported that EGFR-TKI treatment rapidly activates Notch3, and here describe the physical association of Notch3 with -catenin, leading to increased stability and activation of -catenin. We demonstrate that the combination of EGFR-TKI and a -catenin inhibitor inhibits the development of these adaptive persisters, decreases tumor burden, improves recurrence free survival, and overall survival in xenograft models. These results supports combined EGFR-TKI and -catenin inhibition in patients with EGFR mutant lung cancer.
Notch3-dependent β-catenin signaling mediates EGFR TKI drug persistence in EGFR mutant NSCLC.
Specimen part, Cell line
View SamplesLKB1 is a tumor suppressor lost in approximately 30% of lung adenocarcinomas. It is a serine-threonine kinase involved in regulating metabolism, proliferation, and cell polarity. We have characterized its association with mRNA expression profiles in resected tumors and in cell lines, but little is known about the direct effects of LKB1 on the regulation of these genes.
No associated publication
Disease, Disease stage, Cell line
View SamplesOral cancer kills about 1 person every hour each day in the United States and is the 6th most prevalent cancer worldwide. In this study we utilized existing microarray data from a prior oral cancer study to examine the role of chronic pro-inflammatory mediators in oral carcionogenesis by comparing gene expression in oral tumors with adjacent non-tumor oral tissue from the same patient
Deletion of macrophage migration inhibitory factor inhibits murine oral carcinogenesis: Potential role for chronic pro-inflammatory immune mediators.
Disease, Subject
View SamplesThis microarray study was performed to investigate the molecular events in esophageal SCC carcinogenesis in NMBA induced rat esophageal SCC models.
No associated publication
No sample metadata fields
View SamplesTo understand the underlying cause for the observed apoptosis in E2f1-3 deficient myeloid cells. We compared gene expression profiles of Cd11b+ sorted myeloid cells isolated from bone marrow of control (E2F1-/- ) and experimental (Mxcre;E2F1-/-2-/-3f/f ) mice.
E2f1-3 are critical for myeloid development.
Age, Specimen part
View SamplesTo understand the underlying cause for reduced lung metastasis, we compared global gene expression profiles of F4/80+ FACS sorted tumor-associated macrophages (TAMs) PyMT;E2f3 f/f (control) and PyMT;Lys Cre:E2f3 f/f (experimental) mice.
No associated publication
Specimen part
View SamplesPreterm birth is an important unsolved clinical problem. Despite advanced treatments, infants who survive prematurity remain at increased risk for permanent disabilities. In approximately one-third of cases, prematurity is related to infection and/or inflammation, which renders hostile the normally receptive intrauterine environment. Proinflammatory cytokines provoke up-regulation of genes that promote uterine contractions. Using monolayer cultures of human cervical fibroblast cells as a model, we profiled the global pattern of gene expression in response to cytokine challenge.
Progesterone Receptor Signaling Selectively Modulates Cytokine-Induced Global Gene Expression in Human Cervical Stromal Cells.
Treatment
View SamplesGene Expression in d5 wound-edge tissues of MFG-E8 WT and MFG-E8 KO mice
Correction of MFG-E8 Resolves Inflammation and Promotes Cutaneous Wound Healing in Diabetes.
Specimen part
View SamplesThe objective of the study was to compare the wound macs with corresponding macs derived from peripheral blood monocytes (MDMs). Wound site macrophage (wound macs were isolated from human subjects with chronic wounds. Matching blood monocyte derived macrophages (MDM) were obtained from same subjects. Transcriptome profiling (GeneChip, Affymetrix) was performed.The expression values of genes were normalized using global scaling approach.
Prostaglandin E₂ induces oncostatin M expression in human chronic wound macrophages through Axl receptor tyrosine kinase pathway.
Specimen part
View Samples