Oral Cavity Cancer
A 13-gene signature prognostic of HPV-negative OSCC: discovery and external validation.
Sex
View SamplesOSCC is associated with substantial mortality and morbidity. In this study, we built on our previous molecular work to identify and validate a prognostic 13-gene signature that showed a higher ability than tumor stage in predicting survival for patients with
A 13-gene signature prognostic of HPV-negative OSCC: discovery and external validation.
Sex, Specimen part, Treatment
View SamplesOSCC is associated with substantial mortality and morbidity. To identify potential biomarkers for the early detection of invasive OSCC, we compared the gene expressions of OSCC, oral dysplasia, and normal
Gene expression profiling identifies genes predictive of oral squamous cell carcinoma.
Sex
View Samples- Gene expression changes linked to two step immortalization of human mammary epithelial cells (HMEC).
A lincRNA connected to cell mortality and epigenetically-silenced in most common human cancers.
Specimen part
View SamplesThree of the melanoma cell lines show higher expression fold change after stimulation than the other 3.
Loss of IFN-γ Pathway Genes in Tumor Cells as a Mechanism of Resistance to Anti-CTLA-4 Therapy.
Specimen part
View SamplesThe aim of this study was to determine how gene expression is changed after arsenite-induced malignant transformation of prostate epithelial cells.
Coordinate H3K9 and DNA methylation silencing of ZNFs in toxicant-induced malignant transformation.
Specimen part, Cell line, Treatment
View SamplesIn the hematopoietic microenvironment, endothelial cells (ECs) play an important role in the regulation of hematopoietic cell proliferation and trafficking. We previously demonstrated that EC stimulated with tumor necrosis factor alpha (TNF-) induce the generation of dendritic cells from CD34(+) stem cells, whereas in contrast, interleukins were capable of inducing the proliferation of hematopoietic and myeloid progenitors.
Transcriptional profiling of the hematopoietic support of interleukin-stimulated human umbilical vein endothelial cells (HUVECs).
Specimen part, Treatment
View SamplesWe sought to characterize expression profiles signifying the development of atypical adenomatous hyperplasia (AAH) from normal lung parenchyma (NL), and its progression to lung adenocarcinomas (LUAD). Overall design: We performed transcriptome sequencing of 48 samples, comprising NLs, AAHs and LUADs, from 17 patients. Sequencing was performed using the Ion Torrent platform afterwhich gene profiles differentially expressed among the three groups were determined.
Genomic Landscape of Atypical Adenomatous Hyperplasia Reveals Divergent Modes to Lung Adenocarcinoma.
Specimen part, Subject
View SamplesWe have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18INK4C and p16INK4A codeletion. Functional reconstitution of p18INK4C in GBM cells null for both p16INK4A and p18INK4C resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18INK4C in p16INK4A-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16INK4A in primary astrocytes induced a concomitant increase in p18INK4C. Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18INK4C in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation.
Feedback circuit among INK4 tumor suppressors constrains human glioblastoma development.
No sample metadata fields
View SamplesWe have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18INK4C and p16INK4A codeletion. Functional reconstitution of p18INK4C in GBM cells null for both p16INK4A and p18INK4C resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18INK4C in p16INK4A-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16INK4A in primary astrocytes induced a concomitant increase in p18INK4C. Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18INK4C in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation.
Feedback circuit among INK4 tumor suppressors constrains human glioblastoma development.
No sample metadata fields
View Samples