We study the global gene expression profiles of BKV viremia and nephropathy patients using microarrays in order to better understand the immunologic response to polyomavirus BK (BKV).
Genomics of BK viremia in kidney transplant recipients.
Specimen part, Disease
View SamplesWe investigated the clinical, histopathologic and genomic features of donor-specific antibody (DSA) +/C4d- and DSA-/C4d- transplant glomerulopathy (TGP) using microarrays. Comparison of the gene expression profiles of DSA-/C4d- TGP biopsies with ptc+g score > 1 to normal and IFTA (Interstitial Fibrosis and Tubular Atrophy) biopsies by microarrays revealed increased expression of quantitative cytotoxic T cell--associated transcripts (QCAT). However, CAMR (chronic antibody-mediated rejection) and DSA+/C4d- TGP had increased expression of QCAT, interferon-gamma and rejection induced, constitutive macrophage-associated, natural killer cell-associated, and DSA selective transcripts. B cell and endothelial cell associated transcripts expression were upregulated only in CAMR biopsies. Our results suggest that while DSA+/C4d- TGP should be classified under CAMR, DSA-/C4d- TGP with ptc+g score > 1 probably develops through a chronic cellular immune response.
The clinical and genomic significance of donor-specific antibody-positive/C4d-negative and donor-specific antibody-negative/C4d-negative transplant glomerulopathy.
Specimen part
View SamplesWe study the global gene expression profiles of TGP patients with or without graft loss to determine if a clinical and/or gene expression profile can predict allograft survival.
Clinical, Histological, and Molecular Markers Associated With Allograft Loss in Transplant Glomerulopathy Patients.
Specimen part
View SamplesThe presence of Donor-Specific anti-HLA Antibodies (DSA) is associated with an increased risk of both acute and chronic antibody-mediated rejection (AMR) in kidney allografts. AMR has remained challenging in kidney transplantation and is the major cause of late allograft loss. However, not all patients with DSA develop AMR, leading to the question of whether this represents accommodation, if other protective mechanisms exist or if this is actually a state of pre-rejection.
A pathogenesis-based transcript signature in donor-specific antibody-positive kidney transplant patients with normal biopsies.
Specimen part
View SamplesTranscription profiling by array of pancreas from KrasG12D, Ela-Tgfa and KrasG12D Ela-Tgfa mice
Concomitant pancreatic activation of Kras(G12D) and Tgfa results in cystic papillary neoplasms reminiscent of human IPMN.
Age, Specimen part
View SamplesDBZ (dibenzazepine) treatment in C57BL/6 mice, pancreatic gene expression
Notch signaling is required for exocrine regeneration after acute pancreatitis.
Sex, Age, Specimen part, Disease, Compound, Time
View Samplescharacterize the molecular signature of PB-IMC in different stages of tumor development, thus possibly leading to a novel, sensitive and elegant approach for early cancer detection and surveillance. Overall design: Two types of cancer. For each type 4 groups (day 0, day 4, day 8, day 11), for each group 3 biological repeats
The transcriptional profile of circulating myeloid derived suppressor cells correlates with tumor development and progression in mouse.
Specimen part, Cell line, Subject
View SamplesWe report nuclear receptor Esrrb''s responsive genes with or without Esrrb ligand DY131 in DU145 cells. Using Esrrb-null cells, we used RNA-Seq to find Esrrb responsive genes. In addition, we tested DY131-driven Esrrb-dependent genes to test the ligand dependency of Esrrb in regulating gene expression. Overall design: Control vector transfected cells with vehicle treatment, Esrrb expression vector transfected cell with vehicle treatment, control vector transfected cells with DY131 treatment, Esrrb expression vector transfected cell with DY131 treatment.
Messenger RNA profile analysis deciphers new Esrrb responsive genes in prostate cancer cells.
No sample metadata fields
View SamplesWe report Hedgehog signaling responsive genes with or without Esrrb in NI3T3 cells. Using Hh-responsive cells, we used RNA-Seq to find Hh responsive genes. In addition, we tested Esrrb''s modification on Hh target genes'' response. Overall design: Control vector transfected cells with vehicle treatment, Esrrb expression vector transfected cell with vehicle treatment, control vector transfected cells with Hh conditioned medium treatment, Esrrb expression vector transfected cell with Hh conditioned medium treatment,
Genes targeted by the Hedgehog-signaling pathway can be regulated by Estrogen related receptor β.
No sample metadata fields
View SamplesBackground. Androgen receptor splice variant-7 (AR-V7) is a truncated form of the androgen receptor protein which lacks the ligand-binding domain, the target of enzalutamide and abiraterone, but remains constitutively active as a transcription factor. We hypothesized that detection of AR-V7 in circulating tumor cells (CTCs) from men with advanced prostate cancer would be associated with resistance to enzalutamide and abiraterone. Methods. We used quantitative reverse-transcription polymerase-chain-reaction (qRT-PCR) to interrogate CTCs for the presence or absence of AR-V7 from prospectively enrolled patients with metastatic castration-resistant prostate cancer initiating treatment with either enzalutamide or abiraterone. We examined associations between AR-V7 status and PSA response rates, PSA-progression-free-survival (PSA-PFS), clinical/radiographic-progression-free-survival (PFS), and overall survival (OS). Multivariable Cox regression analyses were performed to determine the independent effect of AR-V7 status on clinical outcomes. Results. Thirty-one enzalutamide-treated patients and thirty-one abiraterone-treated patients were enrolled, of which 38.7% and 19.4% had detectable AR-V7 from CTCs, respectively. Among men receiving enzalutamide, AR-V7–positive patients had inferior PSA response rates (0% vs 52.6%, P=0.004), PSA-PFS (median: 1.4 vs 6.0 months, P<0.001), PFS (median: 2.1 vs 6.1 months, P<0.001), and OS (median: 5.5 months vs not reached, P=0.002) compared to AR-V7–negative patients. Similarly, among men receiving abiraterone, AR-V7–positive patients had inferior PSA response rates (0% vs 68.0%, P=0.004), PSA-PFS (median: 1.3 months vs not reached, P<0.001), PFS (median: 2.3 months vs not reached, P<0.001), and OS (median: 10.6 months vs not reached, P=0.006). The negative prognostic impact of AR-V7 was maintained after adjusting for full-length-AR expression. Conclusions. Detection of AR-V7 in CTCs from patients with castration-resistant prostate cancer is associated with resistance to enzalutamide and abiraterone. Overall design: A total of four metastatic castration-resistant prostate tumor samples from four patients were subjected to RNA-seq. Two samples were positive for androgen receptor splice variant 7 and the other two were negative for this variant.
AR-V7 and resistance to enzalutamide and abiraterone in prostate cancer.
No sample metadata fields
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