Comparison of mRNA expression from FACS isolated Gli1 expressing stromal cells from mice given SAG21k versus vehicle
Control of inflammation by stromal Hedgehog pathway activation restrains colitis.
Sex, Specimen part, Treatment
View SamplesComparative analysis of mRNA from colons of mice that were given colitis though use of 5% dextran sulfate in the drinking water (Days 0-5)
Control of inflammation by stromal Hedgehog pathway activation restrains colitis.
Sex, Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Recurrent 8q24 rearrangement in blastic plasmacytoid dendritic cell neoplasm: association with immunoblastoid cytomorphology, MYC expression, and drug response.
Specimen part, Disease, Disease stage, Cell line
View SamplesBlastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare skin-tropic hematological malignancy of uncertain pathogenesis and poor prognosis. We examined 118 BPDCN cases for cytomorphology, MYC locus rearrangement, and MYC expression. Sixty-two (53%) and 41 (35%) showed the classic and immunoblastoid cytomorphology, respectively. Forty-one (38%) MYC+BPDCN (positive for rearrangement and expression) and 59 (54%) MYC-BPDCN (both negative) cases were identified. Immunoblastoid cytomorphology was significantly associated with MYC+BPDCN. All examined MYC+BPDCNs were negative for MYB/MYBL1 rearrangement (0/36). Clinically, MYC+BPDCN showed older onset, poorer outcome, and localized skin tumors more commonly than MYC-BPDCN. MYC was demonstrated by expression profiling as one of the clearest discriminators between CAL-1 (MYC+BPDCN) and PMDC05 (MYC-BPDCN) cell lines, and its shRNA knockdown suppressed CAL-1 viability. Inhibitors for bromodomain and extraterminal protein (BETis) and aurora kinases (AKis) inhibited CAL-1 growth more effectively than PMDC05. We further showed that a BCL2 inhibitor was effective in both CAL-1 and PMDC05, indicating that this inhibitor can be used to treat MYC-BPDCN, to which BETis and AKis are probably less effective. Our data will provide a rationale for the development of new treatment strategies for patients with BPDCN in accordance with precision medicine.
Recurrent 8q24 rearrangement in blastic plasmacytoid dendritic cell neoplasm: association with immunoblastoid cytomorphology, MYC expression, and drug response.
Specimen part, Disease, Disease stage, Cell line
View SamplesBlastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare skin-tropic hematological malignancy of uncertain pathogenesis and poor prognosis. We examined 118 BPDCN cases for cytomorphology, MYC locus rearrangement, and MYC expression. Sixty-two (53%) and 41 (35%) showed the classic and immunoblastoid cytomorphology, respectively. Forty-one (38%) MYC+BPDCN (positive for rearrangement and expression) and 59 (54%) MYC-BPDCN (both negative) cases were identified. Immunoblastoid cytomorphology was significantly associated with MYC+BPDCN. All examined MYC+BPDCNs were negative for MYB/MYBL1 rearrangement (0/36). Clinically, MYC+BPDCN showed older onset, poorer outcome, and localized skin tumors more commonly than MYC-BPDCN. MYC was demonstrated by expression profiling as one of the clearest discriminators between CAL-1 (MYC+BPDCN) and PMDC05 (MYC-BPDCN) cell lines, and its shRNA knockdown suppressed CAL-1 viability. Inhibitors for bromodomain and extraterminal protein (BETis) and aurora kinases (AKis) inhibited CAL-1 growth more effectively than PMDC05. We further showed that a BCL2 inhibitor was effective in both CAL-1 and PMDC05, indicating that this inhibitor can be used to treat MYC-BPDCN, to which BETis and AKis are probably less effective. Our data will provide a rationale for the development of new treatment strategies for patients with BPDCN in accordance with precision medicine.
Recurrent 8q24 rearrangement in blastic plasmacytoid dendritic cell neoplasm: association with immunoblastoid cytomorphology, MYC expression, and drug response.
Specimen part, Disease, Disease stage, Cell line
View SamplesDrugs that target specific gene alterations have proven beneficial in the treatment of cancer. Because cancer cells have multiple resistance mechanisms, it is important to understand the downstream pathways of the target genes and monitor the pharmacodynamic markers associated with therapeutic efficacy.
ERK Signal Suppression and Sensitivity to CH5183284/Debio 1347, a Selective FGFR Inhibitor.
No sample metadata fields
View SamplesPatients who cleared HCV viremia early during therapy tended to show favorable outcomes, whereas patients who needed a longer period to clear HCV had poorer outcomes. We explored the mechanisms of treatment resistance by comparing hepatic gene expression before and during treatment
Differential interferon signaling in liver lobule and portal area cells under treatment for chronic hepatitis C.
Specimen part, Time
View SamplesTET2 is an enzyme for converting methylcytosine (mC) to hydorxymethylcytosine (hmC) and its mutations have been frequently found in myeloid malignancies and T-cell lymphoma in humans. We analyzed Tet2 gene trap mice and found that homozygous mice developed T-cell lymphoma with follicular helper T-cell-like features.
Reduced TET2 function leads to T-cell lymphoma with follicular helper T-cell-like features in mice.
Specimen part
View SamplesTh17 cells are enriched by sorting FR4-CD4+ T cells from SKG mice. A large number of Th17 cells also develop spontaneously when CD4+ T cells from IFN-g-deficient (IFN-g-/-) BALB/c mice are transferred to T cell-deficient RAG2-deficient (RAG2-/-) mice and subjected to homeostatic proliferation, whereas they fail to develop in similar transfer of IL-6-deficient (IL-6-/-) CD4+ T cells to IL-6-/- RAG2-/- mice.
Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model.
Sex, Age, Specimen part
View SamplesGene expression profiling was carried out in Huh-7.5 cells in which miR-27a was over- or under-expressed. Transfection of cells with pre-miR-27a and pre-miR-control, or anti-miR-27a and anti-miR-control enabled down- and up-regulated genes to be determined, respectively.
MicroRNA-27a regulates lipid metabolism and inhibits hepatitis C virus replication in human hepatoma cells.
Cell line, Treatment
View Samples