Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1199538 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31751593.fastq.gz | Fastqsanger.gz | |||
| SRR31751594.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 2 of 2 |
Similar Datasets
Project description:MCF7 breast cancer cell lines: drug-resistant (OHT and ICI) cell lines vs. drug-sensitive (wild type) cell lines. Assessment of association between gene expression and methylation. Two comparisons: OHT-resistant vs. wild type, and ICI-resistant vs. wild type. OHT: 4-hydroxytamoxifen ICI: fulvestrant ((ICI 182780) This submission represents the methylation component of the study.
2011-10-04 | E-GEOD-25519 | biostudies-arrayexpress
Project description:Promoter methylation data: OHT/ICI-sensitive vs. -resistant cell lines
| PRJNA133775 | ENA
Project description:MCF7 breast cancer cell lines: drug-resistant (OHT and ICI) cell lines vs. drug-sensitive (wild type) cell lines. Assessment of association between gene expression and methylation.
2011-10-05 | GSE25519 | GEO
Project description:The heterogenicity of hepatocellular carcinoma (HCC) remains a key obstacle in turning the majority of ‘immune-cold’ tumors ‘hot’ for effective immune checkpoint inhibitors (ICIs). Through analyzing the naturally-existed ‘hot’ HCC variants, we identified fas-associated death domain (FADD) as a key molecule upregulated in patients with dense tumor-filtrating CD8+T cells and better response to ICIs. Apart from the canonical role in apoptosis pathway, our data showed that CRISPR knockout of hepatoma-intrinsic Fadd led to increased tumor weights in immunocompetent but not immunodeficient mice, accompanied with decreased numbers and IFN-γ/TNF-ɑ production of tumor-filtrating CD8+T cells. Mechanistically, phosphorylated FADD translocated into cell nucleus, where it interacted with Sam68 to upregulate NF-κB transcription of CCL5, thereby promoted CD8+T cell tumor infiltration. Interestingly, anti-PD1 triggered FADD phosphorylation by CD8+T cell-derived IFN-γ/TNF-ɑ in ICI-sensitive, but not resistant tumors. Sequential FADD activation through genetic or pharmacologic approaches to orchestrate p-FADD-CD8+T cell axis therefore overcame ICI resistance in ICI-resistant orthotopic and spontaneous HCC mouse models in vivo. Taken together, our findings may provide insights into the combinatory immunotherapy approaches for the majority of HCC patients in the future.
2025-07-07 | PXD057519 | Pride
Project description:Immune checkpoint inhibitors (ICIs) have improved outcomes in advanced cancers, yet resistance remains a major obsticle. Here, we investigated the role of myeloid cells in shaping the immunosuppressive tumor microenvironment that contributes to ICI resistance. Using mutagenized ICI-sensitive and resistant 4T1 breast cancer clones, we performed single-cell RNA sequencing to characterize immune cell populations post-ICI therapy. We identified monocytic dendritic progenitors (MDPs) and common monocytic progenitors (cMOPs) enriched in sensitive tumors, which may differentiate into immunosuppressive cells in resistant tumors. Analysis of public datasets confirmed the presence of MDP-cMOPs in tumors and blood of breast, lung, and colorectal cancer patients. We found high expression of CXCR4 and IL6R in MDP-cMOPs, and inhibiting these pathways blocked their recruitment and differentiation. Combined targeting of CXCR4 and IL6 pathway with ICI improved responses in resistant tumors, highlighting MDP-cMOPs as contributors to immunotherapy resistance and potential therapeutic targets.
2025-06-05 | GSE298984 | GEO
Project description:Immune checkpoint inhibitors (ICIs) provide clinical benefits for various advanced malignancies. However, the predictive factors that determine sensitivity to ICIs have not been fully elucidated. To identify the mechanisms underlying ICI resistance, we performed a microarray analysis to compare the IFN-γ-inducible genes between ICI-sensitive AB1-HA and ICI-resistant LLC in vitro.
2024-11-25 | GSE266384 | GEO
Project description:ER-dependent gene expression was investigated in the LY2 endocrine resistant cell line by treatment with ICI 182780. Cells were steroid depleted for 3 days prior to treatment with ICI for 6 hours. Four biological replicates were processed and analysed.
2014-09-18 | E-MTAB-1870 | biostudies-arrayexpress
Project description:Transcriptome analysis was used to identify changes in mouse kidney cancer cells (RENCA) resistant to sunitinib (SuR) and after short and long term sunitinib withdrawal in vitro (ST-W for 48 hours and LT-W for more than 2 months, respectively).
2018-11-22 | GSE122821 | GEO
Project description:Background: Tumor heterogeneity is one of the key factors leading to chemo-resistance relapse. It remains unknown how resistant cancer cells influence sensitive cells during cohabitation and growth within a heterogenous tumors. The goal of our study was to identify driving factors that mediate the interactions between resistant and sensitive cancer cells and to determine the effects of cohabitation on both phenotypes. Methods: We used isogenic ovarian cancer cell (OC) lines pairs, sensitive and resistant to platinum: OVCAR5 vs. OVCAR5 CisR and PEO1 vs. PEO4, respectively, to perform long term direct culture and to study the phenotypical changes of the interaction of these cells. Results: Long term direct co-culture of sensitive and resistant OC cells promoted proliferation (p < 0.001) of sensitive cells and increased the proportion of cells in the G1 and S cell cycle phase in both PEO1 and OVCAR5 cells. Direct co-culture led to a decrease in the IC50 to platinum in the cisplatin-sensitive cells (5.92 µM to 2.79 µM for PEO1, and from 2.05 µM to 1.51 µM for OVCAR5). RNAseq analysis of co-cultured cells showed enrichment of Cell Cycle Control, Cyclins and Cell Cycle Regulation pathways. The transcription factor E2F1 was predicted as the main effector responsible for the transcriptomic changes in sensitive cells. Western blot and qRT-PCR confirmed upregulation of E2F1 in co-cultured vs monoculture. Furthermore, an E2F1 inhibitor reverted the increase in proliferation rate induced by co-culture to baseline levels. Conclusions: Our data suggest that long term cohabitation of platinum-sensitive and -resistant cancer cells drive sensitive cells to a higher proliferative state, more responsive to platinum. Our results reveal an unexpected effect caused by direct interactions between cancer cells with different proliferative rates and levels of platinum resistance, modelling competition between cells in heterogeneous tumors.
2024-02-11 | GSE244626 | GEO
Project description:Drug resistance is a major public health challenge in Leishmaniasis chemotherapy, particularly in the case of emerging Leishmania/HIV-1 co-infections. Recently, we have delineated the mechanism of cell death induced by the HIV-1 protease inhibitor, Nelfinavir, in the Leishmania parasite. In order to investigate the underlying molecular mechanism involved in Nelfinavir resistance, in vitro Nelfinavir resistant amastigotes were developed by direct drug pressure in culture. RNA expression profiling analyses of closely related Leishmania species were used as a screening tool to compare Nelfinavir-resistant and -sensitive parasites in order to identify candidate genes involved in drug resistance, and several genes were found to be differentially expressed. Comparative gene hybridization (CGH) analyses of Nelfinavir-resistant and -sensitive Leishmania using whole-genome 60-mer oligonucleotide microarrays were also carried out. RNA expression profiles and the CGH of Nelfinavir resistant vs sensitive Leishmania amastigotes suggest that parasites regulate mRNA levels either by modulating gene copy numbers through chromosome aneuploidy, or gene deletion/duplication by homologous recombination. Interestingly, supernumerary chromosomes 6 and 11 in the resistant parasites lead to upregulation of the ABC class of transporters, which are involved in vesicular trafficking. Transporter assays using radiolabeled Nelfinavir suggest that the drug accumulates in greater amounts in the resistant parasites and in a time dependent manner. Furthermore, high-resolution electron microscopy showed an increased number of vacuoles in Nelfinavir-resistant parasites. Together these results suggest that Nelfinavir is rapidly and dramatically sequestered in these intracellular vesicles. Two condition experiment: NFV-sensitive vs resistant. Biological replicates: Three. One dye swap.
2013-06-27 | E-GEOD-42195 | biostudies-arrayexpress