Ontology highlight
ABSTRACT:
PROVIDER: PRJNA635269 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11862400_1.fastq.gz | Fastqsanger.gz | |||
| SRR11862400_2.fastq.gz | Fastqsanger.gz | |||
| SRR11853214_1.fastq.gz | Fastqsanger.gz | |||
| SRR11853214_2.fastq.gz | Fastqsanger.gz | |||
| SRR11853215_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:For many years, immortalized cell lines have been used as model systems for cancer research. Cell line panels were established for basic research and drug development, but did not cover the full spectrum of leukemia and lymphoma. Therefore, we now developed a novel panel (LL-100), 100 cell lines covering 22 entities of human leukemia and lymphoma including T-cell, B-cell and myeloid malignancies. Importantly, all cell lines are unequivocally authenticated and assigned to the correct tissue. Cell line samples were proven to be free of mycoplasma and virus contamination. Whole exome sequencing (WES) and RNA sequencing (RNA-seq) of the hundred authenticated leukemia-lymphoma cell lines were conducted with a uniform methodology to complement existing data on these publicly available cell lines. This part captures WES. This data set will be useful for understanding the function of oncogenes and tumor suppressor genes and to develop targeted therapies.
2019-05-28 | E-MTAB-7722 | biostudies-arrayexpress
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2019-12-17 | PXD016779 |
Project description:For many years, immortalized cell lines have been used as model systems for cancer research. Cell line panels were established for basic research and drug development, but did not cover the full spectrum of leukemia and lymphoma. Therefore, we now developed a novel panel (LL-100), 100 cell lines covering 22 entities of human leukemia and lymphoma including T-cell, B-cell and myeloid malignancies. Importantly, all cell lines are unequivocally authenticated and assigned to the correct tissue. Cell line samples were proven to be free of mycoplasma and virus contamination. Whole exome sequencing (WES) and RNA sequencing (RNA-seq) of the hundred authenticated leukemia-lymphoma cell lines were conducted with a uniform methodology to complement existing data on these publicly available cell lines. This part captures RNA-Seq. This data set will be useful for understanding the function of oncogenes and tumor suppressor genes and to develop targeted therapies.
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Project description:ATAC sequencing data of cell lines of urological malignancies treated with epigenetic agents LAK31, Romidepsin, Quisinostat and MZ-1.
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Project description:High grade serous ovarian cancers (HGSC) are deadly malignancies that relapse despite carboplatin chemotherapy. Many commercially ovarian cancer cell lines are not good models for HGSC. Here we demonstrate that 3 low passage cell lines derived from HGSC have similar transcriptomes to their parental bulk tumors. These cell lines recapitulated tumor characteristics of the primary cancer and had responded to therapy in the same manner as primary HGSC cells, demonstrating they are accurate models for HGSCs. mRNA profiles of low passage high grade serous tumor cell lines and their parental tumors, generated by next generation sequencing, were compared.
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Project description:Protection against deadly pathogens requires the production of high-affinity antibodies by B cells. High-affinity antibody-forming cells are generated in germinal centers (GC) as a result of a developmental program that is commonly altered in B cell malignancies. Identification of regulators of the GC response is crucial to develop targeted therapies for GC B cell dysfunctions including lymphomas. The Histone H3 lysine-27 methyltransferase Enhancer of Zeste homolog 2 (EZH2) is highly expressed in GC B cells and often constitutively activated in GC-derived Non-Hodgkin lymphomas (NHL), but its function in these cells remains largely unknown. Herein, we show that Ezh2 inactivation in mouse GC B cells causes a profound impairment in GC responses, memory B cell formation and humoral immunity. Mechanistically, Ezh2 protected GC B cells against AID mutagenesis, facilitated cell-cycle progression independent of p16INK4a repression and silenced plasma cell determinants Blimp1 and Irf4. Likewise, EZH2 inhibition in GC-derived NHL cells induced tumor suppressor BLIMP1, which impaired tumor growth. In conclusion, in GC B cells Ezh2 sustains AID function and prevents terminal differentiation to allow antibody diversification and affinity maturation. Dysregulation of such mechanisms may facilitate lymphomagenesis and identifies EZH2 as possible therapeutic target in NHL and other GC-derived B cell diseases. In this study, two independent primary samples of splenic GC B cells from C5/BL/6J mice were subjected to H3K27me3 and H3K4me3 ChIP-sequencing. A totale of 6 samples, including input samples, were subjected to ultra-deep sequencing.
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Project description:Hass2017-PanRTK model for single cell
line
The model structure comprises
heterodimerization and receptor trafficking as described in detail
in the article below. For ligand input, set a respective
event. The illustrated event sets the EGF concentration to 2.5 nMol
in the model file.
This model is described in the article:
Predicting ligand-dependent
tumors from multi-dimensional signaling features.
Hass H, Masson K, Wohlgemuth S,
Paragas V, Allen JE, Sevecka M, Pace E, Timmer J, Stelling J,
MacBeath G, Schoeberl B, Raue A.
NPJ Syst Biol Appl 2017; 3: 27
Abstract:
Targeted therapies have shown significant patient benefit in
about 5-10% of solid tumors that are addicted to a single
oncogene. Here, we explore the idea of ligand addiction as a
driver of tumor growth. High ligand levels in tumors have been
shown to be associated with impaired patient survival, but
targeted therapies have not yet shown great benefit in
unselected patient populations. Using an approach of applying
Bagged Decision Trees (BDT) to high-dimensional signaling
features derived from a computational model, we can predict
ligand dependent proliferation across a set of 58 cell lines.
This mechanistic, multi-pathway model that features receptor
heterodimerization, was trained on seven cancer cell lines and
can predict signaling across two independent cell lines by
adjusting only the receptor expression levels for each cell
line. Interestingly, for patient samples the predicted tumor
growth response correlates with high growth factor expression
in the tumor microenvironment, which argues for a co-evolution
of both factors in vivo.
This model is hosted on
BioModels Database
and identified by:
MODEL1708210000.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
| MODEL1708210000 | BioModels
Project description:Development of novel PI3Ks inhibitors is an important strategy to overcome their resistance and poor tolerability in clinical trials. The quassinoid family member Brusatol shows specific inhibitory activity against hematologic malignancies. However, the mechanism of its anti-cancer activity is unknown. We studied the anti-cancer activity of Brusatol on multiple hematologic malignancies derived cell lines by RNA-Seq, mass spectrometry, biochemical pull-down assays, and CRISPR/Cas9 gene knock-out. We demonstrated that the PI3Kgamma isoform was identified as a direct target of Brusatol, and inhibition was lost on PI3Kgamma deficient cells. Novel synthetic analogs were also developed and tested in vitro and in vivo. They shared superior potency in their ability to inhibit malignant hematologic cell lines, and in a xenograft transplant mouse model. They also had minimal toxicity to normal human cells. These new analogs have enhanced potential for development as a new class of PI3K inhibitors for treatment of hematologic malignancies.
2020-03-06 | MSV000085067 | MassIVE