Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1200288 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31812160_1.fastq.gz | Fastqsanger.gz | |||
| SRR31812160_2.fastq.gz | Fastqsanger.gz | |||
| SRR31812161_1.fastq.gz | Fastqsanger.gz | |||
| SRR31812161_2.fastq.gz | Fastqsanger.gz | |||
| SRR31812162_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 36 |
Similar Datasets
Project description:We report the gene expression of human chronic myelomonocytic leukemia by performing whole transcriptome shotgun sequencing of bone marrow mononuclear cells of patients with chronic myelomonocytic leukemia.
2022-02-21 | GSE159543 | GEO
Project description:We established a model for myeloproliferative disease in mice, that is based on primary bone marrow expressing human Thrombopoietin receptor and human mutant Calrdel52. To learn more about cellular and transcriptional rearrangements in the bone marrow we performed single cell RNA sequencing comparing bone marrow cells of empty vector control mice with mice that received MPL-Calrdel52 bone marrow.
2024-05-30 | GSE241364 | GEO
Project description:RNA-sequencing was performed on human CD19- CD138+ bone marrow plasma cells. 4 biological replicates of human CD19- CD138+ bone marrow plasma cells.
2016-05-14 | E-GEOD-81443 | biostudies-arrayexpress
Project description:The paper describes a model of tumor invasion to bone marrow.
Created by COPASI 4.26 (Build 213)
This model is described in the article:
Modeling invasion of metastasizing cancer cells to bone marrow utilizing ecological principles
Kun-Wan Chen, Kenneth J Pienta
Theoretical Biology and Medical Modelling 2011, 8:36
Abstract:
Background: The invasion of a new species into an established ecosystem can be directly compared to the steps involved in cancer metastasis. Cancer must grow in a primary site, extravasate and survive in the circulation to then intravasate into target organ (invasive species survival in transport). Cancer cells often lay dormant at their metastatic site for a long period of time (lag period for invasive species) before proliferating (invasive spread). Proliferation in the new site has an impact on the target organ microenvironment (ecological impact) and eventually the human host (biosphere impact).
Results: Tilman has described mathematical equations for the competition between invasive species in a structured habitat. These equations were adapted to study the invasion of cancer cells into the bone marrow microenvironment as a structured habitat. A large proportion of solid tumor metastases are bone metastases, known to usurp hematopoietic stem cells (HSC) homing pathways to establish footholds in the bone marrow. This required accounting for the fact that this is the natural home of hematopoietic stem cells and that they already occupy this structured space. The adapted Tilman model of invasion dynamics is especially valuable for modeling the lag period or dormancy of cancer cells.
Conclusions: The Tilman equations for modeling the invasion of two species into a defined space have been modified to study the invasion of cancer cells into the bone marrow microenvironment. These modified equations allow a more flexible way to model the space competition between the two cell species. The ability to model initial density, metastatic seeding into the bone marrow and growth once the cells are present, and movement of cells out of the bone marrow niche and apoptosis of cells are all aspects of the adapted equations. These equations are currently being applied to clinical data sets for verification and further refinement of the models.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models .
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.
2024-09-02 | BIOMD0000000793 | BioModels
Project description:The paper describes a model of tumor invasion to bone marrow.
Created by COPASI 4.26 (Build 213)
This model is described in the article:
Modeling invasion of metastasizing cancer cells to bone marrow utilizing ecological principles
Kun-Wan Chen, Kenneth J Pienta
Theoretical Biology and Medical Modelling 2011, 8:36
Abstract:
Background: The invasion of a new species into an established ecosystem can be directly compared to the steps involved in cancer metastasis. Cancer must grow in a primary site, extravasate and survive in the circulation to then intravasate into target organ (invasive species survival in transport). Cancer cells often lay dormant at their metastatic site for a long period of time (lag period for invasive species) before proliferating (invasive spread). Proliferation in the new site has an impact on the target organ microenvironment (ecological impact) and eventually the human host (biosphere impact).
Results: Tilman has described mathematical equations for the competition between invasive species in a structured habitat. These equations were adapted to study the invasion of cancer cells into the bone marrow microenvironment as a structured habitat. A large proportion of solid tumor metastases are bone metastases, known to usurp hematopoietic stem cells (HSC) homing pathways to establish footholds in the bone marrow. This required accounting for the fact that this is the natural home of hematopoietic stem cells and that they already occupy this structured space. The adapted Tilman model of invasion dynamics is especially valuable for modeling the lag period or dormancy of cancer cells.
Conclusions: The Tilman equations for modeling the invasion of two species into a defined space have been modified to study the invasion of cancer cells into the bone marrow microenvironment. These modified equations allow a more flexible way to model the space competition between the two cell species. The ability to model initial density, metastatic seeding into the bone marrow and growth once the cells are present, and movement of cells out of the bone marrow niche and apoptosis of cells are all aspects of the adapted equations. These equations are currently being applied to clinical data sets for verification and further refinement of the models.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models .
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.
2024-09-02 | BIOMD0000000795 | BioModels
Project description:Here we used Illumina NGS for high-throughput profiling of the DNA methylome in two human colon cancer derived cell lines, two human normal bone marrow CD34+ controls and in five human Acutre Myeloid Leukeima patient samples. These data can be used to determine the CpG cytosine methylation pattern at base pair resolution in each sample and to determine differentially methylated cytosines and regions between samples Reduced Representation Bisulfite Sequencing (RRBS) and Extended Reduced Representation Bisulfite Sequencing (ERRBS) on genomic DNA. We used colon cancer cell lines (two) to establish reproducbility and range of assay sensitivity. We used Acute Myeloid Leukemia patient samples and CD34+ bone marrow cells as controls to determine the methylome pattern in the patient samples
2012-06-01 | E-GEOD-37454 | biostudies-arrayexpress
Project description:Transcriptome sequencing was performed on 214 patients with myelodysplasia in this study. RNA was obtained from bone marrow CD34+ cells (n=100) and/or bone marrow mononuclear cells (n=165). Transcriptome sequencing was performed for both cell fractions in 51 patients. We also studied bone marrow CD34+ cells and bone marrow mononuclear cells obtained from three healthy adults each.
| EGAS00001002346 | EGA