Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA149475 | ENA |
REPOSITORIES: ENA
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Project description:Osteosarcoma is thought of arising from the malignant transformation of osteogenic progenitors. The stage-specific embryonic antigen-4 (SSEA-4) labels a subset of TICs specially present in the high-risk subgroup. SSEA-4+ AND SSEA-4-
2014-06-05 | E-GEOD-58209 | biostudies-arrayexpress
Project description:Osteosarcoma is thought of arising from the malignant transformation of osteogenic progenitors. The stage-specific embryonic antigen-4 (SSEA-4) labels a subset of TICs specially present in the high-risk subgroup.
2014-06-05 | GSE58209 | GEO
Project description:Primary human skin cells were gated based on expression of stage-specific embryonic antigen 3 (SSEA3) with the high SSEA3 expressing cells (top 10%, categorized as SSEA3-positive or SSEA3-high) and negative SSEA3 expressing cells (bottom 10%, categorized as SSEA3-negative) purified into two different subpopulations. Sorted cells were allowed to adhere overnight under DMEM/F12 + 10% FBS culture conditions before total RNA was collected and global transcriptional analysis was performed. We isolated primary adult human skin cells with either high SSEA3 expression or negative SSEA3 expression via FACS and analyzed via Affymetrix microarray analysis.
2012-03-01 | E-GEOD-33066 | biostudies-arrayexpress
Project description:Primary human skin cells were gated based on expression of stage-specific embryonic antigen 3 (SSEA3) with the high SSEA3 expressing cells (top 10%, categorized as SSEA3-positive or SSEA3-high) and negative SSEA3 expressing cells (bottom 10%, categorized as SSEA3-negative) purified into two different subpopulations. Sorted cells were allowed to adhere overnight under DMEM/F12 + 10% FBS culture conditions before total RNA was collected and global transcriptional analysis was performed.
2012-03-01 | GSE33066 | GEO
Project description:Pluripotency can be induced in murine and human fibroblast by transduction of four transcription factors (Oct4, Sox2, Klf4 and c-Myc). Previously we reported that two factors (Oct4 and Klf4) are sufficient for reprogramming adult mouse neural stem cells (NSCs) to a pluripotent state. However, although NSCs endogenously express the factors Sox2, c-Myc, and Klf4, our previous report does not elucidate why exogenous expression of either Klf4 or c-Myc is still required for reprogramming. Here we report that exogenous expression of Oct4 is sufficient to generate one-factor induced pluripotent stem (1F iPS) cells without any oncogenic factors, such as c-Myc and Klf4, from mouse adult NSCs, which endogenously express Sox2, c-Myc, and Klf4, and also intermediate reprogramming markers alkaline phosphatase (AP), stage-specific embryonic antigen-1 (SSEA-1). These results extend our previous report proposing that somatic cells can be reprogrammed to a pluripotent state with a reducing number of reprogramming factors when the complementing factors are endogenously expressed in the somatic cells. Experiment Overall Design: 10 hybridizations in total. Experiment Overall Design: NSC-derived iPS cells by one-factor (Oct4) in triplicate: Experiment Overall Design: - NSC_1F_iPS_1 Experiment Overall Design: - NSC_1F_iPS_2 Experiment Overall Design: - NSC_1F_iPS_3 Experiment Overall Design: One-factor (Oct4) iPS cell-derived NSC in triplicate: Experiment Overall Design: - 1F_iPS_NSC_1 Experiment Overall Design: - 1F_iPS_NSC_2 Experiment Overall Design: - 1F_iPS_NSC_3 Experiment Overall Design: Neural stem cell (NSC) derived from brain of OG2/Rosa26 mice: Experiment Overall Design: - NSC_1 Experiment Overall Design: - NSC_2 Experiment Overall Design: - NSC_3 Experiment Overall Design: - NSC_4
2009-02-08 | E-GEOD-12499 | biostudies-arrayexpress
Project description:The cellular heterogeneity of one patient derived orthotopic breast cancer xenograft model (PDBCX) was investigated using flow cytometry , combined with assessment of in vivo tumorigenicity and whole genome expression profiling. Epithelial cell adhesion molecule (EpCAM) was revealed as a highly specific cell surface marker of the human tumor cell population in both xenografts. Based on expression patterns observed in primary tumor tissue, SSEA-4 and CD24 were chosen as markers to further subdivide the luminal tumor cells into four subpopulations. FACS sorting was used to isolate four cell subpopulations. Results: In vivo tumorigenicity assay showed that SSEA-4+/CD24+ cells were non-tumorigenic, while the three other subpopulations were tumorigenic. Tumors resulting from the SSEA-4+/CD24- subpopulation of luminal cancer cells, did not express CD24, while tumors arising from the SSEA-4-/CD24-, and SSEA-4-/CD24+ populations both recapitulated the original tumor containing all four subpopulations. Whole genome expression analysis revealed distinct transcriptional profiles, and 44 genes were significantly differentially expressed when comparing the tumorigenic vs non-tumorigenic populations. Several interesting genes putatively suppressing the cancer cells ability to initiate tumors in vivo were upregulated in the non-tumorigenic population. We here show that tumor initiating cells within one primary tumor evidently included more than one phenotype. Furthermore, with respect to cell surface marker expression, one of the subpopulations produced tumors unlike both the originating cells, and the original tumor. Discussion: Our results imply that subpopulations from one primary tumor can give rise to dissimilar daughter tumors. These tumors may not necessarily respond to the same targeted treatment, and thereby represent a therapy escape mechanism. This study highlights that to remove the risk of breast cancer recurrence, inhibition of the molecules critical for driving the tumor progression in several tumor cell subpopulations might be essential
2015-05-26 | GSE48384 | GEO
Project description:Little is known about the molecular and functional features of pluripotent stem cells (PSCs) in rabbits. To address this, we derived and characterized two types of rabbit PSCs from the same breed of New Zealand White rabbits: four lines of embryonic stem cells (rbESCs), and three lines of induced PSCs (rbiPSCs) that resulted from reprogramming adult skin fibroblasts. All lines were dependent on fibroblast growth factor 2. All rbESC lines exhibited molecular and functional properties typically associated with primed pluripotency. The rbESC lines also exhibited a cell cycle with a prolonged G1 phase and a DNA damage checkpoint prior to entry into the S phase, which are two features typically associated with the somatic cell cycle. In contrast, the rbiPSC lines exhibited some characteristics of naïve pluripotency as defined in rodents, including resistance to single cell dissociation by trypsin, robust activity of the distal enhancer of the mouse Oct4 gene, and expression of naïve-specific genes. According to gene expression profiles, rbiPSCs were closer to the rabbit inner cell mass than rbESCs. We propose that rbiPSCs self-renew in an intermediate state between naïve and primed pluripotency, which represents a key step toward the generation of bona fide naïve PSC lines in rabbits The patterns of stage specific embryonic antigen (SSEA) expression were also assessed between cell lines. All two rbiPSC lines exhibited heterogeneous expression of SSEA1 and SSEA4 that leads to obtain 3 different cell sub-populations (SSEA1+, SSEA1+/4+, SSEA1-/4-). All four rbESC lines expressed only SSEA1 and not SSEA4. Then, for this category of cell lines, we used 3 different cell sub-populations (SSEA1+, SSEA1-, and total which contained all cell types). Three independent experiments were performed for each line and for each cell sub-population.
2013-01-11 | E-GEOD-43403 | biostudies-arrayexpress
Project description:We developed a photosensitive tag (PsT) to label cells that reside in specific areas of interest in (human) primary tissues through specific exposure with violet light, allowing analysis of single cells while preserving their spatial information. As a benchmarking experiment, we used the PsT to assess transcriptional differences between CD8+ T cells that reside in an area containing tumor cells that do express cognate antigen, or an area of tumor cells that do not express the antigen. Single cell RNA sequencing revealed differential expression of activation markers between CD8+ T cells from antigen-positive or antigen-negative areas, demonstrating the value of the PsT to investigate spatially-induced differences between cells residing in primary tissues.
2021-05-31 | GSE175813 | GEO
Project description:The cellular heterogeneity of one patient derived orthotopic breast cancer xenograft model (PDBCX) was investigated using flow cytometry , combined with assessment of in vivo tumorigenicity and whole genome expression profiling. Epithelial cell adhesion molecule (EpCAM) was revealed as a highly specific cell surface marker of the human tumor cell population in both xenografts. Based on expression patterns observed in primary tumor tissue, SSEA-4 and CD24 were chosen as markers to further subdivide the luminal tumor cells into four subpopulations. FACS sorting was used to isolate four cell subpopulations. Results: In vivo tumorigenicity assay showed that SSEA-4+/CD24+ cells were non-tumorigenic, while the three other subpopulations were tumorigenic. Tumors resulting from the SSEA-4+/CD24- subpopulation of luminal cancer cells, did not express CD24, while tumors arising from the SSEA-4-/CD24-, and SSEA-4-/CD24+ populations both recapitulated the original tumor containing all four subpopulations. Whole genome expression analysis revealed distinct transcriptional profiles, and 44 genes were significantly differentially expressed when comparing the tumorigenic vs non-tumorigenic populations. Several interesting genes putatively suppressing the cancer cells ability to initiate tumors in vivo were upregulated in the non-tumorigenic population. We here show that tumor initiating cells within one primary tumor evidently included more than one phenotype. Furthermore, with respect to cell surface marker expression, one of the subpopulations produced tumors unlike both the originating cells, and the original tumor. Discussion: Our results imply that subpopulations from one primary tumor can give rise to dissimilar daughter tumors. These tumors may not necessarily respond to the same targeted treatment, and thereby represent a therapy escape mechanism. This study highlights that to remove the risk of breast cancer recurrence, inhibition of the molecules critical for driving the tumor progression in several tumor cell subpopulations might be essential Gene expression was measured in four cell subpopulations isolated from Patient derived human luminal-like breast cancer xenograft. Four replicates from three subpopulations and three replicates from one subpopulation.
2015-05-26 | E-GEOD-48384 | biostudies-arrayexpress
Project description:The cellular heterogeneity of one patient derived orthotopic breast cancer xenograft model PDX was investigated using flow cytometry, combined with assessment of in vivo tumorigenicity and SNP genotyping array for copy number analysis. Epithelial cell adhesion molecule (EpCAM) was revealed as a highly specific cell surface marker of the human tumor cell population in both xenografts. Based on expression patterns observed in primary tumor tissue, SSEA-4 and CD24 were chosen as markers to further subdivide the luminal tumor cells into four subpopulations. FACS sorting was used to isolate four cell subpopulations. Results: In vivo tumorigenicity assay showed that SSEA-4+/CD24+ cells were non-tumorigenic, while the three other subpopulations were tumorigenic. Tumors resulting from the SSEA-4+/CD24- subpopulation of luminal cancer cells, did not express CD24, while tumors arising from the SSEA-4-/CD24-, and SSEA-4-/CD24+ populations both recapitulated the original tumor containing all four subpopulations. Copy number analysis comparing the four subpopulations between eachother, did reveal high similarity. Although there were some minor differencies between the subpopulations, no differences in genome aberrations could explain their difference in tumorigenicity. Discussion: Our results imply that subpopulations from one primary tumor can give rise to dissimilar daughter tumors. These tumors may not necessarily respond to the same targeted treatment, and thereby represent a therapy escape mechanism. This study highlights that to remove the risk of breast cancer recurrence, inhibition of the molecules critical for driving the tumor progression in several tumor cell subpopulations might be essential
2015-05-26 | GSE54595 | GEO