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Epigenetic drugs selectively target a population of AML cells which are positive for CD123 cell surface markers and are chemoresistant I

ABSTRACT: Epigenetic drugs selectively target a population of AML cells which are positive for CD123 cell surface markers and are chemoresistant I

PROVIDER: PRJNA422583 | ENA |

REPOSITORIES: ENA

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Epigenetic drugs selectively target a population of AML cells which are positive for CD123 cell surface markers and are chemoresistant

Project description:Epigenetic drugs selectively target a population of AML cells which are positive for CD123 cell surface markers and are chemoresistant

| PRJNA472052 | ENA

Epigenetic drugs selectively target a population of AML cells which are positive for CD123 cell surface markers and are chemoresistant II

Project description:Epigenetic drugs selectively target a population of AML cells which are positive for CD123 cell surface markers and are chemoresistant II

| PRJNA472053 | ENA

Epigenetic drugs selectively target a population of AML cells which are positive for CD123 cell surface markers and are chemoresistant

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-28 | GSE114649 | GEO

Epigenetic drugs selectively target a population of AML cells which are positive for CD123 cell surface markers and are chemoresistant II

Project description:Gene expression profiling was performed on OCI-AML2 R50 drug resistant leukemia cell line before or after Romidepsin treatment.

2020-08-28 | GSE114648 | GEO

Epigenetic drugs selectively target a population of AML cells which are positive for CD123 cell surface markers and are chemoresistant I

Project description:Global gene expression profiling was performed on OCI-AML2 leukemia cell line, R3 and R50 drug resistant cell lines.

2020-08-28 | GSE108142 | GEO

Identification of Prognosis-Relevant Subgroups in Patients with Chemoresistant Triple Negative Breast Cancer

Project description:Triple-negative breast cancer (TNBC) patients with residual disease after neoadjuvant chemotherapy generally have worse outcome; however, some patients with residual tumor after neoadjuvant chemotherapy do not relapse. We hypothesize that there are subgroups of chemoresistant TNBC patients with different prognosis. In this study, 25 chemoresistant samples from 47 neoadjuvant chemotherapy-treated TNBC (The Methodist Hospital) are chosen for study We used gene expression data of TNBC patients with residual disease and different prognosis to molecularly define the clinically relevant subgroups, and developed a 7-gene prognostic signature for chemoresistant TNBCs

2013-01-15 | E-GEOD-43502 | biostudies-arrayexpress

Effect of CD33 and/or CD123 KO in the NPM1-mutated AML cell line OCI-AML3

Project description:To reveal which pathways linked to CD33 and CD123 overexpression could be involved in leukemic proliferation, we performed unbiased bulk RNA sequencing comparison between OCI-AML3 wt and CD123 and or CD33 KO clones

2022-07-25 | GSE209518 | GEO

Linezolid suppresses growth of tumours dervived from triple negative breast cancer, cancer chemoresistant and cancer stem-like cells through the induction of mitochondrial dysfunction

Project description:Cancer cells are known to reprogram their metabolism to adapt to adverse conditions dictated by tumor growth and microenvirontment. A subtype of cancer cells with stem-like properties, known as cancer stem cells (CSC) is thought to be responsible for tumour recurrence. These consequences are fatal for cancer patients as metastatic tumors are much more aggressive than the primary tumors from which they originate. Since both CSC and chemoresistant cancer cells may share common qualities and implicate involvement of mitochondria, drugs inducing mitochondrial dysfunction as for example, bactericidal antibiotics, may effectively suppress growth of cancer cells. In the current study, we demonstrate that CSC and chemoresistant cells derived from triple negative breast cancer (TNBC) cells display enrichment of up- and down-regulated proteins from metabolic pathways that suggest a direct link to mitochondria. Both cancer cell types (resistant cells and CSC) can be targeted by antibiotics, in particular, linezolid which decreases tumour growth rate by suppressing mitochondrial functions. As autophagy itself can “feed” cancer cells in their trial to reduce ROS induction by antibiotics, we propose that specific bactericidal antibiotics used in combination with autophagy blocker may suppress cancer cell proliferation and decrease tumour growth.

2018-11-04 | PXD009442 | Pride

Tumor Suppressor Role of INPP4B in Chemoresistant Retinoblastoma

Project description:Chemotherapy of retinoblastoma (RB), a malignant ocular childhood disease, is often limited by the development of resistances against commonly used drugs. We identified inositol polyphosphate 4-phosphatase type II (INPP4B) as a differentially regulated gene in etoposide resistant RB cell lines, potentially involved in the development of RB resistances. INPP4B is controversially discussed as a tumor suppressor and an oncogenic driver in various cancers, but its role in retinoblastoma in general and chemoresistant RB in particular is yet unknown. In the study presented, we investigated the expression of INPP4B in RB cell lines and patients and analyzed the effect of INPP4B overexpression on etoposide resistant RB cell growth in vitro and in vivo. INPP4B mRNA levels were significantly downregulated in RB cells lines compared to the healthy human retina, with even lower expression levels in etoposide resistant compared to the sensitive cell lines. Besides, a significant increase in INPP4B expression was observed in chemotherapy treated RB tumor patient samples compared to untreated tumors. INPP4B overexpression in etoposide resistant RB cells resulted in a significant reduction in cell viability with reduced growth, proliferation, anchorage-independent growth, and in ovo tumor formation. Caspase-3/7 mediated apoptosis was concomitantly increased, suggesting a tumor suppressive role of INPP4B in chemoresistant RB cells. No changes in AKT signalling were discernible, but p-SGK3 levels increased following INPP4B overexpression, indicating a potential regulation of SGK3 signalling in etoposide-resistant RB cells. RNAseq analysis of INPP4B overexpressing, etoposide resistant RB cell lines revealed differentially regulated genes involved in cancer progression, mirroring observed in vitro and in vivo effects of INPP4B overexpression and strengthening INPP4B`s importance for cell growth control and tumorigenicity.

2023-03-15 | GSE226408 | GEO

Gene expression patterns of chemoresistant and chemosensitive serous epithelial ovarian tumors with possible predictive value in response to initial chemotherapy

Project description:Chemotherapy (CT) resistance in ovarian cancer is broad and encompasses diverse, unrelated drugs, suggesting more than one mechanism of resistance. We aimed to analyze the gene expression patterns in primary serous epithelial ovarian cancer (EOC) samples displaying different responses to first-line CT in an attempt to identify specific molecular signatures associated with response to CT. Initially, the expression profiles of 15 chemoresistant serous EOC tumors [time to recurrence (TTR) ≤6 months] and 10 chemosensitive serous EOC tumors (TTR ≥30 months) were independently analyzed which allowed the identification of specific sets of differentially expressed genes that might be functionally implicated in the evolution of the chemoresistant or the chemosensitive phenotype. Our data suggest that the intrinsic chemoresistance in serous EOC cells may be attributed to the combined action of different molecular mechanisms and factors linked with drug influx and efflux and cell proliferation, as possible implications of other molecular events including altered metabolism, apoptosis and inflammation cannot be excluded. Next, gene expression comparison using hierarchical clustering clearly distinguished chemosensitive and chemo- resistant tumors from the 25 serous EOC samples (training set), and consecutive class prediction analysis was used to develop a 43-gene classifier that was further validated in an independent cohort of 15 serous EOC patients and 2 patients with other ovarian cancer histotypes (test set). The 43-gene predictor set properly classified serous EOC patients at high risk for early (≤22 months) versus late (>22 months) relapse after initial CT. Thus, gene expression array technology can effectively classify serous EOC tumors according to CT response. The proposed 43-gene model needs further validation. 2 condition experiment: chemoresistant clinical samples versus chemosensitive samples

2011-07-23 | E-GEOD-28739 | biostudies-arrayexpress

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