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Cyclophosphamide (CTX) Enhances Cancer Antibody Immunotherapy in the Resistant Bone Marrow Niche by Modulating Macrophage FcγR Expression

ABSTRACT: Purpose: To understand the molecular mechanisms underlying the CTX synergization with antibody therapies in resistant niche-specific organs and BM-resident tumors

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE135997 | GEO | 2019/08/20

REPOSITORIES: GEO

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Cyclophosphamide (CTX) Enhances Cancer Antibody Immunotherapy in the Resistant Bone Marrow Niche by Modulating Macrophage FcγR Expression

Project description:Cyclophosphamide (CTX) Enhances Cancer Antibody Immunotherapy in the Resistant Bone Marrow Niche by Modulating Macrophage FcγR Expression

| PRJNA560906 | ENA

Cyclophosphamide Enhances Cancer Antibody Immunotherapy in the Resistant Bone Marrow Niche by Modulating Macrophage Fc?R Expression.

Project description: Not available

| S-EPMC7780711 | biostudies-literature

Niche modulated versus niche modulating genes in multiple myeloma

Project description:Background. Multiple myeloma (MM) cells depend on the bone marrow (BM) niche for growth and survival. However, the tumor genes regulated by the niche are largely unknown. Design and Methods. BM aspiration samples were obtained from MM-patients with a high tumor load. Gene expression profile (GEP) was recorded immediately following aspiration and at subsequent time points. Identification of niche-regulated genes relied on spontaneous gene modulation following loss of niche regulation. Results. Compared to the reference samples fixed immediately following aspiration, the BM samples fixed after longer delay acquired numerous changes in GEP. The top modulated genes included a common subset of ~ 60 genes displaying prompt and sustained “switch” in expression consistently, among which were oncogenes (FOS, JUN) and genes regulating homing (CD69, RGS1), expansion and angiogenesis (AREG, PTGS2, RGS2, NR4A2). Interestingly, the “switch” in GEP was reversible and turned “off” and “on” in culture conditions resuming cell-cell-matrix contact versus re-spread into suspension, respectively. Moreover, the resuming of contact prolonged the survival of the tumor cells out-of-niche and the regression of the “contactless switch” was followed by induction of a new set of genes this time mostly encoding extracellular proteins, including angiogenic factors (IL8, CXCL5), extracellular-matrix proteins (SPP1, FN1), chemokines (CXCL5, CCL2, CCL20) and growth factors (CCL2, IL6). Conclusions. Our dataset, being unique in authentic expression design, uncovered contact-regulated genes capable of controlling homing, expansion and tumorigenesis. The adaptive response of the tumor cells to culture conditions deficient of integral niche components (e.g., vascular vessels) uncovered inducible niche-regulating tumor genes.

2012-02-23 | GSE36036 | GEO

Tellurite-mediated cefotaxime (CTX) potentiation

Project description:Transcriptional profiling comparing Escherichia coli simultaneously exposed to tellurite and CTX with untreated control cells; Tellurite with control; CTX with control Three-condition experiment, antibacterial (tellurite; CTX or tellurite/CTX) vs. Untreated control cells. Biological replicates: 3 control, 3 toxicants exposed cells, independently grown and harvested. One replicate per array.

2013-09-01 | E-GEOD-39696 | biostudies-arrayexpress

Differential expression CTX positive and CTX negative Vibrio cholerae O139 strains

Project description:To gain an insight into the changes between CTX-positive and -negative strain, apart from the CTX phage deletion, we carried out microarray analysis and whole genome sequencing of both strains

2017-10-12 | GSE104843 | GEO

Tellurite-mediated cefotaxime (CTX) potentiation

Project description:Transcriptional profiling comparing Escherichia coli simultaneously exposed to tellurite and CTX with untreated control cells; Tellurite with control; CTX with control

2013-09-01 | GSE39696 | GEO

mRNA-seq analyses for the differentially expressed genes (DEGs) among Con, NF VM-astrocytes, Ctx-astrocytes, and control Ctx-NPCs

Project description:To gain further molecular insight into the observed astrocyte functions, we performed RNA-sequencing (RNA-seq) analysis of the differentiated Ctx-NPCs (control), Ctx-astrocytes and VM-astrocytes used in the co-culture and CM experiments. The genes that are differentially expressed (DEGs) in Ctx-astrocytes compared to differentiated Ctx-NPCs (FPKM>1, log2>1) significantly overlapped with DEGs in VM-astrocytes compared to differentiated Ctx-NPCs

2020-10-25 | GSE106216 | GEO

Gene expression in BM niche populations

Project description:Gene expression in BM niche populations

| PRJNA429030 | ENA

Restoring bone marrow niche function rejuvenates aged hematopoietic stem cells by reactivating the DNA Damage Response [5]

Project description:The bone marrow (BM) niche comprised of BM endothelial cells (BMECs) and LepR+ mesenchymal stromal cells (MSCs), plays a critical role in preserving the fitness of hematopoietic stem cells (HSCs). Aging is associated with defects in the BM niche that impair their ability to support HSC activity. However, mechanisms underlying age-related defects in the BM niche remain poorly understood. In this study, we identify BM niche derived Netrin-1 (NTN1) as a critical regulator of BM niche cell fitness during aging. Conditional deletion of NTN-1 specifically within BM MSCs or BMECs of young mice resulted in premature aging phenotypes within the BM niche including increased vascular leakiness, hypoxia, DNA damage and adiposity. On the other hand, supplementation of aged mice with NTN1 resulted in restoration of these hallmark niche defects and a rejuvenation of HSC activity. Mechanistically, we identify NTN1 as a critical regulator of DNA Damage Response (DDR) within BM niche cells and HSCs. In this experiment, RNA Seq analysis was performed on BM MSCs and BMECs following conditional deletion of NTN1 within BMECs or MSCs to characterize transcriptional alterations within BM niche cells resulting from a deficiency of niche derived NTN1.

2023-04-14 | GSE227147 | GEO

Restoring bone marrow niche function rejuvenates aged hematopoietic stem cells by reactivating the DNA Damage Response [1]

2023-04-14 | GSE227143 | GEO

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