Gene expresson profile at single cell level of myeloid cells from pancreatic cancer tissue.
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE300154 | GEO | 2026/03/22
REPOSITORIES: GEO
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Project description:Gene expresson profile at single cell level of myeloid cells from pancreatic cancer tissue.
| PRJNA1279138 | ENA
Project description:To gain insights into which pathways might be dysregulated in JMML, we compared the transcriptome profiles among hiPSC and sorted CD33+ myeloid cells from control and patient samples. NS/JMML-derived CD33+ myeloid cells showed dysregulation in major biological processes. Moreover, a consistent expression pattern among sets of genes related to pluripotency and myeloid regulation was observed in the control, NS and NS/JMML CD33+ myeloid cells further supporting generally successful myelopoiesis. Total RNA obtained from hiPSC and sorted CD33+ myeloid cells (at day 14 of differentiation) from control and patient samples
2014-01-31 | E-GEOD-54538 | biostudies-arrayexpress
Project description:To gain insights into which pathways might be dysregulated in JMML, we compared the transcriptome profiles among hiPSC and sorted CD33+ myeloid cells from control and patient samples. NS/JMML-derived CD33+ myeloid cells showed dysregulation in major biological processes. Moreover, a consistent expression pattern among sets of genes related to pluripotency and myeloid regulation was observed in the control, NS and NS/JMML CD33+ myeloid cells further supporting generally successful myelopoiesis.
2014-01-31 | GSE54538 | GEO
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Project description:Metastasis of melanoma significantly worsens prognosis and therefore therapeutic interventions that prevent, or slow metastasis could improve patient outcomes. Here, we show using humanized mice that colonization of distant visceral organs with melanoma is dependent upon a human CD33+CD11b+CD117+ progenitor cell subset comprising <4% of the human CD45+ leukocytes. Metastatic tumor-infiltrating CD33+ cells from patients and humanized (h)NSG-SGM3 mice showed converging transcriptional profiles. Single-cell RNAseq analysis identified a gene signature of a KIT/CD117 expressing CD33+ subset that correlated with decreased overall survival in TCGA melanoma samples. Thus, human CD33+CD11b+CD117+ myeloid cells represent a novel candidate biomarker as well as a therapeutic target for metastatic melanoma.
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Project description:Due to scarcity of effective therapeutic targets, metastatic TNBC (mTNBC) has shorter survival times compared to other advanced breast cancer subtypes. Although chemo-immunotherapy with immune checkpoint inhibitors (ICIs) in PD-L1+ mTNBC has shown promise, survival benefit remains modest. Therefore, it is crucial to gain improved insight into the mechanisms underlying response and resistance to checkpoint inhibition in mTNBC. We employed single cell-RNA-sequencing, single cell secretomics, and flow cytometry to identify transcriptomic and proteomic peripheral immune cell signatures associated with response and non-response to anti-PD-1/PD-L1 therapy and chemotherapy in mTNBC. Transcriptomic analysis revealed divergent transcriptional programming of CD33+ myeloid cells between responders and non-responders, even in pretreatment PBMC samples. This divergence, in responders, was characterized by an immune-promoting CD33+ cell phenotype involving IL-1b signaling versus, in non-responders, an immunosuppressive phenotype marked by IL-1b inhibition. These baseline differences expanded during the course of treatment. Differences in CD33+ cell phenotype resulted in functional differences in lymphocyte activities between responders and non-responders. To confirm this causal role of myeloid cells, we depleted CD33+ cells in pre-treatment samples from non-responders, which led to a rescue of T cell effector function. Our findings highlight CD33+ cell phenotype as a key determinant of response to chemo-immunotherapy, which can be assessed from peripheral blood. This offers a valuable tool in the context of metastatic TNBC, in which tissue sampling is often challenging.
2024-10-31 | GSE270235 | GEO
Project description:Galectin-9 (Gal-9) is a versatile immuno-modulatory protein. Its contribution to the expansion of suppressive myeloid cells in human tumors remain to be investigated. For this aim, we used in vitro models bringing together carcinoma cells derived from nasopharyngeal carcinomas (NPC) and CD33+ myeloid precursors. We found that Gal-9 expression in carcinoma cells enhances the generation of HLA-DR-CD33+CD11b+ myeloid-derived suppressor cells (MDSCs) in bystander cells. The underlying mechanisms involve both the intra-cellular and secreted Gal-9. Inside carcinoma cells, Gal-9 up-regulates the expression of a variety of pro-inflammatory cytokines which are critical for MDSC differentiation and recruitment, including IL-1b, IL-6, CCL22, and CX3CL1. This effect is mediated by accelerated degradation of the STING protein resulting from direct interaction of the Gal-9 carbohydrate recognition domain 1 with the STING C-terminus and subsequent enhancement of the TRIMP29-mediated K48-linked ubiquitination of STING. Moreover, we showed that extracellular Gal-9 secreted by carcinoma cells can enter the myeloid cells and trigger the same signaling cascade. Consistently, clinical data from NPC patients show that high concentrations of Gal-9 in tumor cells and plasma samples are associated with shortened disease-free survival. These findings unearth a novel contribution of Gal-9 to the generation of an immunosuppressive microenvironment which favors tumor development.
2020-07-13 | GSE125942 | GEO
Project description:In human patients and in mouse models, immunosuppressive regulatory T cells(Tregs)accumulate in Pancreatic Intraepithelial Neoplasia (PanIN), the precursor lesions to pancreatic cancer. Tregs are considered a potential therapeutic target with the goal to reverse immunosuppression in a number of malignancies, including pancreatic cancer. Here, using a genetically engineered mouse that allows at will depletion of Tregs during pancreatic carcinogenesis, we determined that Treg depletion failed to relieve immunosuppression. Contradicting the current paradigm, depletion of Tregs led to accelerated tumorprogression. We demonstratedthat Treg depletion resultsin changes in the fibroblast population, exemplified by loss of Smooth Muscle Actinexpression and an increase the myeloid recruiting chemokines Ccl3, Ccl6, and Ccl8. Treg depletion further resulted ina compensatoryinflux of suppressive myeloid cells, thereby preventing an anti-tumor immune response. Mechanistically, we show that themyeloid recruitment was driven through the CCR1 axis, with the receptor expressed on tumor associated myeloid cells and several ligands up-regulated in epithelial cells and fibroblasts upon Treg depletion. Finally,blockade of CCR1 signalingcombined with Treg-depletionsuccessfully inhibitedtumorigenesis, uncovering the immune-suppressive myeloid CCR1 axis as a potential therapeutic targetin pancreatic cancer.
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Project description:Suppressive myeloid cells play a central role in cancer escape from anti-tumor immunity and exert multiple pro-tumoral activities, including the promotion of cancer cell survival, invasion and metastasis. Recent evidence suggests that certain subsets may also influence tumor heterogeneity and cellular plasticity. However, their role in cancer stem cell promotion and plasticity and the underlying molecular mechanisms have yet to be deciphered. Here we demonstrate that human immunosuppressive myeloid cells, generated in vitro or isolated from patients with breast cancer, induce cancer stem-like cells exhibiting mesenchymal features. This cancer-stemness-inducing function was restricted to CD52-expressing myeloid subset. Single cell transcriptomic- and surface proteome-based interactome analyses identify membrane-bound TGF-β1 as a potential mediator of this effect. Functional inhibition of the TGF-β1 pathway block stem-like feature induction by suppressive myeloid cells. These results provide insights into the cancer stemness-promoting capacity of suppressive myeloid cells and its associated molecular mechanisms in breast cancer.
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