Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The effect of Gemcitabine chemotherapy on lung intertiatial macrophages (IMs) from tumor-free mice

ABSTRACT: The effect of Gemcitabine chemotherapy on lung intertiatial macrophages (IMs) from tumor-free mice

PROVIDER: PRJNA896950 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22142453.fastq.gz	Fastqsanger.gz
	SRR22142454.fastq.gz	Fastqsanger.gz
	SRR22142455.fastq.gz	Fastqsanger.gz
	SRR22142456.fastq.gz	Fastqsanger.gz
	SRR22142457.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

The effect of Gemcitabine chemotherapy on lung intertiatial macrophages (IMs) from tumor-free mice

Project description:Chemotherapy offers long-term clinical benefits to many cancer patients. However, several pre-clinical studies have demonstrated that certain cytotoxic drugs enhance metastasis via multiple mechanisms. These studies have mainly focused on tumor cell-derived inflammation. The importance of host responses triggered by chemotherapy in regulating cancer metastasis has not been fully explored. Our recent studies have showed that multi-dose Gemcitabine (GEM) treatment promoted breast cancer lung metastasis in a transgenic spontaneous breast cancer animal model. Both CCR2+ macrophages and monocytes were increased in the lungs of GEM-treated mice. Further, the increase of CCR2+ macrophages and monocytes were observed in naïve (tumor-free) mice after GEM treatment. These changes were largely caused by chemotherapy-induced reactive myelopoiesis that are biased toward monocyte development. Importantly, the host responses following chemotherapy promote tumor metastasis, which is dependent on CCL2/CCR2 axis. To understand how lung macrophages contribute to the pro-metastatic effect of chemotherapy, the expression profile of lung interstitial macrophages (IMs) from GEM treated and PBS control tumor-free mice was examined.

2023-03-22 | GSE217105 | GEO

Multi-omics Study Reveals the Synergistic Anti-tumor Effects of Aspirin and Gemcitabine-based Chemotherapy on Pancreatic Cancer and the Underlying Mechanism

Project description:Pancreatic cancer is a highly malignant tumor that is well known for its poor prognosis. It has been reported that aspirin can reduce the risk of various cancers, but the potential role of aspirin and gemcitabine in pancreatic cancer pathogenesis and chemotherapy has not been studied.

2023-09-08 | E-MTAB-11517 | biostudies-arrayexpress

Chemotherapy-polarized macrophages from human breast cancer

Project description:Chemotherapies have been shown to enhance anti-tumor immunity, but whether chemotherapies affect tumor-associated macrophages (TAMs) is still unclear. We found TAMs is different before and after chemotherapy by comparing proteomic profiles of TAMs before and after chemotherapy.

2021-02-16 | PXD022673 | Pride

Comparison of de novo refilled to original lung interstitial macrophages by bulk RNA-sequencing

Project description:Lung interstitium macrophages (IMs) are non-alveolar resident tissue macrophages which contribute to the lung homeostasis. These cells were reported to be heterogeneous by our group and other teams, which contains two main distinct subpopulations: CD206+ IMs and CD206- IMs. However, the exact origin of IMs and the transcriptional programs that regulate IM differentiation remains unclear. In recent report, we analyzed the refilled IMs in the course of time after induced IM depletion with single-cell RNA sequencing (10X Genomics Chromium) and bulk RNA sequencing. In this study, the de novo refilled CD206+ and CD206- IMs on Day 14 post-depletion were compared to those without depletion. Alvelar macrophages (AMs) samples were also included in this analysis and served as a reference. Results of clustering and PCA analyses showed high similarity between de novo refilled and original IMs for both CD206+ and CD206- subsets. Only 9 genes were find upregulated in refilled IMs: AA467197, Cd109, Igf2r, Rarb and S100a4.

2023-02-07 | GSE194020 | GEO

mRNA Expression profiles of parental Panc cell lines and Gemcitabine resistance Panc1cell lines

Project description:Gemcitabine (GEM) is a key drug for treating PDAC, and it is commonly used for adjuvant chemotherapy. Although the majority of PDAC is sensitive to GEM at first, GEM cannot control PDAC for very long, suggesting that PDAC develops resistance to GEM after prolonged exposure. No reliable predictors of susceptibility to gemcitabine chemotherapy exist in pancreatic ductal adenocarcinoma. This study assesses gemcitabine resistant PDAC for its specific mRNA expression pattern. Gemcitabine resistant variants of Panc1, a human pancreatic adenocarcinoma cell line, were established. mRNA screening was investigated by microarray.

2016-04-26 | GSE80617 | GEO

SAGE analysis of alveolar macrophages from metastatic lung and untreated lung

Project description:Macrophages in lungs can be classified into two subpopulations, alveolar macrophages (AMs) and interstitial macrophages (IMs), which reside in the alveolar and interstitial spaces, respectively. Accumulating evidence indicates the involvement of IMs in lung metastasis but the roles of AMs in lung metastasis still remain elusive. An intravenous injection of a mouse hepatocellular carcinoma (HCC) cell line, BNL, caused lung metastasis foci with infiltration of AMs and IMs. Comprehensive determination of arachidonic acid (AA) metabolite levels revealed increases in leukotrienes (LTs) and prostaglandins in lungs in this metastasis model. A 5-lipoxygenase (LOX) inhibitor but not a cyclooxygenase inhibitor reduced the numbers of metastatic foci, particularly those with larger sizes. A major 5-LOX metabolite, LTB4, augmented in vitro cell proliferation of human HCC cell lines as well as BNL cells. Moreover, in this lung metastasis course, AMs exhibited higher expression levels of the 5-LOX and LTB4 than IMs. Consistently, 5-LOX-expressing AMs increased in the lungs of human HCC patients with lung metastasis, compared with those without lung metastasis. Furthermore, intratracheal clodronate liposome injection selectively depleted AMs but not IMs, together with reduced LTB4 content and metastatic foci numbers in this lung metastasis process. Finally, IMs in mouse metastatic foci produced CCL2, thereby recruiting blood-borne, CCR2-expressing AMs into lungs. Thus, AMs can be recruited under the guidance of IM-derived CCL2 into metastatic lungs and can eventually contribute to the progression of lung metastasis by providing a potent AA-derived tumor growth promoting mediator, LTB4.

2018-02-16 | GSE106987 | GEO

Chemotherapy-polarized macrophages from breast tumor of PyMT mice

2021-02-16 | PXD022674 | Pride

Single-cell RNAseq analysis (10X Genomics Chromium) of refilled lung interstium macrophages on day 4 after depletion

Project description:Lung interstitium macrophages (IMs) are non-alveolar resident tissue macrophages which contribute to the lung homeostasis. These cells were reported to be heterogeneous by our group and other teams, which contains two main distinct subpopulations: CD206+ IMs and CD206- IMs. However, the exact origin of IMs and the transcriptional programs that regulate IM differentiation remains unclear. In recent report, we analyzed the refilled IMs in the course of time after induced IM depletion with single-cell RNA sequencing (10X Genomics Chromium) and bulk RNA sequencing. The IMs in Day 4 post-depletion were compared to the those without depletion. Results showed that refilled IMs had a lower ratio of CD206+ IM vs CD206- subpopulation comparing to IMs without depletion, but they shared high similarity to each other, indicating that the de novo IM population had been established before Day 4 post-depletion.

2023-02-07 | GSE193894 | GEO

microRNA Expression profiles of parental Panc1 cell lines and Gemcitabine resistance Panc1 cell lines

Project description:Gemcitabine (GEM) is a key drug for treating PDAC, and it is commonly used for adjuvant chemotherapy. Although the majority of PDAC is sensitive to GEM at first, GEM cannot control PDAC for very long, suggesting that PDAC develops resistance to GEM after prolonged exposure. No reliable predictors of susceptibility to gemcitabine chemotherapy exist in pancreatic ductal adenocarcinoma. MicroRNAs (miR) are epigenetic gene regulators with tumorsuppressive or oncogenic roles in various carcinomas. This study assesses gemcitabine resistant PDAC for its specific miR expression pattern. Gemcitabine resistant variants of Panc1, a human pancreatic adenocarcinoma cell line, were established. MicroRNA screening was investigated by microarray.

2016-04-26 | GSE80616 | GEO

Expression data from gemcitabine treated pancreatic CAFs

Project description:Pancreatic ductal adenocarcinoma (PDAC) has a characteristically dense stroma comprised predominantly of cancer associated fibroblasts (CAFs). CAFs promote tumor growth, metastasis and treatment resistance. We aimed to investigate the molecular changes and functional consequences associated with chemotherapy treatment of PDAC CAFs. Chemoresistant immortalized CAFs (R-CAFs) were generated by continuous incubation in 100nM gemcitabine. Gene expression differences between treatment naÃ¯ve CAFs (N-CAFs) and R-CAFs were compared by array analysis. Immortalized human pancreatic CAFs were grown for 30 days in either control media or media containing 100nM gemcitabine. RNA was then isolated and hybidized on U133 Plus 2.0 Affymetrix arrays.

2016-03-09 | E-GEOD-78982 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data