Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15321300.fastq.gz | Fastqsanger.gz | |||
| SRR15321301_1.fastq.gz | Fastqsanger.gz | |||
| SRR15321301_2.fastq.gz | Fastqsanger.gz | |||
| SRR15321302_1.fastq.gz | Fastqsanger.gz | |||
| SRR15321302_2.fastq.gz | Fastqsanger.gz |
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Project description:Brain metastases (BrMs) are a devastating complication of solid tumors with challenging clinical management. In this study, immunogenomic and digital spatial analyses were applied to interrogate the peripheral blood and tumor specimens derived from 53 unique patients with metastatic brain tumors originating from different solid tumors including melanoma, breast cancer, lung cancer and renal cell carcinoma. In the peripheral blood, lower levels of neutrophil -lymphocytes ratio (NLR) were detected at time of craniotomy in patients with melanoma-derived brain metastasis (MBM) vs. non-melanoma- derived brain metastasis (non-MBM). Independently from the primary tumor of derivation, patients with BrMs and increased NLR levels were characterized by shorter overall survival (OS) following craniotomy. In the tumor microenvironment (TME), molecular evaluations performed on FFPEs revealed higher expression of genes and mRNA signatures identifying NK cells, CD8 cells and B cells in MBM (n=13) vs. non-MBM brain metastasis (n=41). Focusing on CD8 cells, higher infiltration of CD8+ cells were observed in patients with MBM with longer OS following craniotomy. Spatial proteomic analysis further highlighted the infiltration of CD8+ cells, antigen presenting cells- (HLA-DR+, CD11c+, B2M+), agonists of T cell activity (CD137+, CD40+) and B cells (CD20+) enriched in MBM vs non-MBM. On the contrary, an increased expression of genes associated with neuro-development, cell- cell adhesion, neutrophil enrichment together with the increased infiltrations of cells promoting neuro-differentiation (Neun+, S100+), immune regulatory functions (CD25+, CD127+), and granulocytes aggregation (CD66b+) were observed in non-MBM vs. MBM. These findings highlight that the TME of BrMs plays a pivotal role in the pathogenesis and therapeutic resistance of BrMs derived from different solid tumors. Our results also suggest that distinct neuro-immune interplay may contribute to treatment resistance in BrMs.
2024-09-11 | GSE245467 | GEO
Project description:Bulk ATAC-seq on 24 patient-derived cell lines corresponding to 4 melanoma brain metastases (MBM) and 4 peripheral/extracranial melanoma metastses (ECM).
2022-07-06 | GSE205033 | GEO
Project description:We performed single-cell/nuclei RNA-sequencing (sc/snRNA-seq) of 22 treatment-naïve melanoma brain metastases (MBM; 5 samples using scRNA-seq and 17 snRNA-seq) from 21 patients and 10 treatment-naïve extracranial (peripheral) metastases (MPM; all snRNA-seq) from 10 patients . In total, we recovered 145,555 cell transcriptomes in 32 samples including 73,369 cells from MBM and 72,186 from MPM.
2022-07-06 | GSE200218 | GEO
Project description:Melanoma brain metastasis (MBM) is linked to dismal prognosis, low overall survival, and is detected in up to 80% of patients at autopsy. Circulating tumor cells (CTCs) are the smallest functional units of cancer and precursors of fatal metastasis. We previously employed an unbiased multilevel approach to discover a unique ribosomal protein large/small subunits (RPL/RPS) CTC gene signature associated with MBM. Here, we hypothesized that CTC-driven MBM secondary metastasis (?metastasis of metastasis? per clinical scenarios), has targeted organ specificity for liver. We injected parallel cohorts of immunodeficient and newly-developed humanized NBSGW (HuNBSGW) mice with cells from CTC-derived MBM to identify secondary metastatic patterns. We found the presence of a melanoma brain-liver metastasis axis in humanized NBSGW mice. Further, RNA-Seq analyses of tissues showed a significant upregulation of the RPL/RPS CTC gene signature linked to metastatic spread to liver. Additional RNA-Seq of CTCs from HuNBSGW blood revealed extensive CTC clustering with human B cells in these mice. CTC:B cell clusters were also upregulated in blood of primary melanoma patients, and maintained either in CTC-driven MBM or MBM CTC-derived cells promoting liver metastasis. CTC-generated tumor tissues were interrogated at single-cell gene and protein expression levels (10x Genomics Xenium and HALO spatial biology platforms, respectively). Collectively, our findings suggest that heterotypic CTC:B cell interactions can be critical at multiple stages of metastasis. This study provides important insights for relevance of pro-metastatic CTC:B cell clusters extending from primary metastatic disease, and identifies new targets for therapies of clinical metastasis to improve patient care.
2025-01-14 | GSE280739 | GEO
Project description:We performed matched TCR-seq and single-cell RNA-sequencing of 5 treatment-naïve melanoma brain metastases (MBM) from 5 individual patients.
2022-07-06 | GSE200215 | GEO
Project description:Bulk RNA-seq on 24 patient-derived cell lines corresponding to 4 melanoma brain metastases (MBM) and 4 peripheral/extracranial melanoma metastses (ECM).
2022-07-06 | GSE200217 | GEO
Project description:We analyzed cell-free microRNAs (cfmiRs) in blood, tissue, and urine samples of melanoma patients to find potential biomarkers for monitoring and assessing early detection of melanoma metastasis. This study demonstrates that identifying cfmiR signatures in body fluids may allow for detection and assessment of melanoma brain metastasis (MBM) and metastatic melanoma patients undergoing checkpoint inhibitor immunotherapy treatments.
2020-07-15 | GSE150956 | GEO
Project description:food waste & fish MBM-BSFL frass
| PRJNA758603 | ENA
Project description:Metastatic (as well as tumor) microenvironments contain both cancer-promoting as well as cancer restraining factors. The balance between these opposing forces determines the fate of cancer cells that disseminate to secondary organ sites. In search for microenvironmental drivers or inhibitors of metastasis, we identified, in a previous study, the beta subunit of hemoglobin (HBB) as a lung-derived antimetastatic factor. In the present study, exploring mechanisms leading to melanoma brain metastasis, we discovered that brain-derived factors restrain proliferation and induce apoptosis and necrosis of brain-metastasizing melanoma cells. Employing various purification procedures, we identified a heterodimer composed of hemoglobin alpha and beta chains that performs these anti-metastatic functions. Neither the alpha nor the beta subunit alone were inhibitory. An alpha/beta chain dimer chemically purified from human hemoglobin inhibited the cell viability of primary melanomas, melanoma brain metastasis (MBM), and breast cancer cell lines. The dimer-induced DNA damage, cell cycle arrest at the SubG1 phase, apoptosis, and significant necrosis in four MBM cell lines. Proteomic analysis of dimer-treated MBM cells revealed that the dimer downregulates the expression of BRD4, GAB2, and IRS2 proteins playing crucial roles in cancer cell sustainability and progression.
2023-03-08 | GSE225459 | GEO
Project description:Indications of PD-1/L1- and MAPK-targeted therapies cross cancer histologies. Rationally sequencing and/or combining them may overcome innate and acquired resistance. We observed increased clinical benefit of BRAF andV600MUT/MEK inhibitors in patients with advanced BRAFV600MUT melanoma who were previously treated with immune checkpoint therapy (ICT). To test whether ICT primes MAPK inhibitor (MAPKi) efficacy, we compared sequential/combinatorial regimens in subcutaneous mouse tumors driven by BrafV600, Nras, Nf1 or Kras mutations. The most efficacious regimen consisted of anti-PD-L1 lead-in preceding MAPKi combination and specifically promoted intratumoral pro-inflammatory macrophages and clonal expansion of IFNhi, CD8+ cytotoxic T-cells (relative to CD4+ regulatory T-cells) that highly expressed activation and cytolytic genes. Since melanoma brain metastasis (MBM) and its propensity for therapeutic resistance limit patient survival, we developed an experimental metastasis model of BrafV600MUT MBM. Sequencing anti-PD-L1 before MAPKi combination resulted in superior MBM control and survival as well as robust intratumoral T-cell clonal expansion both intracranially and extracranially. We propose that brief anti-PD-1/L1 dosing prior to MAPKi co-treatment suppresses resistance.
2021-08-19 | GSE177901 | GEO