IL10 as Cancer Biomarker

González‐Garza, María Teresa; Cruz-Vega, Delia Elva; Maldonado‐Bernal, Carmen

doi:10.5772/intechopen.90806

Cited by 13 publications

(11 citation statements)

References 94 publications

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“…In TME IL-10 is mainly produced by M2 macrophages and Th2 cells but also monocytes, mast cells, Treg cells, and by subsets of activated T and B cells [ 62 ]. This cytokine plays a primarily immune suppressive role in TME.…”

Section: Reviewmentioning

confidence: 99%

“…Immune suppressive and tumor-promoting action of IL-10 was supported by finding that IL-10 deficiency enhanced the efficacy of DC-based immunotherapy, reduced MDSC and Treg levels in the TME, and promoted Th1-type antitumor responses in mice [ 70 ]. In contrast, in vitro studies have shown, that low levels of IL-10 could exert the antitumor effect via activation of NK cells, T lymphocytes, and macrophages [ 62 ]. These data show that the role of IL-10 still has to be fully explained.…”

Section: Reviewmentioning

confidence: 99%

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Systemic Interleukins’ Profile in Early and Advanced Colorectal Cancer

Czajka-Francuz

Cisoń-Jurek

Czajka

et al. 2021

IJMS

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Tumor microenvironment (TME) is characterized by mutual interactions of the tumor, stromal and immune cells. Early and advanced colorectal tumors differ in structure and present altered serum cytokine levels. Mutual crosstalk among TME infiltrating cells may shift the balance into immune suppressive or pro-inflammatory, antitumor response this way influencing patients’ prognosis. Cancer-related inflammation affects all the body and this way, the systemic level of cytokines could reflect TME processes. Despite numerous studies, it is still not known how systemic cytokines levels change during colorectal cancer (CRC) tumor development. Better understanding tumor microenvironment processes could help in planning therapeutic interventions and more accurate patient prognosis. To contribute to the comprehension of these processes within TME, we reviewed cytokines levels from clinical trials in early and advanced colorectal cancer. Presented data were analyzed in the context of experimental studies and studies analyzing tumor infiltration with immune cells. The review summarizes clinical data of cytokines secreted by tumor microenvironment cells: lymphocytes T helper 1 (Th1), lymphocytes T helper 2 (Th2), lymphocytes T helper 17 (Th17), regulatory T cells (Treg cells), regulatory T cells (Breg cells), M1/M2 macrophages, N1/N2 neutrophils, myeloid-derived suppressor cells (MDSC), dendritic cells (DC), innate lymphoid cells (ILC) natural killer (NK) cells and tumor cells.

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Section: Reviewmentioning

confidence: 99%

Section: Reviewmentioning

confidence: 99%

Systemic Interleukins’ Profile in Early and Advanced Colorectal Cancer

Czajka-Francuz

Cisoń-Jurek

Czajka

et al. 2021

IJMS

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“…3E ) (46). The B-lymphoid lineage of T/My MPAL showed significant enrichment of the IL-10 pathway that has been extensively explored as a prognostic marker for leukemias (47). Also, in T/My MPAL B cells, the upregulated CSK pathway is associated with the promotion of B-cell activation, while the IFN-γ pathway is associated with inhibition of B-cell activation ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Single Cell RNA Sequencing Driven Characterization of Pediatric Mixed Phenotype Acute Leukemia

Mumme

Raikar

Bhasin

et al. 2022

Preprint

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BackgroundMixed phenotype acute leukemia (MPAL) is a rare subgroup of leukemia characterized by blast cells that display both myeloid and lymphoid lineage features, making this cancer difficult to diagnose and treat. A deeper characterization of MPAL at the molecular level is essential to better understand similarities/differences to the more common and better-studied leukemias, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). Therefore, we performed single-cell RNA sequencing (scRNAseq) on MPAL bone marrow (BM) samples in an attempt to develop a more granular map of the MPAL microenvironment landscape.MethodsWe analyzed ∼16,000 cells from five pediatric MPAL BM samples collected at diagnosis to generate a single-cell transcriptomic landscape of B/Myeloid (B/My) and T/Myeloid (T/My) MPAL blasts and associated microenvironment cells. Cell clusters were identified using principal component analysis and uniform manifold approximation and projection (UMAP). Unsupervised analysis was performed to determine the overall relationship among B/My MPAL, T/My MPAL, and other acute leukemias – B-ALL, T-ALL, and AML. Supervised differentially expressed gene (DEG) analysis was performed to identify B/My and T/My MPAL blast-specific signatures. MPAL sample transcriptome profiles were compared with normal BM stem and immune cells to identify MPAL-specific dysregulation. Gene set enrichment analysis (GSEA) was performed, and significantly enriched pathways were compared in MPAL subtypes. Comparative analysis was performed on diagnostic samples based on their future minimal residual disease (MRD) and relapse status.ResultsB/My MPAL and T/My MPAL blasts displayed distinct subtype-specific blast signatures. UMAP analysis revealed that B/My MPAL samples had greater overlap with B-ALL samples, while T/My MPAL samples clustered separately from other acute leukemia subtypes. Genes overexpressed in both MPAL subtypes’ blasts compared to other leukemias and healthy controls included PLIN2, CD81, and UBE2S. B/My MPAL blast-specific genes included IRS2, SMIM3, and HBEGF, whereas T/My MPAL blast-overexpressed genes included IER5, BOD1L1, and HPGD. Sirtuin signaling, p38 MPAK signaling, and PI3K signaling pathways were upregulated in B/My MPAL blasts while oxidative phosphorylation and Rho family GTPases signaling pathways were upregulated in T/My MPAL blasts. Transcriptomic, pathways, and cell communication level differences were observed in the MPAL samples based on future MRD and clinical outcome status.ConclusionsWe have for the first time described the single-cell landscape of pediatric MPAL and demonstrate that B/My and T/My MPAL have unique scRNAseq profiles distinct from each other as well as from ALL and AML.

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“…Evidence suggests that cancer cells can synthesize themselves, thereby causing an imbalance in the homeostasis of the immune system and causing tumors to escape. 13…”

Section: Resultsmentioning

confidence: 99%

The Role of IFN gamma and IL-10 in Breast Cancer

Prihatina¹,

Sandhika²,

Ariani³

2021

Indian Journal of Forensic Medicine & Toxicology

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Inflammation in the tumor microenvironmentisanessentialaspectof tumor biologicalactivity. Interferon γ and IL-10 are pro-inflammatoryand anti-inflammatorycytokinesthatplay a crucialrole in regulatingthehost'simmuneresponseto cancer cells. IFN-γ and IL-10 expression are associatedwithpoor prognosis andlowsurvivalrate in breastcarcinomapatients.This cross-sectional study was performed on the 60 paraffin-embedded samples of radical mastectomy during

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IL10 as Cancer Biomarker

Cited by 13 publications

References 94 publications

Systemic Interleukins’ Profile in Early and Advanced Colorectal Cancer

Systemic Interleukins’ Profile in Early and Advanced Colorectal Cancer

Single Cell RNA Sequencing Driven Characterization of Pediatric Mixed Phenotype Acute Leukemia

The Role of IFN gamma and IL-10 in Breast Cancer

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