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Articles by Linbin Yang
Neutrophil extracellular traps promote liver metastasis by impairing NK cell-dependent tumor surveillance via CCDC25
Abstract Tumor metastasis requires constant crosstalk between primary tumor cells and immune cells in distant organs, yet how this interaction shapes the evolving immune landscape of metastatic sites remains unclear. Here, using longitudinal single-cell RNA sequencing in a 4T1 orthotopic breast cancer model, we observe a progressive infiltration of neutrophils, robust NETosis and an immunosuppressive niche during metastatic progression in the liver.
Prostaglandin E2 induces dendritic cell dysfunction in skin involvement of breast cancer - Cell Death & Disease
Abstract The skin involvement (SI) of breast cancer exhibits suboptimal to standard treatment and poor prognosis. Dendritic cells (DCs) are essential to maintain immune homeostasis. However, the role of cutaneous DCs in skin lesions of breast cancer remains elusive, limiting the development of therapeutic approaches. Here, skin tissues from 47 breast cancer patients were analyzed for different immune cell infiltration, showing a significant reduction in DC number and activation in lesional skin.
On a One‐Component Blow‐Up Criterion for Inhomogeneous Axially Symmetric Navier-Stokes Equations
Conflicts of Interest The authors declare no conflicts of interest. Data Availability Statement I confirm that my Data Availability Statement complies with the Expects Data Policy. References 1 and , Mathematical Study of Flows of Nonhomogeneous Fluids Novosibirsk: (Lecture Notes, Novosibirsk State University, 1973). 2 and , “The Existence of Nonhomogeneous, Viscous and Incompressible Flow in Unbounded Domains,” Communications in Partial Differential Equations 17 (1992): 1253–1265.
Liver-breast communication of adipocyte-oriented exosomes drives primary mammary cancer progression
Keywords breast cancer nonalcoholic fatty liver disease exosome adipocyte N1 methyladenosine Get full text access Log in, subscribe or purchase for full access. References 1. Fan, J.G. ∙ Kim, S.U. ∙ Wong, V.W.S. New trends on obesity and NAFLD in Asia J. Hepatol. 2017; 67:862-873 2. Thomas, J.A. ∙ Kendall, B.J. ∙ El-Serag, H.B. ... Hepatocellular and extrahepatic cancer risk in people with non-alcoholic fatty liver disease Lancet Gastroenterol. Hepatol. 2024; 9:159-169 3.
Tumor‐Associated Sympathetic Nerves Promote the Progression of Epstein‐Barr Virus‐Positive Diffuse Large B‐Cell Lymphoma
1 Introduction Epstein-Barr virus-positive (EBV+) diffuse large B-cell lymphoma (DLBCL) is a distinct entity recognized by the World Health Organization (WHO) since 2016, for which there is currently no established standard-of-care therapy.[1-3] Most patients are treated with the same regimens used for newly diagnosed DLBCL, not otherwise specified (NOS)[4, 5], yet they typically experience poorer outcomes compared to those with DLBCL, NOS[6-8], underscoring the urgent need to elucidate the...
Extracellular vesicle-packaged HIF-1α-stabilizing lncRNA from tumour-associated macrophages regulates aerobic glycolysis of breast cancer cells
Abstract Metabolic reprogramming is a hallmark of cancer. Here, we demonstrate that tumour-associated macrophages (TAMs) enhance the aerobic glycolysis and apoptotic resistance of breast cancer cells via the extracellular vesicle (EV) transmission of a myeloid-specific lncRNA, HIF-1α-stabilizing long noncoding RNA (HISLA). Mechanistically, HISLA blocks the interaction of PHD2 and HIF-1α to inhibit the hydroxylation and degradation of HIF-1α.
Neutrophil extracellular traps induced by IL-8 promote diffuse large B cell lymphoma progression via the TLR9 signaling
Abstract Purpose: Over 30% of patients with diffuse large B cell lymphoma (DLBCL) experience treatment failure after first-line therapy. Neutrophil extracellular traps (NETs), a pathogen-trapping structure in tumor microenvironment, can promote the transition of autoimmunity to lymphomagenesis. Here, we investigate whether NETs play a novel role in DLBCL progression and its underlying mechanism.
NKILA lncRNA promotes tumor immune evasion by sensitizing T cells to activation-induced cell death
T cells were transduced with lentivirus carrying an NKILA expression cassette (NKILA) or an empty vector (vec), or NKILA-shRNA (shNK1, shNK2), GFP-shRNA (shGFP) or shRNA control vector (shvec), followed by PHA activation (a, f, n) or co-culturing with autologous DCs pulsed with MUC1-peptide (b, c), MDA-MB-231/NCI-H1703 lysates (d, e, j-m) or primary tumor lysates (g, h, i) for indicated days.
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