Skip to content

Tumour microenvironment

Immune suppression, metabolic competition, stroma and myeloid cells: how the tumour microenvironment decides response.

81 selectedRelated topicsImmunotherapySingle-cell and spatial omicsOncology

Latest picks

21–40 of 81
Oct 17Sat
  1. youtube.com71

    Fc receptor engagement lets anti-CD25 antibodies deplete intratumoral Tregs, experts explain

    Experts on ImmuneZoom discuss how anti-CD25 antibodies deplete intratumoral Tregs through Fc receptor mechanisms. A non-IL-2-blocking CD25 antibody (NIB) achieved 100% complete regression as a single agent in inflamed tumors, and in a glioblastoma model, combined with an anti-EGFRv3 antibody, also reached 100% complete regression via IL-2-driven CD8 expansion and IFN-gamma activation of macrophages. The humanized anti-CD25 RG6292 depleted Tregs in blood and was well tolerated but achieved under 2-fold, unstable intratumoral depletion, which may explain clinical failure; the team now studies boosting Fc receptor activity in the tumor microenvironment.

    Why it matters: Expert analysis of why Fc-mediated intratumoral Treg depletion determines anti-CD25 antibody efficacy in cancer.

Oct 16Fri
  1. mp.weixin.qq.com70

    Tumor Cells Use SLC52A2 to Seize Vitamin B2 and Drive T Cell Ferroptosis

    Tumor cells outcompete T cells for vitamin B2 (riboflavin) in the tumor microenvironment by preferentially using the transporter SLC52A2 rather than the SLC52A3 that T cells rely on. Riboflavin is converted to FMN and FAD, cofactors central to mitochondrial energy production and antioxidant defense, and its depletion promotes ferroptosis, a 2012-named iron-dependent form of cell death marked by lipid peroxide accumulation, in T lymphocytes. The finding points to nutrient competition as a mechanism of immune suppression in solid tumors.

    Why it matters: It identifies SLC52A2-mediated riboflavin competition as a new route to T cell ferroptosis in solid tumors.

  2. youtube.com80

    STAMP In Vivo Imaging Platform Dissects Heterogeneity and Dynamics of the Tumor Immune Microenvironment

    Global ImmunoTalks broadcast an expert lecture by Christine Moussion of Genentech, introducing STAMP, an in vivo imaging platform developed by her team. The platform uses a laser micropore array to implant clonally identical GFP+ tumor cells in mouse skin.

    Why it matters: STAMP combines clonal tumor array implantation with 30-day live imaging, giving a transferable paradigm for multi-phenotype parallel controls within a single mouse.

Oct 14Wed
  1. mp.weixin.qq.com77

    Resident Macrophages Feed Pancreatic Cancer Selenium Transporter to Evade Ferroptosis

    Resident tissue macrophages in pancreatic cancer supply a selenium transporter protein to tumor cells, protecting them from ferroptosis and supporting an invasive EMT state, a study from Bai Yong Shen and Florent Ginhoux at Shanghai Jiao Tong University's Ruijin Hospital published in Cell shows. The work identifies RTM-Selenop as an axis of metabolic support in the tumor microenvironment and positions Mrc1 as a reliable marker distinguishing resident tissue macrophages from monocyte-derived macrophages, which have different transcriptional profiles.

    Why it matters: It reframes macrophages as direct metabolic donors to tumors, not just immune regulators.

  2. youtube.com70

    Thommen Team Decodes PD-1^high Exhausted T Cells in Human Cancers as Immunotherapy Biomarker

    A GLOBAL IMMUNOTALKS video lecture summarizes the Thommen team's series of studies on T cell immunity in human cancer. They propose that PD-1^high (PD-1^T) CD8 T cells are a distinct exhausted subpopulation that has lost classical effector secretion but specifically expresses high levels of CCL3, and that these cells are enriched in intratumoral tertiary lymphoid structures (TLS).

    Why it matters: The lecture reviews evidence that PD-1^high exhausted CD8 T cells mark immunotherapy response, with IHC more sensitive than PD-L1 testing.

Oct 13Tue
  1. bioRxiv Cancer Biology50

    Malignant and stromal partial EMT programmes and cetuximab outcome in head and neck cancer

    Standard bulk partial EMT (pEMT) scores in head and neck squamous cell carcinoma mainly measure stroma: across three single-cell datasets, the malignant arm (laminin-332 and hemidesmosome genes) sat in malignant cells while the stromal arm (fibrillar collagens, vimentin) sat in fibroblasts. A classifier and 12-gene core recovering the malignant arm predicted long progression-free survival in 40 patients given platinum and cetuximab (AUC 0.78 and 0.82), but the malignant arm tracked the Basal subtype, whose score performed as well or better (0.93) and also in two xenograft panels.

    Why it matters: It shows bulk pEMT scores reflect stroma rather than tumour cells and that the Basal subtype score captures cetuximab outcome.

Oct 11Sun
  1. Sci Adv77

    Extracellular matrix-targeted TNC-scFv armoring enhances CAR T cell persistence and antitumor activity in solid tumors.

    Armoring CAR T cells with a secreted tenascin-C-targeted single-chain variable fragment (TNC-scFv) enhanced cytotoxicity, persistence, and reduced exhaustion in vitro and in xenograft tumor models. Single-cell transcriptomics showed the approach reprograms the tumor microenvironment toward a CD8+ T cell-enriched, functionally active immune landscape, and humanized tumor models showed robust antitumor responses with minimal systemic toxicity. Combining the armoring with interleukin-2 further increased efficacy while mitigating cytokine-associated toxicity, establishing extracellular matrix-directed armoring as a generalizable strategy for solid tumors.

    Why it matters: It offers a generalizable armoring strategy that improves CAR T cell function against solid tumors, where efficacy has been limited.

Oct 10Sat
  1. Oncol Rep33

    Expression of V‑domain Ig suppressor of T cell activation in ovarian cancer and its regulation of follicular regulatory T‑cell function via the AKT/MAPK pathway

    VISTA expression rises with ovarian cancer progression and tracks with infiltration of FOXP3+CXCR5+ Tfr-like cells in tumor tissues. In vitro, VISTA overexpression and silencing showed VISTA drives Tfr-like cell proliferation and secretion of IL-10 and TGF-beta 1, suppresses IL-21 and granzyme B, and reduces AKT and ERK1/2 phosphorylation. The work links VISTA to immunosuppressive Tfr function via the AKT/MAPK pathway, supporting VISTA-targeted immunotherapy in ovarian cancer.

    Why it matters: Identifies VISTA as a checkpoint controlling follicular regulatory T-cell immunosuppression in ovarian cancer.

  2. medicalxpress.com65

    Tracking molecular malfunctions in metastatic colorectal cancer to find new avenues for treatment

    Hokkaido University researchers, working with an international team led by University of South Florida Health and Tampa General Hospital, have shown that the 30-year-old sphingolipid rheostat model operates in the tumor microenvironment rather than inside cancer cells in metastatic colorectal cancer. Analysis of 574 human colon cancer tissue samples showed that rising sphingosine-1-phosphate and falling long-chain ceramide create a biochemical barrier that excludes cytotoxic T cells. In lab experiments, blocking S1P/S1PR3 let killer T cells attack tumors again, pointing to a combination strategy with immunotherapy.

    Why it matters: It explains a mechanism of immunotherapy resistance in metastatic colorectal cancer and identifies a druggable pathway.

Oct 9Fri
  1. mp.weixin.qq.com70

    Bian Yingjie team's Cell study: cancer cells seize vitamin B2 to suppress antitumor immunity, supplementation boosts immunotherapy

    A team led by Yingjie Bian at Guangzhou Medical University reports in Cell that cancer cells take up vitamin B2 to suppress the antitumor function of T cells, and that B2 supplementation can improve immunotherapy outcomes. The background notes that cancer cells compete with T cells for nutrients such as glucose, amino acids and lipids to evade immune surveillance, but which SLC transporters mediate this process was previously unclear.

    Why it matters: The article extends tumor-T cell nutrient competition from glucose and amino acids to vitamin B2 and identifies a specific testable metabolic pathway.

  2. medicalxpress.com68

    Electrical ablation boosts CAR-NK cell therapy against liver cancer, offering new strategy for refractory solid tumors

    Irreversible electroporation (IRE) combined with GPC3-targeted CAR-NK cells, made with lipid nanoparticle gene delivery, produced substantially stronger tumor control than either treatment alone in hepatocellular carcinoma. IRE reshaped the immunosuppressive tumor microenvironment: chemokine levels rose, recruiting NK cells early, while IRE-induced reactive oxygen species left residual tumor cells more susceptible to NK cell killing. Across multiple preclinical models the combination showed superior tumor suppression and prolonged survival.

    Why it matters: It combines three clinically near-term technologies into a workable strategy against immunosuppressive solid tumors.

Oct 8Thu
  1. doi.org76

    Mechanotherapy enhances nanodrug uptake by overcoming the actin cytoskeleton damping effect

    Matrix stiffness in hepatocellular carcinoma suppresses nanoparticle uptake by driving F-actin polymerization and stress-fiber formation that mechanically damps the plasma membrane-actin interface. Tumor softening with β-aminopropionitrile reduced this mechanical resistance and improved NP penetration and cellular uptake. Combined softening with donafenib-loaded PLGA NPs cut endpoint tumor weight by 87.8% versus free donafenib, but increased pulmonary metastasis, exposing an efficacy-safety trade-off.

    Why it matters: Links matrix mechanics to nanodrug uptake at the membrane level and quantifies both the benefit and the metastasis risk.

Oct 7Wed
  1. Cell81

    Cancer competition for vitamin B2 creates metabolic checkpoint for T cell ferroptosis.

    Tumors use the transporter SLC52A2 to scavenge vitamin B2 and outcompete T cells, which depend on SLC52A3-mediated B2 uptake. Deprived T cells lose mitochondrial respiration and glutathione regeneration, undergo mitophagy, labile iron accumulation, and lipid peroxidation, and die by ferroptosis. Deleting tumor SLC52A2 restores T cell function in immunocompetent hosts, and B2 supplementation or SLC52A3 overexpression boosts CAR-T antitumor efficacy. High tumoral SLC52A2 correlated with T cell dysfunction and poor survival.

    Why it matters: It identifies a specific nutrient-competition mechanism causing T cell ferroptosis and a targetable transporter axis for immunotherapy.

  2. mp.weixin.qq.com69

    Serpins Weave a Fibrin Immunosuppressive Niche in Pancreatic Ductal Adenocarcinoma

    Serpins help pancreatic ductal adenocarcinoma build a fibrin-rich, immunosuppressive niche, pointing to why PDAC resists anti-PD-1 therapy despite a five-year survival rate of only about 13%. Using the Perturb-map platform, the team combined in vivo CRISPR knockout with Pro-Code protein barcoding and multiplex immunofluorescence imaging, tracking 35 Pro-Code-labeled KPC cells in orthotopic tumors. A Pro-Code/CRISPR library targeting coagulation and fibrinolysis genes, with F8-targeting guide RNA as control, was implanted in the pancreata of immunocompetent mice and spatially imaged at days 7, 14 and 21.

    Why it matters: It identifies a serpin-fibrin axis that may explain checkpoint-inhibitor failure in PDAC.

Oct 6Tue
  1. Cell78

    Cancer competition for vitamin B2 creates metabolic checkpoint for T cell ferroptosis

    T cells take up vitamin B2 through the transporter SLC52A3, while tumors rely on SLC52A2 to outcompete them for the vitamin, driving T cell ferroptosis. A CRISPR screen of solute carriers identified this transport split. Enforcing SLC52A3 overexpression in T cells reversed the competition and enhanced their antitumor activity.

    Why it matters: Identifies a nutrient-competition mechanism that can be engineered into T cells to improve antitumor activity.

  2. mp.weixin.qq.com67

    Cell Study Maps Spatial Evolution of Cachexia-Promoting Microenvironment in Pancreatic Cancer

    More than 80% of pancreatic cancer patients develop cachexia, the progressive loss of skeletal muscle and adipose tissue that progresses from a pre-cachexia stage. A team led by Xu Jingyong at Beijing Hospital and the National Center of Gerontology, with the Cancer Institute and Hospital of CAMS and the University of Oklahoma, mapped how a cachexia-promoting microenvironment evolves spatially in pancreatic cancer to drive skeletal muscle wasting. The work appears in Cell as "Spatial evolution of a cachexia-promoting microenvironment in pancreatic cancer."

    Why it matters: It identifies a spatial mechanism linking pancreatic cancer to skeletal muscle wasting, the hallmark of cachexia.

  3. youtube.com74

    Sympathetic Nerves Drive Skin CD8+ TRM Formation Through Epidermal Stem Cells, Not Immune Cells Directly

    Sympathetic nerves regulate skin immunity through epithelial stem cells rather than by acting on immune cells directly. Sympathetic nerve terminals form synapse-like structures of about 200 nm facing epidermal stem cells; suppressing sympathetic signaling raises the stem cells' CXCL16, which recruits CXCR6-expressing effector and memory T cells and promotes antigen-specific CD8+ TRM formation. In a B16 melanoma skin graft model, the resulting CD8+ TRM increase strengthened local anti-tumor defense.

    Why it matters: It recasts neuro-immune crosstalk in skin as nerve-to-stem-cell signaling that controls CD8+ TRM formation and anti-tumor immunity.

Oct 5Mon
  1. youtube.com69

    David Tuveson Maps Pancreatic Cancer Biology and Stromal Targets in CSHL Lecture

    David Tuveson of Cold Spring Harbor Laboratory gave a CSHL Leading Strand lecture on pancreatic cancer biology, covering how oncogenic mutations drive epigenomic and microenvironmental change. He described atypical WNT7 activation that drives fibroblast overactivation and matrix production, RAS dependence on farnesylated membrane localization, and a new target validated genetically in mitochondrial metabolism with antagonist compounds designed using cryo-EM. His group uses organoids, single-cell data and in vivo metabolite perturbations such as auxin to find and test targets.

    Why it matters: A leading pancreatic cancer researcher outlines new stromal and metabolic targets and organoid-based validation methods.

  2. youtube.com64

    CSHL interview: Elham Azizi on AI models for mapping the tumor microenvironment

    Cold Spring Harbor Laboratory interviewed Columbia's Elham Azizi about using machine learning, from probabilistic models to generative and foundation models, to characterize the tumor microenvironment from spatial transcriptomics, including deconvolution of mixed signals in sequencing-based platforms like Starfish. In ER-positive breast cancer, her cell-interaction algorithms suggest cytotoxic T cell infiltration correlates with worse outcomes, possibly because T cells increase tumor dependence on estrogen receptor programs, pointing to better treatment combinations. Her long-term goal is a TME foundation or world model that predicts patient trajectories across treatment doses and schedules, requiring large paired pre- and post-treatment cohorts and out-of-distribution generalization.

    Why it matters: Shows how spatial transcriptomics and foundation models could turn TME analysis into predictive treatment selection.

Oct 4Sun
  1. youtube.com74

    Third Military Medical University's Lilin Ye identifies TDLN memory T cells as key responders to PD-1 checkpoint blockade

    Lilin Ye of Third Military Medical University described CD8+ T cell exhaustion in chronic infection and cancer and identified tumor-specific memory T cells (TTSM) in tumor-draining lymph nodes as the responding population for PD-1 checkpoint blockade. PD-1 blockade drives TTSM in tumor-draining lymph nodes to differentiate into effector and exhausted T cells that migrate into tumors, which he says explains common tumor recurrence after PD-1 therapy. He proposes combining PD-1 blockade with inducing tumor pyroptosis via GSDMB/GSDME and engaging cDC1 to steer TTSM toward functional effector cells and secondary memory.

    Why it matters: Reframes the cellular basis of PD-1 response and recurrence, with direct implications for combination immunotherapy design.

CBACBA Frontier Insights (CFI)Chinese Biopharmaceutical Association (CBA)www.cba-usa.org

Disclaimer CBA Frontier Insights uses AI-assisted methods to aggregate, summarize, and analyze publicly accessible biopharmaceutical information. Content is provided for informational and educational purposes only and does not represent the official views of original sources or affiliated organizations. AI-generated content may contain errors; please verify important information against primary sources. Intellectual property rights remain with their respective owners. For copyright concerns or corrections, please contact us through the website’s feedback page.