All articles tagged with #tumor microenvironment
Researchers using real-time imaging show CD169-positive macrophages at the edges of melanoma tumors actively engulf live cancer cells and help signal the immune system, constraining tumor growth even without T cells or B cells. Similar macrophages are found in human samples, suggesting these cells could be mobilized to convert cold tumors to hot and broaden the reach of immunotherapies like checkpoint inhibitors.
A large single‑cell and spatial transcriptomics study of pretreatment TNBC identifies four cancer-cell archetypes and eight ecotypes defined by cancer cells and the tumor microenvironment, reveals macrophage and interferon‑related programs linked to better neoadjuvant chemotherapy response, and provides cell-state– and gene-based classifiers (including a 13‑gene panel) to predict pathological complete response, offering new insight into TNBC heterogeneity and potential immune targets such as LAG3 and HAVCR2.
The study shows that metastasis-associated oncofetal cell states arise at the very onset of invasion in colorectal cancer and are shaped by interactions with submucosal fibroblasts. Using multiregional organoids, spatial transcriptomics, and organoid–fibroblast co-cultures, it demonstrates that trophocyte-like cancer-associated fibroblasts at the invasive front induce these fetal-like states, establishing that microenvironmental context—not just tumor genetics—dictates when and where oncofetal plasticity first appears. Although common in early cancers, additional bottlenecks such as immune evasion explain why many lesions do not metastasize.
Researchers at the University of Waterloo are engineering Clostridium sporogenes bacteria to invade oxygen-poor tumor cores and consume nutrients from inside, potentially destroying tumors. They added an oxygen-tolerance gene and use quorum sensing to activate it only after enough bacteria accumulate, limiting safety risks. Next steps combine both features in a single strain and test in preclinical trials, showcasing interdisciplinary synthetic-biology cancer research.
Researchers at Cold Spring Harbor Laboratory uncovered a self-sustaining loop in early pancreatic cancer: myCAFs (fibroblasts) lure sympathetic nerves, whose norepinephrine signals activate the fibroblasts and recruit more nerves, accelerating tumor development. Blocking nerve activity slowed growth by about 50% in mice/human cell experiments, pointing to therapies that disrupt the nerve–fibroblast crosstalk alongside existing cancer treatments.
University of Geneva researchers find that neutrophils recruited to tumors are reprogrammed to produce the chemokine CCL3, which promotes tumor growth. This shift helps explain why some cancers become more aggressive and points to CCL3 activity in neutrophils as a potential prognostic biomarker and therapeutic target. The team used genetic tools to selectively suppress CCL3 in neutrophils and reanalyzed multiple studies to confirm the link.
Researchers report that MakA, a toxin from Vibrio cholerae, when delivered systemically, slows colorectal tumor growth in mice by increasing tumor cell death and reshaping the tumor's immune environment, with no observable harm to healthy tissue or organs, suggesting a tumor-targeted anti-cancer strategy that requires further clinical study.
Brazilian researchers identify periostin produced by pancreatic stellate cells as a key driver that remodels surrounding tissue, enabling pancreatic cancer cells to invade nerves early and spread, creating a dense desmoplastic microenvironment that hinders chemotherapy and immunotherapy; targeting periostin or the stellate cells offers a potential path for precision therapies to curb invasion and metastasis.
KAIST researchers inject lipid nanoparticles carrying CAR mRNA and immunostimulants directly into tumors to reprogram resident tumor-associated macrophages into anticancer CAR-macrophages, boosting local and potentially systemic anti-tumor immunity and showing strong tumor suppression in animal models.
This study explores how epigenetic changes and immune microenvironment interactions drive early immune evasion in colorectal cancer, highlighting chromatin architecture's role in suppressing neoantigen expression and the importance of early immune escape mechanisms in tumor evolution.
COVID-19 mRNA vaccines enhance the effectiveness of immune checkpoint inhibitors in cancer treatment by stimulating innate and adaptive immune responses, increasing tumor PD-L1 expression, and potentially restoring immune sensitivity in 'cold' tumors, leading to improved survival outcomes in patients with NSCLC and melanoma.
This study used spatial transcriptomics, proteomics, and genomics to analyze the tumor immune microenvironments in diffuse large B-cell lymphoma (DLBCL), identifying distinct cellular neighborhoods and communication patterns that influence immune cell function and tumor behavior, with implications for targeted immunotherapy.
New research reveals that physical pressure from surrounding tissues can trigger epigenetic changes in cancer cells, making them more invasive and resistant by involving proteins like HMGB2 and structural remodeling, which complicates treatment strategies.
The article explores how neuronal activity and innervation, particularly via the vagus nerve, influence the initiation, progression, and metastasis of small cell lung cancer (SCLC), highlighting the role of neuron-tumor interactions, synaptic communication, and membrane depolarization in tumor growth within the lung and brain.
Scientists have discovered that certain macrophages in prostate cancer are reprogrammed to support tumor growth and suppress immune responses. Targeting these cells, specifically the SPP1 protein, in mice improved the effectiveness of immunotherapy, offering a potential new approach for treating advanced prostate cancer.