Articles tagged with Tumor Microenvironments
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A multidisciplinary team developed a dual-scale Capillary-Cell microscope to visualize tumor metabolism and vasculature dynamics. The platform revealed complex relationships between tumor vascular network and metabolic behavior, highlighting distinct adaptations based on local conditions.
A study led by Aaron Hobbs and Rachel Burge reveals the distinct cell signaling and tumor microenvironment behind a slower-growing pancreatic tumor mutation. G12R KRAS mutations lead to better patient outcomes, including earlier diagnoses and longer survival times.
Active aldehydes promote toxic lipid peroxidation, impairing FAO and activating glycolysis in killer T cells, accelerating exhaustion. This vicious cycle exacerbates T cell differentiation and dysfunction.
The study reveals that low levels of CTDNEP1 drive early and deadly pancreatic tumors, highlighting its role as a tumor suppressor. Tumors with low CTDNEP1 expression showed stronger metabolic activity and immune evasion.
Tumor-specific MHC-II expression is a critical driver of antitumor responses, modulating CD4⁺ T-cell priming, differentiation, and memory formation. This review highlights MHC-II as a promising biomarker and therapeutic target for next-generation cancer treatments.
Researchers have identified a protein complex that drives T cell exhaustion in tumors and show that disrupting it can revive exhausted anti-tumor CTLs. The study's findings offer new hope for improving the efficacy of cancer immunotherapy.
A new study from Mass General Brigham researchers identified distinct T-cell infiltration patterns in colorectal cancer precursor lesions and cancer tissues. The findings suggest that understanding these patterns could help detect CRC earlier by predicting risk and develop therapeutic approaches.
Researchers at Sanford Burnham Prebys Medical Discovery Institute found that aging accelerates pancreatic cancer progression, leading to faster tumor growth and metastasis. By understanding the impact of age on the tumor microenvironment, they developed a new approach to treating this disease in frail patients.
A study published in Chinese Medical Journal identified tumor-promoting keratinocytes linked to HPV infection and poor prognosis. These cells were found to interact with immune cells, promoting tumor proliferation and differentiation.
Researchers at MD Anderson Cancer Center identified distinct cellular microenvironments in diffuse large B-cell lymphoma tumors, providing a framework to develop therapies that engage the patient's immune system. Additionally, a study found widespread misbeliefs about the cancer risks of alcohol among Americans, highlighting the need f...
The review highlights how T cells specifically recognize and eliminate malignant cells through antigen recognition mechanisms. It also explores how tumors evade immune surveillance through various mechanisms and discusses potential therapeutic strategies, including combination therapies to improve response rates for cancer patients.
A new study by Texas A&M University Health Science Center reveals how TFE3 oncofusions hijack RNA to build liquid-like hubs that promote cancer growth. The researchers also created a molecular switch to dissolve these hubs, cutting off tumor growth at its source.
Recent studies suggest that cell cycle proteins, including cyclins and CDKs, play a regulatory role in the tumor microenvironment. Inhibiting these proteins has shown promise in converting immunologically 'cold' tumors into 'hot' tumors and suppressing tumor progression.
Organoids are transforming biomedical research with their ability to model complex diseases like cancer, Zika virus infection, and cystic fibrosis. They enable high-throughput drug testing, personalized treatment prediction, and safety assessment.
ACTM-838, a novel bacterial immunotherapy, enriches in solid tumors and delivers IL-15/IL-15Rα and STING payloads to engage innate and adaptive immunity. The therapy shows durable anti-tumor efficacy and synergizes with anti-PD1 drugs, improving outcomes in treatment-resistant tumor models.
Researchers developed a new strategy to boost immunotherapy in solid tumors by targeting senescent immune cells, which contribute to treatment resistance. The approach showed improved efficacy and lower toxicity compared to existing treatments.
The University of Texas MD Anderson Cancer Center and Springer Nature will host a free conference on the tumor ecosystem, featuring presentations on cancer immunology, microbiome, disease evolution, and metastasis. Researchers can register for the event and submit abstracts to share their findings.
Researchers have identified a potential new strategy for treating glioblastoma multiforme (GBM), the most common and aggressive type of adult brain cancer. Disabling a protein called ADAR1 can stall GBM cell proliferation while reprogramming the tumor microenvironment to an anti-tumoral state.
This study reveals that GPNMB modifies the tumor microenvironment by repurposing macrophages into immunosuppressive tumor-associated macrophages. The interaction between GPNMB and Siglec-9 enables this reprogramming, leading to increased cancer cell motility and invasiveness.
Researchers discovered that breast cancer cells co-opt iron-recycling immune cells in bone marrow to acquire essential minerals, disrupting red blood cell production. This adaptation enables cancer cells to survive in low-oxygen environments and proliferate, ultimately leading to anemia and poor patient outcomes.
The study reveals how tumors manipulate amino acid metabolism to gain a competitive edge, starving immune cells and reshaping the tumor immune microenvironment. Amino acids, once seen as passive nutrients, are now known to steer cell fate, immune suppression, and resistance to immunotherapy.
A study of ovarian tumor immune landscapes reveals four distinct immunologic subtypes, with those with T cells surviving longer and having better outcomes. The researchers also found that myeloid cells play a key role in reestablishing the immune landscape upon recurrence.
Senescent T cells exhibit genomic instability, protein imbalance, and mitochondrial dysfunction, impairing immune function and recognizing tumor antigens. The presence of senescent T cells is associated with poor prognosis and reduced immunotherapy efficacy.
A decade-long study reveals that the source of dietary fat, not adiposity itself, is the primary factor influencing tumor growth in obese mice. High-fat diets derived from animal fats compromise anti-tumor immunity and accelerate tumor growth, while plant-based fats have a neutral effect.
Researchers at Sanford Burnham Prebys found that blocking macropinocytosis reshapes the tumor microenvironment, allowing more access to immune cells. This change made immunotherapy and chemotherapy more effective in treating PDAC tumors in mice.
The study reveals diverse microbial profiles within different tumor types, with notable diversity in species composition and spatial localization. Functional effects of intratumoral microbiota on the tumor microenvironment range from immunostimulatory to protumor.
The EVOaware project aims to develop an innovative platform that addresses tumour resistance to therapies by using advanced tissue imaging technologies and integrating genetic screening, lineage tracing, and spatial omics techniques. This platform has the potential to accelerate the discovery and development of new cancer therapies.
The interplay between exosomes and metabolic reprogramming shapes breast cancer progression and resistance. Targeting this axis offers novel diagnostic and therapeutic strategies, including exosome-based liquid biopsy techniques and combination therapies.
Researchers developed patient-specific Cancer Chips to model esophageal tumor microenvironments, enabling accurate prediction of chemotherapy responses. The approach can rapidly stratify patients into responders and non-responders, paving the way for personalized medicine.
Scientists at Nagoya University discovered that dying cancer cells can trigger an inflammatory feedback loop that promotes tumor growth. When macrophages consume dying cancer cells, they produce cytokines that activate growth signals in remaining cancer cells.
Researchers developed self-propelled ferroptosis nanoinducers to enhance cancer therapy by inducing programmed cell death. The nanotherapeutics exhibited enhanced diffusion and deep tumor penetration while maintaining biocompatibility.
The SOLFEGE project aims to investigate how different types of cells coordinate with each other through signals in the tumour microenvironment. Researchers will develop novel experimental tools to observe the influence of soluble factors on cellular organisation and immune cell coordination.
Scientists at Terasaki Institute engineer a novel 3D glioblastoma model that mimics brain tissue and pericyte role, showing increased resistance to chemotherapy. The model increases sensitivity of GBM cell lines to TMZ by 22-32%.
The review highlights three key regulatory layers of T-cell plasticity: cellular signals, metabolic reprogramming, and physical and biological factors. Innovative therapeutic strategies, such as immune checkpoint therapy and adoptive cell therapy, aim to restore T-cell function and enhance antitumor immunity.
Researchers discovered that ascites fluid produced by ovarian cancer suppresses cytotoxic lymphocytes, crippling immune cells' ability to kill cancer cells. Fats in ascites cripple NK cells, T cells, and innate T cells, which are attractive candidates for cellular immunotherapies.
Researchers at MD Anderson Cancer Center have made breakthroughs in understanding pancreatic cancer metastases and identifying potential biomarkers for treatment-resistant pancreatic cancer. A comprehensive spatial map provides insights into lineage shifts in cancer cells transitioning from primary tumors to organ-specific metastases.
A new study reveals the spatial organization and tumor microenvironment of primary testicular diffuse large B-cell lymphomas. The research identifies exhausted CD8+ T cells and B1 cells as playing a role in tumor progression, while E2F and CREB inhibition shows promise as novel therapeutic targets.
Long non-coding RNAs (lncRNAs) play a crucial role in regulating the tumor microenvironment, influencing processes such as immune evasion, angiogenesis, and metastasis. They mediate interactions between tumor cells and their surrounding microenvironment, modulating stromal cell activities and promoting tumor growth and survival.
Researchers discovered that lipid accumulation promotes immune suppression and therapy resistance in triple negative breast cancer. Blocking Omega-6 fatty acid intake reversed treatment resistance. Disrupting lipid droplet formation also resensitized tumors to chemotherapy and immunotherapy.
Recent research highlights the crucial role of circadian rhythms in tumor biology, demonstrating their contribution to tumorigenesis, progression, and metastasis. Disruptions in these rhythms also influence the tumor immune microenvironment and the efficacy of anticancer therapies.
Researchers identified four distinct cell populations in PDAC, including MMP1+ and S100A2+ tumor cells, CCL2+ macrophages, and OMD+ fibroblasts. These cell subsets contribute to a pro-tumor microenvironment, predicting unfavorable prognosis.
A recent study has identified that the neuronal subtype responds best to immunotherapy, while other subtypes exhibit lower response rates. The researchers developed a machine-learning algorithm using large public data sets to predict treatment response based on tumor mutational burden and immune cell infiltration.
A study found that MAGE-4 drives the accumulation of plasma immune cells suppressing antitumor immunity in mouse and human non-small cell lung cancer models. The protein promotes tumor progression by losing a tumor suppressor gene, PTEN, accelerating development into metastasis.
Researchers discover mitochondrial transfer between cancer cells and immune cells as a key immune evasion strategy. Cancer cells can reshape the tumor microenvironment to weaken tumor-infiltrating lymphocytes, and mitochondria play a significant role in this process.
The Micro Immune Response On chip (MIRO) replicates tumours and their environment, allowing researchers to study the efficacy of immunotherapy treatments. This technology has been tested with breast cancer samples and shows promise in understanding how the immune system interacts with tumours.
The study analyzed 63 tumor samples from 10 common malignancies, revealing how malignant cells specialize in growing tumors and non-cancer cells contribute to the immune system's suppression. The findings suggest a hierarchical structure of tumors with specific hallmark expression patterns.
Concordia researchers propose a novel method using ultrasound-guided microbubbles to stimulate critical cytokine secretion in T cells, potentially re-activating them and increasing the release of proteins needed to fight cancer. The approach could complement existing treatments and improve outcomes.
A new study found that inhibiting TBK1 increases CAR-T cell activity and makes cancer cells more susceptible to immune cell targeting. The researchers used patient-derived organotypic tumor spheroids (PDOTS) models to investigate the mechanisms of treatment resistance in solid tumors.
HCC-derived exosomes reprogram immune and stromal cells to create an environment conducive to tumor growth. Exosome engineering holds promise for targeted therapies that enhance the efficacy of existing treatments.
Researchers found that treating the Golgi apparatus with hydrogen sulfide creates T-cells that can take more stress, leading to a better chance of controlling tumors. The study suggests sorting T-cells into high and low Golgi groups could be a new therapeutic target.
The conference explores molecular determinants of cancer therapy resistance, a major challenge in the fight against cancer. Researchers discuss new therapeutic approaches and address resistance mechanisms involving tumour cells and the tumour microenvironment.
Researchers at Anglia Ruskin University are investigating the complex relationship between fat tissue and colorectal cancer. The study aims to enhance knowledge of the tumour microenvironment, uncover new molecules crucial for cancer growth, and develop more effective treatments.
Researchers have developed an immunotherapy that targets glioblastoma by turning its microenvironment against it. The treatment uses CAR T-cells with a blueprint for a molecule that blocks tumor signals, allowing macrophages and microglia to support the attack on cancer cells.
Researchers developed a single-cell RNA-sequencing atlas of the Multiple Myeloma immune microenvironment across disease stages. The atlas reveals potential resistance mechanisms and identifies conventional dendritic cells as a targetable population in MM.
Researchers at MD Anderson Cancer Center present promising new treatments, including a gastric cancer therapy using T cell antigen coupler technology. Additionally, COVID-19 mRNA vaccines are shown to improve responses to immune checkpoint inhibitors in patients with non-small cell lung and melanoma cancers.
Researchers at the University of Pittsburgh found that blocking the uptake of lactic acid, a key factor in T cell exhaustion, can reinvigorate these cells. This new approach shows promise for improving tumor control and treatment outcomes in various cancers.
Researchers at Michigan Medicine found that SLC13A3 transporter impairs tumor immunity by endowing ferroptosis resistance. This discovery suggests a potential target for improving immunotherapy responses in cancer patients.
Research highlights the role of gut dysbiosis in pancreatic ductal adenocarcinoma (PDAC), with specific microbial profiles associated with PDAC. Fecal microbiota transplantation (FMT) is proposed as a potential adjunct therapy to improve patient outcomes through microbiome modulation and immune system recalibration.
A new method to construct protein complex-based therapeutics has been discovered using a polymer cloak, which stabilizes the delivery of protein complexes and enables tumor-targeted immunomodulation. The study presents an IL-15 nanosuperagonist with enhanced efficacy and specificity, promising a safer therapy for cancer treatment.
Researchers have identified a 'forcefield-like' defense system in solid tumors, which uses small extracellular vesicles to block nanoparticle-based therapies. The study found that tumor cells release sEVs carrying proteins that block the activity of cytotoxic T cells and intercept nanoparticles like a decoy.