A study published in eLife has identified two strategies used by cancer to survive treatment with immunotherapies, including one that disables energy production in cancer-killing T-cells. Researchers found that some human cancer cells release molecules that inhibit the activity of energy-producing mitochondria in T-cells.
New research on cancer cells' interaction with their environment reveals the importance of physical cues in guiding cell migration. A novel optical tweezer-based tool probes mechanical cues to study tumor behavior.
The study found that SLC25A32 inhibition resulted in anti-proliferative effects on certain tumor cell lines, potentially by increasing reactive oxygen species. Treatment with riboflavin and glutathione rescued cancer cell proliferation upon SLC25A32 down-regulation.
Researchers at CNIO propose a novel approach using CDK4/6 inhibitors after chemotherapy to prevent tumor cells from resisting treatments. This strategy shows promising results in preventing tumor growth and death in mice with pancreatic adenocarcinoma, suggesting new avenues for improving cancer treatment.
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Researchers developed a nanoparticle delivery method that tags implanted human cancer cells with molecular signals, making them visible to the immune system. The treatment showed promise in mice with melanoma and colon cancer, with some surviving up to 60 days without tumor growth.
Researchers discovered that healthy lung cells support the survival of breast cancer cells, allowing them to form secondary tumours. Targeting the growth of cell protrusions on breast cancer cells can prevent secondary tumour formation.
Scientists create tiny nanoparticles made of dendritic polyglycerols to target cancer cells via EGFR receptors. The particles are designed to visualize tumor cells using imaging techniques and can be modified to carry therapeutic agents, offering a potential therapeutic approach.
A Cornell-led team employed a statistical modeling technique from physics to analyze breast tumor cells' behavior in the microenvironment. They found that chemokine CCL19 caused targeted cancer cells to move faster and increased heterogeneity.
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A team of researchers has created a detailed cell atlas of an entire salivary gland tumor in a mouse model, revealing that the tumor is composed of various cell types, including cancer stem cells. The study uses single-cell RNA sequencing technologies to identify these cells, which make up less than one percent of the tumor population.
Scientists have developed a new technique to analyze signaling molecules in individual cancer cells, revealing complex communication networks that contribute to tumor growth and treatment resistance. The technique, tested on bowel cancer cells, detected 28 key signaling molecules across six cell types in over 1 million cells.
Researchers at UCL have developed a new mass spectrometry platform to measure communication signals in millions of single cells from bowel cancer mini-tumours. This breakthrough enables the study of how cancer cells interact with healthy cells and the immune system, leading to new personalized cancer treatments.
Researchers identified Merkel cell polyomavirus in 7 out of 18 patients with Merkel cell carcinoma, a rare skin cancer. The study suggests that most MCC cases in India are likely caused by UV-linked damages, while some may be virus-positive, offering new targets for therapy and diagnosis.
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Cancer cells can change their developmental identity, enabling them to spread and evade the immune system. Researchers identified specific cell types involved in lung development that are also present in cancer metastases.
A new biochemical switch involved in M2 macrophage polarization and proliferation has been identified, which can be targeted to inhibit cancer growth. The discovery was made by a research team from the University of Vienna and could lead to novel therapies against systemic diseases and cancer.
Researchers mapped genomic changes throughout the human lifespan to create a timeline for cancer development. The study suggests that tumour progression may start years or even decades before diagnosis, providing a new window of opportunity for early detection and treatment.
Researchers developed a microfluidic device to assess tumor cells' physical ability to adhere, which could improve cancer prognosis. Weakly adherent cells are more likely to migrate and invade other tissues, increasing the risk of tumor recurrence.
Researchers at UNC Lineberger Comprehensive Cancer Center have discovered a way to regulate co-stimulatory molecules in genetically engineered immune cells, allowing for the fine-tuning of CAR-T activity. This could lead to improved therapeutic strategies against blood cancers and potentially solid tumors.
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A study found that increased LOXL2 protein levels in alveolar rhabdomyosarcoma cells promote metastasis. The protein's role in regulating metastatic function remains unclear, but it interacts with vimentin, a cytoskeletal protein involved in cell migration.
Researchers from Brazil, the UK, and Italy developed a novel palladium compound that acts selectively and powerfully against ovarian tumor cells without affecting healthy tissues. The compound has shown twice the potency of cisplatin against resistant tumor cells.
Research reveals frequent RB1 intragenic rearrangements in non-smoking patients with EGFR mutations, indicating higher resistance to EGFR inhibitors. The alteration may favor growth and tumoural versatility of resistant clones.
Immune cells facilitate glioblastoma growth by clearing necrotic areas while ignoring tumour cells. Researchers aim to train microglia and macrophages for tumour elimination through immunotherapy or other strategies.
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Brazilian scientists led by Rodrigo Ramos Catharino found that Zika virus inhibits tumor cell proliferation in prostate cancer cells, even when inactivated. The study, supported by FAPESP, used a human prostate adenocarcinoma cell line and identified markers of metabolic changes caused by the virus.
Researchers have successfully used copper-based nanomaterials to eliminate tumour cells in mice, combining with immunotherapy for long-lasting immune effects. The breakthrough offers a novel approach to treating lung and colon cancers without the use of chemotherapy.
Researchers found that blocking androgen receptors can increase the density of prostate-specific membrane antigen (PSMA) sites on tumor surfaces, allowing for more targeted radiation therapy. This breakthrough could lead to more efficient treatment of advanced prostate cancer.
Researchers discovered that reactivating the PPP2R2A gene can slow or stop prostate cancer progression. The study found that patients with only one functional copy of the gene have shorter survival rates, and that reconstituting PP2A protein ultimately kills prostate cancer cells.
A Northwestern University study discovered an inverse relationship between patient survival and the plasticity of tumor cells. Cancer cells with disorderly chromatin packing are more likely to adapt to treatments, but researchers can now develop new therapies that target chromatin packing to make cancer cells more vulnerable.
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Researchers found that pancreatic tumor cells secrete interleukin-1β (IL-1β) to reduce anti-cancer immune responses, promoting PDA tumor growth. Blocking IL-1β with an antibody treatment doubled T cell infiltration and increased PD-1 blockade efficacy by 40%.
Researchers have developed a low-intensity ultrasound approach that exploits the unique physical and structural properties of tumor cells to target them. By tuning the frequency to match the target cells, they were able to break apart several types of cancer cells without harming healthy blood cells.
Researchers have made a breakthrough in understanding cancer prediction by developing a new method to evaluate cell dynamics and tumor initiation. Their calculations reveal that fixation times are a more important metric than lifetime risks, and that some mutated cells may fix tumors faster than expected.
A new method called scPred uses single cell analysis techniques with machine learning algorithms to identify specific types of cells. This can help diagnose cancer and autoimmune diseases earlier, and personalize treatments for individual patients.
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Pancreatic cancer cells use a process called macropinocytosis to engulf nutrients, which are then broken down into building blocks for cell growth. The study identified key molecular steps involved in boosting this process, including the activation of protein kinase A and v-ATPase.
The European Research Council has awarded €2 million to Ruben van Boxtel's research on late effects of childhood cancer treatment, focusing on developing second cancers. Van Boxtel aims to identify the components of treatment that cause DNA changes and predict patient risk for developing a second novel cancer.
A team of researchers identified a cell surface receptor, CXCR2, essential for hormone-resistant prostate cancer cells. They showed that targeting this receptor can halt tumor growth using a drug originally intended for lung diseases.
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Researchers found that MALT1 levels correlate with patient survival in brain cancer, and blocking the gene with MALT1 inhibitors causes glioblastoma stem cells to undergo cellular suicide. This discovery points to the potential of further exploring MALT1 inhibitors as a treatment for glioblastoma.
A research team identified that several types of highly aggressive pediatric brain tumors originate from stalled development of progenitor cells in the pons and forebrain. The findings represent a significant advance in understanding these diseases, which are the leading cause of cancer-related deaths in children.
Researchers analyzed pleural effusion fluid from patients with non-small cell lung cancer and malignant mesothelioma, discovering unique cytokine profiles that may influence the tumor environment. The study suggests harnessing the local pleural immune environment could lead to improved treatment outcomes.
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In a mouse model of liver cancer, researchers found that activating the Hippo molecular signaling pathway in tumor cells drives growth, while suppressing it in surrounding healthy cells inhibits tumor growth. Systemic inhibition of Yap and Taz could have unwanted consequences by blocking tumor-suppressing abilities of healthy cells.
Researchers found that circular extrachromosomal DNA in cancer cells dramatically amplifies mutant oncogenes, promoting aggressive behavior and resistance to therapy. This unique shape enables tumor cells to generate massive amounts of growth-promoting oncogenes and evolve quickly.
Researchers identify a hyperploid salvage survival pathway in high-grade serous carcinoma cell line models that bypasses apoptosis and emerges as viable large hyperploid cells. This pathway may contribute to acquired resistance and genomic diversity of recovering tumor cells.
Researchers found that CD95 activation triggers apoptosis in individual cells, but stimulates growth in clusters of cancer cells. The study suggests new ways to transform growth-stimulating signals into cell death signals for cancer cells.
Researchers at FEFU developed a method to synthesize biologically active derivatives of fascaplysin, a compound found in sea sponges. The new compounds, including 14-bromoreticulatine and 3,10-dibromofascaplysin, show selective effects on cancer cells, particularly Pseudomonas Aeruginosa bacteria and human prostate cancer cells.
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Researchers have discovered a way in which leukemia cells can change their identity to become macrophages, a process known as transdifferentiation. This transformation occurs through epigenetic changes that alter the cell's genetic material, allowing it to acquire new functions and behaviors.
A study published in Nature Cell Biology has identified a protein called CD9 that drives growth of pancreatic cancer and could be a target for new treatments. The researchers found that CD9 is present on the surface of cancer stem cells, which are a driving force behind cancer growth.
Scientists at Shinshu University discovered a compound in grape stems that induces cell cycle arrest and suppresses the invasive activity of prostate cancer cells. The study found significant anti-cancer activity, with potential applications for metastasis prevention and cancer treatment.
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Researchers have discovered that mitochondria undergo reprogramming under low oxygen conditions, a process that could provide new therapeutic targets for pancreatic cancer. This reprogramming enables cancer cells to adapt to energy scarcity by switching to glycolysis, allowing them to continue growing despite limited nutrients and oxygen.
A compound developed by Johns Hopkins researchers has been shown to slow tumor growth, alter the tumor microenvironment, and promote durable and highly active anti-tumor T cells. The drug, a prodrug version of glutamine antagonist DON, was designed to target cancer cells' high demand for glutamine.
Researchers found that oxygen-starved tumor cells have a four times greater probability of becoming viable circulating tumor cells than those under normal oxygen conditions. These cells also have six times the probability of forming lung metastases, suggesting that oxygen starvation enhances their metastatic capabilities.
A team of scientists has identified a specific gene, eIF2B5, that is essential for the survival of colon cancer cells with APC mutations. Inhibiting this gene causes programmed cell death in mutated cells but not in healthy cells, providing a promising new target for antitumor therapies.
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Researchers analyzed pleural effusions from NSCLC patients, mesothelioma, and benign cases, identifying distinct cytokine levels that may influence tumor growth and immune response. The study suggests modifying the local pleural immune environment with antibody-based therapeutics could enhance anti-tumor effects.
The study found that tumor cells undergoing epithelial to mesenchymal transition (EMT) play a key role in metastasis. However, the reverse transition, MET, is occurring at the metastatic site, suggesting that EMT is not always required for metastasis.
Researchers at Linköping University have successfully captured the instantaneous image of the MYC protein bound to TBP, shedding light on its role in cancer. The study reveals that MYC's adaptability and dynamic structure enable it to interact with over 300 proteins, making it a promising target for new cancer therapies.
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Gajewski's research found that a 'hot' or T cell inflamed tumour microenvironment is key to unlocking immunotherapy efficacy. STING agonists and targeted therapies are being developed to combat 'cold' tumours with limited immune response.
Weiqiang Chen, an assistant professor at NYU Tandon School of Engineering, has been awarded a $1.7 million NIH grant to develop personalized approaches to CAR-T cell therapy for cancer treatment. The grant will support the development of microfluidic systems to model disease environments and study cell interactions.
Researchers created a 3D-printed cell trap that captures white blood cells and filters out red blood cells, leaving behind tumor cells for diagnosis and research. The device can process large volumes of blood at low cost, making it suitable for clinics and hospitals.
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Researchers at UNIGE have developed a new formula, C2, composed of four anti-cancer drugs that target and kill tumour cells while leaving healthy cells intact. The formula has shown promising results in reducing the risk of resistance and side effects associated with high-dose treatments.
A USC study reveals that circulating tumor cells have a unique molecular signature that predicts specific organ targets, such as the brain. The discovery provides potential treatment targets to prevent cancer spread and improves detection and monitoring methods.
Researchers found that cells on a tumor's periphery are softer and more likely to invade surrounding tissues. This softness enables the cells to spread through the body's vasculature, forming 'invasive tips' that break away from the tumor.
Researchers at Washington University and USF Health developed a peptide-based nanoparticle that delivers siRNA to suppress KRAS-driven cancer growth without adverse effects. The nanoparticles effectively target tumor cells, reducing tumor cell death and slowing cancer growth.
A compound has been identified as effective in killing chemotherapy-resistant glioblastoma-initiating cells (GICs), a major challenge in treating this devastating cancer. The research also showed that the compound is non-toxic to normal cells, raising hopes for developing drugs with low toxicity.
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Researchers developed a 3D in vitro system to examine dynamic interactions between brain tumors and the surrounding extracellular matrix. The study found that fetal ECM supported tumor growth better than adult ECM, and lipid droplets released by glioblastoma cells may contribute to lower drug sensitivity.