Researchers genetically engineered olfactory ensheathing cells to carry an anticancer drug, reducing tumor growth and improving survival in a mouse model. The treatment delivered the medication directly to glioblastoma cells while sparing healthy tissue, leading to a significant reduction in tumor size and prolonged survival.
Researchers develop new theory to explain how tumors spread, revealing competition between forces that shape their growth. The 'active wetting' model suggests tumors behave like active drops, with cells creating forces and moving on their own.
Researchers at CWRU School of Medicine are exploring the role of long noncoding RNAs in colon cancer. They have identified potential targets for treatment, including lincDUSP, and found that depleting its levels can slow tumor growth.
A study found that bacteria in the intestines fuel tumor growth in the colon, with chronic inflammation having no effect on cancer development. Microbial therapy is considered a promising approach when more about bacterial flora composition is known.
Researchers developed an mRNA-based nanotherapeutic to reintroduce functional copies of PTEN into cancer cells, restoring tumor suppressor function and killing cancer cells. The therapy showed significant suppression of tumor growth and progression in mouse models of prostate cancer.
Researchers at Massachusetts General Hospital discovered how NF-2 gene mutations lead to hyper-responsiveness to growth factor signaling, driving out-of-control cellular proliferation. This phenomenon is mediated by macropinocytosis, a process that enables cells to engulf fluids and nutrients from their environment.
Researchers have developed a new method using TOF-SIMS to map the flow of biomolecules in and around solid tumors. This technique reveals how tumors signal to their microenvironment and sap local tissue resources.
Researchers found a synthetic chemical, KHS101, which disrupts the mitochondria and metabolism of glioblastoma cells, leading to their self-destruction. The study showed promising results in mice, with a 50% decrease in tumour growth and an increase in survival.
Researchers discovered elephants' ability to resist cancer stems from the 'zombie LIF6' gene, which kills cells poised to become cancerous. This strategy may inspire new treatments for humans by mimicking the gene's behavior or activating its existing copies.
A team of researchers has confirmed that healthy tumor hybrid cells contribute to metastasis by forming spontaneously in live animals. Gene expression profiles show a mix of genes from both cell types, aiding metastatic cells in survival and potential groundwork for other tumor cells.
Medical researchers from MSU propose a new targeted cancer therapy by increasing the activity of wild-type p53, which supports genetic stability and prevents malignant tumor formation. The study reveals that p53 also regulates metastasis formation through various programmed cell death pathways.
Researchers have found that the cell layer surrounding breast milk ducts acts as an active defense mechanism to prevent cancer cells from spreading, grabbing stray cells and pulling them back in up to 92% of the time. This discovery challenges previous assumptions about the myoepithelial layer's role in cancer invasion.
A study by Weizmann Institute researchers found that a gene normally protecting against cancer, p53, can switch allegiance in the tumor microenvironment, supporting cancer growth. Eliminating this protein from cancer-associated fibroblasts reduced their ability to promote tumor growth and metastasis.
AEP enhances checkpoint inhibitor drug effects on cancer cells and autoimmune diseases; measuring AEP levels may help identify patients responding to treatment with PD-1 inhibitors.
A magnetic wire used to snag scarce tumor cells could prove swift and effective for early cancer detection. The technique attracts up to 80 times more tumor cells than current methods, making it a potent tool to catch the disease earlier.
Researchers at Brigham and Women's Hospital have developed engineered cancer cells that can home in on and destroy tumors using CRISPR technology. The treatment shows promise in preclinical models across multiple types of cancer, establishing a potential roadmap for clinical translation.
Researchers identified a mechanism where tumor cells display both PD-L1 and PD-1 proteins, neutralizing the PD-L1 'brake' on T cells. This could explain why some patients don't respond to immunotherapy, suggesting alternative mechanisms may be employed by tumors.
Researchers at Georgia State University and Vanderbilt University Medical Center have identified xCT, an amino acid transporter, as a potential therapeutic target for non-small cell lung cancer. The study found that inhibiting xCT using sulfasalazine reduced tumor formation in laboratory tests and improved survival rates in mice.
Researchers have identified 52 distinct cell types in lung tumors, far more than previously thought, offering new avenues for treatment and research. The study's findings will help develop strategies to fight tumor growth and test new immunotherapy targets.
Researchers discovered that cancerous cells in an aggressive type of childhood brain tumour work together to infiltrate the brain. The study found that DIPG cells can exert a profound influence on each other, leading to tumour growth and spread.
Researchers identify epigenetic enzyme TET2 as a key player in controlling dormant tumor cells that can lead to cancer recurrence. A novel biomarker, 5-Hydroxymethylcytosine (5hmC), is also discovered to detect these treatment-resistant cells and predict patient outcomes.
Scientists have developed a novel therapy that reprograms the metabolism of tumor cells, increasing their level of reactive oxygen species and leading to death. By pushing oxidative stress levels to the point where cancer cells become deadly, this treatment shows promise in treating various types of cancer.
A new microscope system can image living tissue in real time and molecular detail, allowing for the study of concurrent processes within cells and tissue. This technology has the potential to track tumor progression and improve cancer diagnosis.
Researchers at Temple University Health System discover a dual synthetic lethality approach to eradicate cancer cells by inhibiting two backup repair pathways simultaneously. The strategy effectively narrows down the number of secondary repair pathways available, helping to ensure cancer cell eradication.
Researchers identify dominant immune cells contributing to tumor tolerance and find that silencing these cells allows T cell attack on tumors. Jointly inhibiting both cell types substantially inhibits tumor growth in mouse models.
Researchers discovered a key molecular machinery driving DNA segregation in yeast cells, which may hold insights into human chromosome maintenance and cancer development. Cells lacking this machinery, RSC, exhibit abnormal DNA segregation and spontaneous chromosome duplication.
Scientists discovered that altered cohesin SA2 variant influences gene expression and favours loss of differentiation in tumour cells. The two cohesin variants have distinct functions, with SA1 involved in topological domains and SA2 regulating gene expression through local chromatin loops.
Scientists are exploring ways to develop innovative therapies for treating non-small cell lung cancer (NSCLC) by understanding the role of deregulated protein kinases, or MAPKs. Elevated levels of these enzymes in NSCLC tissue have been linked to tumor progression and immune evasion.
Kanazawa University researchers discover that interstitial and alveolar macrophages play key role in spreading liver cancer to lungs. The study reveals the production of inflammatory lipid leukotriene B4 promotes tumor growth and invasiveness, sparking hope for novel treatment approaches.
Researchers found that an antifungal medication can halt the growth of dormant cells within bowel tumours in mice. The study suggests that this drug could be effective in treating advanced bowel cancer by targeting drug-resistant cells.
A study found that baking soda can reverse acidity-induced dormancy and drug resistance in cancer cells, making them more susceptible to therapy. Researchers discovered that baking soda neutralizes the acidity of hypoxic patches in tumors, restoring mTOR activity and protein production.
Researchers developed a computer model that forecasts tumour changes, allowing for early disease course prediction and personalized treatment. The study reveals driver mutations can accelerate tumour growth by up to 30%.
Triple-negative breast cancer patients have fewer effective treatments due to high levels of immune suppressor cells. Researchers identified a metabolic pathway linking glycolysis and C/EBP-beta expression, which supports suppressor cell growth and reduces patient outcomes.
Researchers at IRB Barcelona identify p38 as a protective mechanism for tumor cells against excessive DNA accumulation, which would cause cell death. Combining p38 inhibitors with chemotherapy shows promise in shrinking tumors and killing cancer cells.
Researchers discovered colon cancers are composed of two different cell types that can replace each other when one is killed. Targeting both cell populations simultaneously showed strong repressive effects on tumor cell proliferation and increased cell death, resulting in slower tumor growth and prolonged survival times.
Researchers discovered that colon cancer cells rely on unusually long RNA strands, called lincRNAs, to evade cell death and promote unregulated growth. Targeting these molecules could lead to effective treatments.
Researchers have developed a technique to quantify 3D forces within cells using elastic microspheres filled with fluorescent nanoparticles. The study found that these mechanical forces play a fundamental role in cell physiology and may help unlock mysteries related to embryonic development and cancer stem cells.
Researchers discovered pterocarpanquinones and carbapterocarpans, LQB-118 and LQB-223, with anti-tumor activity against MDR leukemias. The compounds target various mechanisms of drug resistance, including FoxM1 and NF-B regulation, promoting apoptosis and inhibiting cell cycle progression.
Researchers have identified a key protein, MIP-1β, that enables ovarian cancer cells to spread through the peritoneal cavity by making mesothelial cells sticky. This discovery could lead to new therapies targeting this protein and its related adhesion protein P-selectin.
A new study found that cells with abnormal centrosomes are present before they transform into cancer cells in patients with Barrett's esophagus. Centrosome amplification was found to be a hallmark of human tumors and may contribute to the initiation and progression of various cancers.
The study shows that ST1-ADC selectively inhibits tumor cell proliferation and induces tumor cell death in both in vitro and in vivo ovarian cancer models. The data provide promising results for the development of new therapeutic options to treat ovarian cancer.
Researchers discovered Zika virus can infect and destroy human CNS tumor cells, reducing tumor mass and increasing survival rates. The virus shows a greater affinity for CNS tumor cells than healthy neural stem cells.
Glioblastoma tumors exhibit cell-to-cell differences that contribute to therapy resistance. Extrachromosomal DNA is found to play a key role in oncogene amplification, driving cancer progression and evolution. Researchers are developing novel combination therapies targeting ecDNA elements to improve treatment outcomes.
Researchers at Université libre de Bruxelles identified different tumor transition states during cancer progression and metastasis. They found that cells with intermediate EMT phenotypes are the most metastatic populations.
A microfluidic device developed by Lehigh University engineers can capture and release circulating tumor cells with high efficiency. The device's wavy-herringbone design and magnetic particles allow for selective capture of tumor cells while rejecting unwanted blood cells, enabling early cancer detection and treatment evaluation.
Researchers developed a method to measure proton nuclear resonance dispersion profiles at low magnetic fields, revealing the water exchange rate of tumor cells. This enables direct assessment of tumor status and metabolic activity, which is characteristic of aggressive and highly metastatic tumors.
PharmaMar presents newly discovered oncogenic properties of eEF1A2, the target of plitidepsin. The protein's interaction with eEF1A2 favors tumor growth, but plitidepsin inhibits this bond, inducing cell death and apoptosis.
Researchers at Stanford Medicine have developed a CAR-T therapy that eradicates diffuse intrinsic pontine glioma (DIPG) tumors in mice, leaving few residual cancer cells. The treatment targets the GD2 sugar molecule on DIPG tumors and has shown promising results, but side effects such as brain swelling must be carefully managed.
A new liquid biopsy-based cancer model has revealed insights into the development of chemotherapy resistance in small-cell lung cancer. The study found that intratumoral heterogeneity, or differences in gene expression between tumor cells, contributes to rapid chemotherapy resistance.
Researchers shed light on functional mechanism of ABC exporters, which transport a wide range of molecules out of cells. This understanding could lead to new therapeutic approaches by specifically influencing or inhibiting these processes.
Researchers from the Wellcome Sanger Institute used single-cell technology and organoids to study colorectal cancer cells, discovering that each cell is genetically unique and has many more mutations than normal cells. The study may allow for targeted prevention or treatment of cancer.
A study published in Cell reveals that tumor cells can be tracked using stemness indices, which help understand cancer progression. The researchers used machine learning algorithms on genomic data from 12,000 samples to identify molecular characteristics of healthy stem cells and differentiated cells.
Researchers developed an index measuring similarity between cancer cells and pluripotent stem cells to predict tumor aggressiveness, treatment resistance, and clinical outcome. The index may help identify novel therapeutic targets against cancer by pinpointing the point at which tumor cells acquire stem cell-like characteristics.
Researchers found that ionizing radiation softens extracellular matrix stiffness, reducing cancer growth and migration. This could lead to improved fractionated radiation therapy and targeted drug delivery.
Researchers used a unique approach combining cell culture studies with mathematical modeling to determine how heterogeneity within a tumor and surrounding environment affect responses to targeted therapies. The study suggests that using a combination of drug inhibitors may be necessary to target diverse tumor cells.
A team of researchers found that lung tumor cells can revert to a developmental program similar to their nearest relatives when a key gene is lost. This discovery highlights the remarkable resilience and adaptability of cancer cells.
A new computational method, Lancet, enables more accurate identification of rare gene mutations in cancer cells by jointly analyzing tumor and normal cell genomes. This approach outperforms existing methods in detecting somatic variants with higher accuracy and sensitivity.
A study by Hiroshima University researchers found that a specific gene group controls DNA damage response in hypoxic cancer cells, weakening the effectiveness of anticancer therapies. Suppressing this gene, DEC2, made cancer cells more sensitive to radiation treatment.
A new study found that some types of glioblastoma tumors shed extracellular vesicles containing PDL-1, which helps them evade the immune system. The presence of PDL-1 DNA in blood samples from patients with glioblastoma may serve as a biomarker for the disease.
A signaling protein called Daple, normally a tumor suppressor, can be manipulated by growth factors to become a driver of malignant growth and metastasis in cancer cells. This discovery highlights the complexity of crosstalk between major signals that drive cancers.