Articles tagged with Tumor Cells
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%.
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.
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 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.
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.
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.
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 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.
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.
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.
Researchers at Johns Hopkins Kimmel Cancer Center found that tumor-associated epigenetic states evolve erratically during early stages of tumor development. This may help refine biomarkers for cancer risk stratification by screening specific genes in individuals of every age group.
Researchers create a computer program that predicts glioblastoma tumor growth with high accuracy, focusing on the role of L1CAM in accelerating cell spread. The model offers new opportunities for researchers to simulate various scenarios and test potential treatments.
Induced pluripotent stem cells have strong immunogenic properties that provoke a systemic, cancer-specific immune response. The study suggests iPS cells may one day be used as a patient-specific cancer vaccine, potentially preventing tumor development months or years later.
Researchers crack genetic code of malignant peripheral nerve sheath tumors and identify Lats1/2 as a gene that suppresses cancer, leading to rapid cell expansion. Disrupting overactive TAZ-YAP signaling reduces tumor growth in mice and human cells, offering new hope for MPNST treatment.
Researchers have discovered that naked mole rats are able to inhibit metabolic processes of senescent cells, making them less pathogenic. The rodents' cells also display increased resistance to DNA damage, which may be essential for their longevity and cancer resistance.
A team of researchers developed a fluorescent sensor, TiY, that selectively stains tumor initiating cells (TICs) in various cancer tissues. The sensor can distinguish TICs from non-TICs and inhibit sphere formation, leading to suppressed tumor growth in mice xenograft models.
A new study reveals how basal cell cancer responds to treatment and offers new ideas for controlling this disease. The researchers found that the relative location of a cell within a tumor can have a big effect on its sensitivity to drug treatment.
Researchers have created a stealth virus that effectively recognizes and infects tumor cells using adapter molecules. The virus is protected by a novel protein shield that prevents immune system elimination, opening up avenues for treating aggressive cancers.
Researchers discover that low levels of microRNA miR-125a-5p correlate with high levels of protein TIMP-1 in human lung cancer cells. Increasing miR-125a-5p levels reduces cancer spread and increases cell death. TIMP-1's role is also explored, revealing its dual function in promoting or inhibiting tumor growth.
A new video database has been created to track cellular migration, providing insights into normal processes and alterations involved in diseases like cancer. The database contains 52 videos analyzed from the Cell Tracking Challenge, offering a guide for researchers to select algorithmic solutions.
Researchers have developed a multifunctional vehicle using gold nanoparticles to transport and release the CRISPR-Cas9 system for targeted gene editing in tumors. The platform combines hyperthermal cancer therapy with genetic modification, offering a promising approach for tumor therapy.
A team of researchers has discovered that chromosomal instability can cause cancer cells to leak DNA, leading to a chronic inflammatory response that enables their spread. This finding opens up new possibilities for targeting metastasis in cancer treatment.
Scientists create nanoparticles that can penetrate extracellular matrix surrounding tumors, delivering chemotherapies specifically to cancer cells. The 'protocell' nanoparticle overcomes previous limitations by carving through the matrix and releasing drugs in acidic cell interiors, showing promise for treating solid tumors.
Rhabdomyosarcoma, the most prevalent soft tissue cancer in children, arises from immature progenitor cells that would normally develop into blood vessel cells, not muscle cells. The discovery opens a path for better treatments and may lead to new therapeutic drug targets.
A recent study published in the Journal of Experimental Medicine reveals that a common CLL treatment may be less effective in patients with a specific protein marker. Combining ibrutinib with drugs blocking this protein could prevent tumor cells from sheltering in lymphoid organs, leading to improved patient outcomes.
Researchers at the Medical University of South Carolina found that cancer cells use the unfolded protein response to alter their circadian rhythm, contributing to tumor growth. Misfolded proteins cause disruptions in this natural clockwork, allowing cancer cells to survive conditions that would kill normal cells.
Researchers developed a technique to pinpoint potential targets for cancer therapies that rely on the immune system. The technique identified two human antigens relevant to immunotherapies and found evidence of shared self-antigens between patients, offering a key to developing effective treatments.
IRB Barcelona researchers have discovered a new target for treating advanced prostate cancer, the TFIIF protein. Removing this protein's interaction with the androgen receptor could make treatment effective again in resistant tumors.
A study published in Journal of Cell Biology identifies SUV420H2 as an epigenetic orchestrator of pancreatic cancer cells' aggressive behavior. Reducing SUV420H2 levels makes pancreatic cancer cells more vulnerable to existing therapies.
A new drug approach targets breast cancer's stem-like cells, slowing their spread before metastasis occurs. Researchers found co-expression of integrin αvβ3 and Slug identifies these cells in up to 20% of primary breast cancers.
Researchers found that low PUMA expression distinguishes stem-like cells in cancer patients who experienced tumor recurrence. Reducing PUMA restores metastasis in cultured cells, highlighting a possible Achilles heel in aggressive breast cancers.
A team from Technical University of Munich has discovered a 'shut-off switch' in immune cells called PD-1 that prevents T cell Non-Hodgkin's lymphoma. The study found that PD-1 can turn off defective T cells at an early stage, preventing them from becoming tumor cells.
A new treatment aims to direct an immune response against a misshapen protein found exclusively on cancer cells, offering hope for children with deadly diffuse intrinsic pontine glioma. The protein target is a neoantigen that can be used to develop more selective and potent immunotherapies.
Researchers found that leftover cancer cell debris can stimulate tumor growth, but resolvins can block this response. The study suggests a new approach to enhance cancer therapy and prevent recurrence.
A new method using single-cell genomics can help identify potentially lethal prostate tumors before surgery, improving risk assessment and treatment decisions. The approach analyzes genomic patterns in biopsy cores, assigning a score based on clonality and genetic aberrations.
Research reveals that bone marrow-derived cells contribute to lung cancer progression by stimulating the production of specific neutrophils. These neutrophils exhibit increased expression of genes associated with tumor-promoting processes, leading to worse patient survival in a small study.
Researchers at Beth Israel Deaconess Medical Center have shown that chemotherapy-generated debris can stimulate tumor growth, but resolvins can suppress this effect. The findings offer a novel treatment approach to prevent cancer recurrence.
Researchers discovered that chemotherapy can stimulate tumor growth by inducing an inflammatory reaction in the body. Resolvins, a family of molecules, have been found to suppress this response, suggesting new ways to enhance cancer therapy effectiveness.
A new study at the University of Michigan identifies a pathway that links efferocytosis, the process of removing dead cells, to tumor growth in metastatic prostate cancer. The researchers found that a pro-inflammatory protein called CXCL5 accelerates tumor growth and sheds light on novel effective cancer therapies.
Researchers have identified a possible way to reengage a tumor suppressor protein, Growth Differentiation Factor 11, in triple-negative breast cancer cells. This could lead to the development of novel medications that can stop the aggressive form of cancer by intervening in its progression.
Scientists at NIST have discovered a way to make tiny colonies of cells grow in three-dimensional structures inside petri dishes, paving the way for more realistic biological environments for testing pharmaceuticals. The method could help bridge the gap between lab and living creature testing, speeding up drug development.