Articles tagged with Tumor Cells
Researchers from Fraunhofer-Gesellschaft have developed nanoparticles that selectively deliver doxorubicin to cancer cells, reducing side effects. In laboratory tests, encapsulated doxorubicin was found to be 5 times more effective than unencapsulated form in eliminating malignant cells.
Researchers at Johns Hopkins Medicine developed flattened football-shaped artificial particles that mimic immune cells, outperforming traditional basketball-shaped particles. These particles activated T-cells more effectively, leading to improved tumor reduction and increased survival rates in mice.
Researchers found that re-activating normal aging in tumor cells can inhibit proliferation, offering a potential new therapeutic target for treating diffuse large B-cell lymphoma. The study identified Smurf2 as a key player in this process and suggests that increasing its expression may lead to improved treatment outcomes.
Researchers at the University of Cincinnati have discovered a biomarker, phosphatidylserine, that can be effectively targeted to kill pancreatic cancer cells. The use of a biotherapy consisting of saposin C and dioleoylphosphatidylserine combined in nanovesicles shows promising results in animal models.
A new study led by Oxford University researchers explains the dual natures of the 'Jekyll-and-Hyde' protein E2F, which can boost tumour cell growth and suppress it. The discovery provides a potent target for developing new cancer drugs, with compounds blocking E2F's change into 'Mr Hyde' resulting in cancer cell death
A new technique for single-cell analysis of gene expression, named Smart-seq2, has been developed to identify rare cell subpopulations in tumors. This method captures three to four times as many RNA molecules as current methods, allowing for a more granular analysis of how subtle differences contribute to biology and disease.
A recent study published in Cell Reports identified a protein called RIP1 as a key regulator of cell division and death in glioblastoma cells. The researchers found that switching off RIP1 can inhibit the growth of these aggressive brain tumors, offering new hope for treatment options.
Researchers developed a microfluidic device to study cancer cell extravasation, the process by which cells escape blood vessels. The device revealed that most arrested cells are trapped and eventually squeeze through, with their nuclei escaping even earlier than expected. Understanding this process can help identify therapies to preven...
Researchers found that Notch 1 is required for initial tumor growth and survival of cancer cells. Disabling Notch 1 leads to increased cancer cell death through increased p53 stability.
Researchers found that the signaling protein calcineurin upregulates Ang-2, promoting angiogenesis in lung endothelial cells. This pathway is crucial for metastasis, offering new targets for lung cancer therapy.
A multi-disciplinary study by University of Pennsylvania researchers has illuminated a crucial step in the process of cell movement. The protein Exo70 induces a reshaping of the cell's plasma membrane, necessary for cell migration from one location to another.
The study identifies over 10,000 different proteins in cancer cells, with more than 5,000 present in varying abundance across all types of tissue. The researchers found that the protein pattern determines the effectiveness of cancer drugs, providing new insights into personalized medicine.
A clinical trial found that tumor cell vaccination increased complete remission rates and induced leukemia-specific T-cells in patients with advanced Chronic Lymphocytic Leukemia (CLL). The study suggests that this approach may enhance anti-tumor responses following allo-HSCT.
Researchers found that high dietary sugar acts together with oncogenes to increase insulin sensitivity specifically in tumor cells. A three-drug combination blocking sugar conversion, Ras/Src signaling, and Wingless/Wnt signaling substantially reduced tumor size and progression.
Scientists have identified a unique enzyme that is abundant in cancer cells but rare in normal adult tissues. By silencing this enzyme, researchers were able to stop the growth of cancer in laboratory mice without causing harm.
A study published in PNAS found that dampening a feedback loop between a DNA repair checkpoint and its controlling pathways may promote tumor growth in pediatric solid tumors. This discovery provides new insights into the cause of childhood cancers and offers a potential target for future therapies.
A team of international researchers has identified a self-perpetuating signaling circuit in connective tissue cells that allows them to form a front and back and propel themselves in a particular direction. This propulsion is similar to the movement used by tumor cells to invade healthy tissue during cancer metastasis.
Researchers found that TAp73 supports proliferation of human and mouse tumor cells by activating G6PD, increasing PPP activity, and directing glucose to pathways for macromolecule synthesis. This reprogramming allows rapid generation of nucleic acids, lipids, and proteins, enabling tumor cells to thrive.
Research by a University of North Carolina-led team shows that inhibiting MerTK signaling in macrophages can activate the immune system to kill cancer cells, slowing tumor growth and metastasis. The study's findings suggest combining this approach with existing therapies may offer a new avenue for activating anti-tumor immunity.
The study reveals that noncoding 5S rRNA regulates the Hdm2-p53 checkpoint, allowing p53 to rise and induce cell death. This discovery suggests an ancient evolutionary link between ribosome biogenesis and cancer.
Researchers from Max Planck Institute discovered the P2Y2 receptor molecule on blood platelet walls enables tumor cells to enter organs via blood vessel openings. Blocking this key molecule may lead to new therapeutic approaches for malignant tumors.
A recent study published by researchers at Penn State College of Medicine found that protein km23-1 is crucial for the spread of colon cancer cells. The team discovered that reducing km23-1 levels decreases the production of TGF-beta and reduces a framework structure associated with cancer cell movement.
Researchers found gliomas produce quinolinic acid, a metabolite of tryptophan, to generate NAD+, evading cell death. A new enzyme, QRPT, enables this process, potentially leading to therapy resistance.
Researchers at the University of Pennsylvania School of Medicine have created a human-cell model of early-disease progression in pancreatic cancer using induced pluripotent stem cells. The study identified biomarkers that could be used for early detection, treatment, and prognosis.
Researchers describe 'chase and run' cell movement mechanism that explains process of metastasis. Cancer cells recruit healthy cells using small chemical molecules, promoting directional collective migration.
A study by University of Pennsylvania researchers found that the tumor suppressor protein Par-4 plays a crucial role in preventing breast cancer recurrence. Low Par-4 expression is associated with an increased risk of recurrence and poor response to chemotherapy, highlighting potential new therapeutic strategies.
A new mathematical method simplifies cancer-cell genome data, identifying recurrent events and revealing tumor evolution. The CORE technique improves prognosis and treatment decision-making by distinguishing subpopulations of cancer cells.
Researchers at Berkeley Lab identified the microenvironment surrounding microvasculature as a niche where dormant breast tumor cells reside. The study reveals that stable microvasculature suppresses growth and creates a dormant niche, while sprouting neovasculature sparks micrometastatic outgrowth.
Researchers discovered that targeting CTLA-4 and OX-40 proteins on regulatory T cells can help eliminate cancer cells. Mice treated with antibodies against these proteins had smaller tumors and improved survival, including clearance of brain metastases.
Researchers at Salk Institute discover that protein TGF-β can promote cancer growth and survival in premalignant cells, offering hope for new treatment methods. The study's findings suggest that novel treatments may be able to halt cancer development in these cells.
Researchers have identified a new compound class that promotes neuroblastoma cell differentiation, which can stop tumor cells from dividing and growing. This breakthrough could lead to the development of novel treatments for high-risk childhood cancer.
Scientists at Nanyang Technological University and Lund University have bioengineered a novel molecule, HAMLET, which has been proven to successfully kill tumour cells. The molecule is based on a natural protein present in human breast milk and has been shown to suppress colon cancer in laboratory mice.
A Johns Hopkins study found that suppressing a key gene, HMGA1, in tumor cells reduces their aggression and growth. The researchers hope to develop a new therapy based on this principle to treat tumors resistant to current drugs.
Researchers from Queen Mary University of London are using bioengineering techniques to grow the first complex 3-dimensional human tumour microenvironment in the laboratory. The goal is to understand how this 'tumour microenvironment' supports cancer growth and develop new treatments that target it.
A study found that ATP11B expression is correlated with higher tumor grade and cisplatin-resistance in human ovarian cancer samples. Loss of ATP11B restored sensitivity to cisplatin and reduced ovarian tumor growth in mice.
Researchers found a few hundred super-enhancers control key genes in healthy cells, but cancer cells create their own to overproduce harmful oncogenes leading to aggressive tumors.
Researchers found that TRAP1 disrupts cancer cell metabolism, but inhibiting it could stimulate tumor progression. The protein regulates a metabolic 'switch' at the level of glucose digestion, which affects tumor stage and aggressiveness.
Researchers at UNC have found that protein palladin enhances cancer-associated fibroblasts' ability to break down barriers and create pathways for tumors to spread. This discovery could lead to new treatments and screening options for pancreatic cancers.
A groundbreaking UK study found that aggressive triple-negative breast cancer cells lack the enzyme FBP1, leading to a glucose anabolic pathway that 'feeds' the cancer. This metabolic switch enables tumor cells to survive in low-oxygen environments, making it a promising target for new treatments.
Researchers discovered a molecular mechanism that makes glioblastoma resistant to mTOR inhibitors, leading to the development of a new treatment approach. The novel combination therapy combines an mTOR inhibitor with low-dose arsenic to reverse resistance and induce tumor cell death.
Moffitt researchers found that silencing the retinoblastoma gene can regulate the differentiation of myeloid-derived suppressor cells into a more aggressive form. This discovery may lead to new therapeutic strategies targeting these cells in cancer treatment.
Researchers at Scripps Research Institute have identified a mechanism controlling tumor aggressiveness and developed a simple treatment that inhibits cancer progression. In mice, the treatment prolongs life when tested with drugs already used for other conditions.
Researchers found that IQGAP1, a molecule controlling cell shape and movement, can suppress the growth of liver tumors when active in surrounding cells. The study provides new insight into cancer metastasis and points to potential therapeutic targets for preventing or treating liver metastases.
Scientists have identified a molecule called Gfi1 that represents the disease's Achilles' heel and could be targeted to develop a new approach. This discovery has direct implications for the treatment of acute lymphoblastic leukemia, a cancer of the bone marrow and blood that progresses rapidly.
A recent study published in Cell Reports found that sunitinib, an anticancer drug, does not cause lingering risks for patients after their treatment ends. The research suggests that sunitinib works by slowing tumor growth and prolonging survival during treatment, without altering tumor biology after the drug is stopped.
A recent study found that the epigenetic marker 5-hydroxymethylcytosine (5hmC) plays a vital role in the selective expression of genes, particularly in healthy brain cells. The study also discovered that changes in 5hmC distribution are associated with gene silencing and may contribute to cancer development.
Researchers at Stanford University School of Medicine have discovered an antibody that can inhibit the growth of gastrointestinal stromal tumor (GIST) cells resistant to other treatments. The antibody targets KIT receptor mutations, stimulating immune cells to kill rogue cells.
Biologists at Tufts University have identified a unique bioelectric signal in cells that are likely to develop into tumors, which they can use to detect early cancer. By manipulating the electrical charge across cells' membranes, they can lower the incidence of cancerous cells and suppress abnormal cell growth.
Researchers at UT MD Anderson Cancer Center found that tumor endothelial cells can trigger changes in cancer cells, making them more resistant to chemotherapy and more likely to spread. This signaling process involves the activation of the Notch molecular pathway and may be targeted by existing drugs under development.
Researchers found a subset of leukemia cells with slower metabolism, allowing them to survive better. An experimental drug tailored to this unique status is being tested for its ability to attack the disease.
Researchers found that cancer cells use unfolded protein response (UPR) to manipulate immune cells, making them ineffective against tumors. Tumor cells exploit UPR to promote their survival and growth, and this mechanism is being targeted for potential therapy and improved cancer vaccines.
Scientists have developed a new device that captures and preserves cancer cells circulating in the bloodstream, allowing for non-invasive diagnosis and insight into cancer spread. The technology could enable doctors to detect tumor cells earlier and provide valuable information on how cancer spreads throughout the body.
A team of researchers has discovered that the cellular reprogramming gene SOX2 is directly regulated by the tumor suppressor CDKN1B(p27) gene, which is also associated with cancers such as lung and pituitary cancer. The study also highlights the potential role of adult stem cells in cancer.
Researchers at University of California, San Diego School of Medicine discovered the reversible EMT switch in metastasis, resolving a decade-long debate. Activation of Twist1 gene promotes carcinoma cells to disseminate into blood circulation, while turning off EMT switch is crucial for proliferation and formation of secondary tumors.
A study published in Cancer Discovery reveals that microRNAs can modify gene expression, converting normal fibroblasts into cancer-associated fibroblasts that promote tumor growth. The researchers identified three microRNAs involved in this process and found that inhibiting these signals could disrupt the cancer's support system.
Researchers have created a new stem-like state of adult epithelial cells, which exhibit attributes favoring regenerative medicine. These cells do not express genes found in embryonic stem cells and induced pluripotent stem cells, making them stable and less prone to forming tumors.
A new gene delivery vehicle has been developed to target tumor cells with the TNFα cytokine, allowing for improved drug delivery and reduced resistance. The treatment approach combines the cytokine with a DNA-intercalating drug doxorubicin, showing promise in reducing tumor growth and metastasis.
A team of researchers found that tumour cells form alliances with surrounding healthy cells, called stroma, to colonize other organs during metastasis. This discovery could lead to a test to predict relapse and tailored treatment regimes for patients.
Resveratrol, a compound found in grape skins and red wine, has been shown to increase the susceptibility of prostate tumor cells to radiation treatment, leading to higher mortality rates. This discovery offers new hope for developing effective treatments for all types of prostate cancer, including aggressive tumors.
Researchers found that nisin slows or stops tumor growth by interrupting the cell cycle in cancer cells but not healthy ones. The study's findings suggest that nisin triggers cell death through the activation of protein CHAC1, which is a new role for this protein.