Research on the biology of tumor cells. Covers tumor spread, cell-particle diagnostics, new anti-tumor molecules, and cancer-killing immune cells.
Researchers found that macrophage populations actively phagocytose tumor cells following monoclonal antibody treatment. Optimized therapies may enhance macrophage recruitment and activity to improve removal of circulating tumor cells in cancer patients.
Researchers at Johns Hopkins Medicine have identified a small molecule compound called BMH-21 that targets and disrupts a key pathway in cancer cells, preventing their growth. By shutting down the RNA Polymerase pathway, BMH-21 prevents mutant cancer genes from communicating with cells and replicating.
The Damon Runyon Cancer Research Foundation has awarded over $2.8 million to 20 top young scientists for their innovative cancer research projects. The award provides independent funding to early career investigators to pursue novel ideas and aims to make paradigm-shifting breakthroughs in cancer prevention, diagnosis, and treatment.
Researchers found that activating p53 in normal cells induces Par-4 secretion, killing cancer cells. The paracrine effect targets tumor cells at distant sites, offering a new approach to treating tumors resistant to other treatments.
The study identifies MAX as a tumor suppressor gene in aggressive lung cancer, which regulates the expression of BRG1 through direct recruitment to the MAX promoter. The depletion of BRG1 hinders cell growth and is synthetic lethal with MAX-deficient tumors.
Engineered immune cells, called CARTmeso cells, have shown antitumor activity in two patients with advanced cancers that failed prior treatments. The temporary CARs are safe and trigger a response against the patient's own tumor, providing a new tool for solid cancer therapy.
A study published in Stem Cells reveals that bladder cancer originates from distinct stem cells for muscle-invasive and non-muscle invasive types. Genetic profiling identified specific gene signatures associated with each cell population, which predicted tumor stage and patient survival.
Senescent cells, a key mechanism of aging, have been identified by researchers. They found that satellite DNA unravels as cells enter senescence, leading to cell division inhibition. This discovery could lead to new treatments for cancer and age-related diseases like Progeria.
Research reveals that fusion between cancer cells and macrophages empowers cancer cells to spread, forming tumors more rapidly. The study's findings suggest a new mechanism by which cancer progression is driven.
Researchers at Johns Hopkins Medicine have identified a unique class of breast cancer cells that lead the invasion process into surrounding tissues. The team found that these 'leader cells' express a protein called K14, which is essential for their invasive behavior and may be a new target for therapy.
A team of University of Pennsylvania scientists has discovered a new mechanism of cancer spread by identifying the split personalities of a protein called Exo70. The research found that one form of Exo70 promotes cell movement and invasion, while the other helps maintain cellular structure and organization.
A new gene sequencing project identifies a family of drugs that enhance oxidative stress to kill rhabdomyosarcoma tumor cells and boost chemotherapy effectiveness. The study offers hope for treating this aggressive childhood cancer, particularly for patients with recurrent disease.
Researchers from Penn Medicine report promising results from a study of 59 leukemia patients treated with cell therapy, achieving high response rates and durable remissions. The treatment, known as CTL019, has shown long-term effectiveness in patients with both acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL).
Researchers found that PKM2 controls mitosis, allowing cancer cells to safely divide and promoting brain tumor growth. Depleting PKM2 led to programmed cell death in tumor cells.
A microchip-based device developed by MGH researchers may simplify the monitoring of patients' response to treatment for ovarian cancer. The team isolated and identified tumor cells from ascites, an accumulation of fluid in the abdomen that often occurs in abdominal cancers.
Researchers have discovered that tumour cells adopt the 'break-induced replication' (BIR) pathway to repair damaged replication forks, allowing for genome duplication. This pathway is common in cancer cells but rare in healthy cells, revealing a significant difference between these two types of cells.
A study published in the Journal of Clinical Investigation found that two p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes. Additionally, a new gene therapy approach may not require immunosuppression, as regulatory T cells promote long-term expression.
Researchers found that two p53 isoforms, Δ133p53 and p53β, play a crucial role in regulating senescence. The study suggests that altering the ratio of these isoforms may be an effective therapeutic strategy for treating immunosenescence disorders.
Researchers at the University of Pennsylvania School of Medicine have developed a method to isolate and expand antitumor T cells from human tumor tissue. These T cells recognize specific proteins on cancer cells, making them potential candidates for targeted immunotherapy.
The university's premier biomedical instrument is expected to provide breakthroughs in treating animal and human health conditions, including cancer. The instrument uses thermal cell therapy and high-resolution imaging to target specific cells and tumors.
Mount Sinai researchers uncover the role of TGFβ2 in determining tumor cell behavior, revealing its potential as a biomarker for dormant cancer cells. The study confirms the 'seed and soil' theory of metastasis, suggesting that conditions within each organ influence tumor cell growth.
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.
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...
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 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.
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.
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.
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.
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.
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.
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.
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.
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.
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 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.
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.
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.