Research on the biology of tumor cells. Covers tumor spread, cell-particle diagnostics, new anti-tumor molecules, and cancer-killing immune cells.
A new method called Time-lapse Imaging Microscopy in Nanowell Grids (TIMING) allows researchers to study immune cells and cancer cells in isolation, enabling the identification of high-performing outliers. This technology has the potential to expand cancer immunotherapy treatment options for more patients.
A Brazilian antibody developed by Recepta Biopharma with FAPESP support will be used to create a new cancer drug. The technology has been licensed to US-based company Mersana Therapeutics, which will use it to develop an immunoconjugate against target tumor cells.
Researchers developed a biosensor to measure Mitochondrial Pyruvate Carrier (MPC) activity in malignant cells, finding low MPC activity compared to healthy cells. Treating cancer cells with a new compound restored normal MPC activity, suggesting the carrier's dysfunction is responsible for its inactivity.
Researchers have discovered that protein Hsp90 triggers cancer cell metabolism, providing a potential therapeutic target. The modified protein is toxic to cells in neurodegenerative disorders but acts as a pro-survival agent in tumor cells.
Researchers discovered that CA125-negative tumor cells have an enhanced ability to repair their DNA and resist programmed cell death, making them dangerous. Combining chemotherapy with birinapant significantly improved disease-free survival in laboratory models of human ovarian cancer.
Researchers at Lawson Health Research Institute have identified LKB1 as a key player in promoting and surviving ovarian cancer cells. This discovery contradicts previous studies, which suggested that LKB1 acts as a tumour suppressor in ovarian cancer.
Researchers at University of Pennsylvania implicated defects in mitochondria as a key factor in cancerous cell transition. Disrupting mitochondrial components led normal cells to adopt cancerous characteristics, including increased glucose consumption and invasive behavior.
Natural killer cells are impaired in the tumor microenvironment, but can be restored in normal conditions. Researchers identified two key factors blocking NK cell function: inflammatory cytokine IL-10 and down-regulated NKG2D ligands.
A recent study discovered that Daple protein is a tumor suppressor in the early stages of colorectal cancer, but may actually facilitate disease spread at later stages. Researchers found that higher levels of Daple were associated with better patient survival rates and lower tumor growth.
Ghajar is investigating two approaches: keeping dormant cells asleep or destroying them altogether to prevent breast cancer metastasis. He aims to identify factors that keep cells asleep and profile molecules that mediate chemo resistance, potentially providing a lasting cure for cancer patients.
Scientists at the Salk Institute discovered that telomeres play a more central role in a self-destruct program in cells that prevents tumors than previously thought. This process, called crisis, can be exploited to improve cancer therapies by targeting telomeres and making cells more susceptible to chemotherapy.
A new study suggests that cell fusion can initiate cancerous processes and tumor formation through 'genomic catastrophe', leading to chromosomal instability and DNA damage. Fused cells from rat intestinal epithelial cells formed tumors in immunodeficient mice, providing evidence for a molecular mechanism driving neoplastic transformation.
The combination of MEDI4736 and tremelimumab has been shown to have manageable toxicity and clinical activity in advanced NSCLC patients, including those with PD-L1 negative tumors. Eight out of 31 evaluable patients achieved a partial response.
Differences in tumor cell metabolism lead to more aggressive behavior in the center of a tumor. Mathematical modeling shows that cells with high glucose metabolism and acid production become invasive and cause tumor recurrence.
Researchers developed a microfluidic device called the Cluster-Chip to capture clusters of two or more cells, which are significantly more likely to cause metastases. The device proved 40-50% better at finding clusters with targeted markers and 1000% better at capturing cells without them.
Dying daughter cells release protein Pvf1, binding to nearby mother stem cells' receptors, preventing apoptosis. This allows stem cells to survive until they can regenerate damaged tissue. The discovery may lead to new cancer treatments by targeting protective signals in tumor-initiating cells.
Scientists at The Wistar Institute have identified a way that cells can reprogram their metabolism to overcome senescence, a tumor-suppressing mechanism. This reprogramming allows for the proliferation of cells that should have become senescent and has the potential to lead to tumor formation.
Researchers at the University of Notre Dame investigate the clinical potential of microvesicles, shedding light on their role in promoting tumor invasion and metastasis. The study identifies key proteins that guide the formation of these vesicles and suggests a potential link to biomarker development.
Researchers discovered that Myc's primary function is to repress well-being genes, making cancer cells vulnerable to cell death. This finding suggests a new approach for cancer therapies, targeting the downregulation of well-being genes to enhance the killer activity of Myc in tumor cells.
Researchers have identified a novel approach to treating pancreatic cancer by introducing the protein E47, which can reprogram cancer cells back to their original state. This breakthrough offers new therapeutic possibilities and may lead to improved patient outcomes.
Scientists at MIT created a new cancer therapy that activates both the innate and adaptive immune systems to attack tumors. The treatment combines an antibody drug with IL-2, which boosts immune responses, resulting in complete tumor disappearance in 80-90% of mice.
Researchers discovered that cancerous tumor cells in soft-shell clams are contagious and can spread from one animal to another. The study found that the cancer originated from a single lineage of tumor cells and has persisted ever since.
Researchers at MIT and Whitehead Institute discover that glioblastoma cells rely on enzyme GLDC to break down glycine, which can be exploited to kill cancer cells. Blocking GLDC activity could offer a new approach to combating brain tumors.
Researchers at Cold Spring Harbor Laboratory have discovered that tumor cells can form tubular networks resembling blood vessels, facilitating metastasis in breast cancer. This phenomenon, known as vascular mimicry, allows tumor cells to access the bloodstream and colonize new sites.
A new review emphasizes the need to decipher immune response dynamics to enhance cancer immunotherapy. Researchers suggest developing combination therapies and biomarker panels to increase treatment impact, as single biomarkers are unlikely to predict patient responses.
Researchers have designed a drug called MP-MUS that targets the energy source of brain tumor cells, crippling their ability to grow and divide. In animal models and human tissue cultures, MP-MUS destroyed 90-95% of malignant glioma cells without affecting healthy brain cells.
Cancer cells with high stress granule levels are more likely to metastasize. Removing YB-1 reduces stress granule formation and decreases metastatic spread in animal models.
Researchers discovered how NORE1A prevents excessive cell proliferation associated with cancer. Overexpressing NORE1A induced cell senescence, whereas removing the protein enhanced cancer-promoting Ras mutations. This study highlights the critical role of NORE1A in regulating tumor growth.
A study published in Veterinary and Comparative Oncology reveals an association between frizzled-6 protein expression and more aggressive behavior in canine bone cancer. The findings may provide a new pathway for tumor formation and improve outcomes for dogs with the disease.
Researchers at Mayo Clinic and the University of Oslo have identified a molecule that transforms normal pancreatic cells into duct-like structures, which can become cancerous. Inhibiting this gene, PKD1, may halt progression and spread of pancreatic cancer.
Researchers are developing an irreversible electroporation technique to target and destroy therapy-resistant cells in glioblastoma. The treatment has shown success in animal trials and is now being tested on human cells.
A new test, PLA test, evaluates the effectiveness of cancer vaccines by detecting tumor antigens presented on MHC molecules. The test has shown promising results in identifying glioma tumors and melanoma cells with specific antigens.
Researchers found that collagen cross-links play a crucial role in regulating stromal stiffness and determining tumor cell metastatic fate. The study identified two types of collagen cross-links, HLCC and LCC, which are associated with different levels of tumor growth and spread.
Chronic inflammatory conditions are directly associated with several types of cancer, but the cellular mechanisms behind this link were unclear. An international team of scientists has identified a multistep process showing how these cancers develop, providing potential therapeutic targets for halting tumor cell formation.
Researchers employed a 'Big Bang' model to trace the origins of colorectal cancer cells, revealing clues to why tumor cells become good or bad and potential ways to stop them before they start growing. The study highlights the importance of understanding the early stages of tumor development to prevent cancer.
Researchers at Griffith University have discovered that mitochondria can transfer genetic material between healthy and cancerous cells, leading to rapid proliferation of tumour cells. This finding has implications for our understanding of human biology and may shed light on other diseases with defective mitochondrial DNA.
Researchers discovered that cells with low levels of profilin 1 protein in breast tumors have increased capacity to metastasize and invade other tissues. The protein regulates the formation of invasive structures called invadopodia, which play a critical role in tumor invasion and metastasis.
Researchers discovered that gene NR2F1 induces dormancy in tumor cells when activated, preventing rapid growth and division. Combining azacytidine and retinoic acid significantly increased NR2F1 activity, leading to improved therapeutic outcomes.
Researchers at CNIC identified the molecular mechanism regulating transport of Rac1 between nucleus and cytoplasm. Sustained presence of Rac1 in nucleus promotes nuclear deformation to facilitate cell migration through confined spaces. The study provides potential targets for future therapies.
Researchers propose a novel approach to cancer therapy by subtly hardening cancer cells to prevent metastasis. They've identified a compound, 4-HAP, that shows promise in fighting pancreatic cancer.
Researchers discovered that Twist1, a developmental regulator, primes cells for stem-cell-like properties when activated transiently. This leads to cellular plasticity and regenerative potential. Conversely, chronic Twist1 activity promotes invasive, non-proliferative phenotypes in tumor cells.
A study led by St. Jude Children's Research Hospital scientists has identified the population of white blood cells that tumors use to enhance growth and suppress the disease-fighting immune system. Monocytes are primarily responsible for T cell suppression around tumors.
Researchers found a mutated region in human mantle cell lymphoma DNA that disables programmed cell death. Cells with this mutation grow uncontrollably, but a new therapy approach targets the ubiquitin ligase responsible for the defect.
Researchers at Centenary Institute used a super-resolution microscope to study the role of DPP9 in cell movement. They found that inhibiting this enzyme can slow down living cancer cells and prevent tumors from growing or spreading.
Researchers at the Buck Institute discovered that senescent cells secrete PDGF-AA, which accelerates wound closure and heals wounds normally. This finding suggests that cellular senescence may play a beneficial role in human health throughout the lifespan.
Researchers develop a new approach to customize nuclear medicine treatment for cancer, using targeted alpha therapy with customized radiolabeled antibody cocktails. This method has great potential for treating various diseases, including those with disseminated tumor cells.
Researchers at Dana-Farber Cancer Institute have discovered an effective treatment for small cell lung cancer using the compound THZ1, which targets tumor cells' basic survival machinery. Clinical trials are underway to test its safety and efficacy in human patients.
Geneticists identified double minutes in glioblastoma cells with specific oncogenes, which amplify malignancy and give cancer cells an adaptive edge. The presence of these mini-chromosomes is detected in most aggressive cancers.
Researchers found malignant mesothelioma tumors to be polyclonal, resulting from the growth of multiple mutant cells. This challenges the long-held belief that cancers are caused by a single cell mutation.
A new study identifies TET1 as a master regulator in cancer progression by silencing tumor suppressor genes. Adding TET1 back to cancer cells reactivates these genes, reducing abnormal proliferation.
A study by MD Anderson Cancer Center researchers found that the enzyme PKM2 controls cell division, promoting tumor cell proliferation. PKM2's role in regulating cytokinesis was also identified as crucial for brain tumor development and malignant tumor progression.
Scientists have developed a novel delivery platform that allows for the inhibition of microRNA activity, leading to controlled cancer growth. The breakthrough uses a peptide with low-pH induced transmembrane structure to target tumor cells, providing a promising new model for cancer therapeutics.
Researchers have discovered that tumor cells secrete exosomes containing proteins capable of transforming neighboring cells into tumor cells, promoting tumor growth. Dicer protein is identified as a key factor in this process and may serve as a biomarker or therapeutic target.
Researchers from Berkeley Lab have developed a new method to create immortal human mammary epithelial cells with normal genomes. This breakthrough could facilitate the examination of cell immortalization as it occurs in cancer development and potentially lead to new therapeutic approaches.
Researchers have successfully triggered the self-destruct process in lung cancer cells, paving the way for a new treatment approach that leaves healthy cells unharmed. The breakthrough was achieved using a combination of two drugs, TRAIL and a CDK9 inhibitor, which altered the molecular switches in the cell suicide process.
Researchers identified CD44 as a potential marker to select patients unresponsive to Sorafenib, a common liver cancer treatment. Patients with a less differentiated mesenchymal phenotype expressing CD44 tend to resist Sorafenib's action, highlighting the need for alternative therapies.
A personalized cellular therapy called CTL019 achieved complete remission in 27 of 30 patients with relapsed or refractory acute lymphoblastic leukemia, with 78% remaining alive six months post-treatment. The treatment involves infusing engineered immune cells that target cancer cells.
Researchers found that nuclear factor kappa B (NF-kB) enables cancer cells to evade the immune system by suppressing genes that inhibit the immune response. Inhibiting NF-kB may make tumor cells more vulnerable to elimination by the immune system.
Researchers have identified a class of chemical compounds that make cancer cells more sensitive to chemotherapeutic drugs. The compounds, referred to as T8, specifically target the protein disulfide isomerase enzyme and induce programmed cell death in rapidly dividing cancer cells.
A study found that postpartum mice develop metastatic disease due to dying tumor cells triggering anti-inflammatory cytokines that promote wound healing. Mice lacking a receptor for macrophage clearance of dying cells did not develop metastasis, highlighting potential targets for limiting postpartum breast cancer severity.