Research on the cell biology of tumors. Covers cancer-cell vulnerabilities, tumor spread, nanoreactor therapies, and AI-guided cancer research.
Researchers found that ovarian cancer cells colonize milky spots in the omentum, which promotes cell growth and spread. The study suggests an alternative model of omental colonization, where both milky spots and fat cells play a role in attracting cancer cells.
A LSUHSC researcher has been awarded a five-year, $1.5 million NCI grant to investigate the connection between chronic inflammation and cancer development. The project aims to understand how p53 dysfunction in normal cells surrounding cancer cells can lead to an inflammatory microenvironment that supports tumor growth.
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.
A study by Weill Cornell Medicine found that even healthy-looking smokers have damaged airway cells with characteristics similar to those in aggressive lung cancer. The researchers discovered that these cells express human embryonic stem cell genes, which are normally only active in developing embryos.
Researchers have discovered a way to kill cancer cells by blocking a specific protein that enables them to survive nutrient starvation. This breakthrough could lead to a more targeted and effective treatment for various types of cancer.
Researchers have gained groundbreaking knowledge about proteases, enzymes that play a role in cancer cell development. The study reveals that proteases can bind to each other instead of just cleaving, which may lead to the development of new anticancer drugs.
A team of scientists at the Salk Institute for Biological Studies has identified a critical pathway in cell cycle control that, when disrupted, leads to cancer cell proliferation. Shortened telomeres, which occur with cellular aging, activate a DNA damage response that arrests cell growth.
Researchers have developed a new method for identifying cell of origin of proteins in multicellular environments, enabling comprehensive mapping of cell-cell communication. This technique, CTAP, exploits amino acid biosynthesis and stable isotope labeling to link proteins directly to specific cell types.
Researchers at UTMB found that colon cancer cells produce large amounts of hydrogen sulfide, which they use to make energy and grow. Blocking the production of this compound, CBS, was shown to curb tumor growth in mice.
Scientists have successfully targeted a malfunctioning immune system enzyme to eliminate diseased cells from patients with myelodysplastic syndrome (MDS), a blood disorder and precursor to leukemia. The research provides a molecular target for designing new drugs, offering a promising treatment option.
Researchers identify unique properties of K11-linked polyubiquitin chains, suggesting new cellular processes involved in disease maintenance. These findings may lead to novel treatments for diseases like cancer and diabetes.
Cancer originates from a default genetic 'safe mode', where cells revert to an ancient programming, leading to uncontrolled proliferation. The theory suggests that cancer-causing genes are reactivated in adulthood due to triggers like chemicals or radiation, adding weight to the radical new idea.
Researchers at the Buck Institute manipulated a signaling pathway implicated in Barrett's esophagus, suggesting a change in stem cell function as the cause of this transformation. This discovery may lead to new targets for therapies and inform the development of more effective treatments for Barrett's esophagus.
Researchers discovered that forced telomere elongation promotes cancer cell differentiation, suppressing genes involved in tumor malignancy. Telomeres may modulate cell behavior by controlling gene expression, potentially leading to new cancer treatments.
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 at MIT have discovered a mechanism that allows cells to read their own DNA in the correct direction and prevents most of the so-called 'junk DNA' from copying into RNA. This process helps explain the existence of many recently discovered types of short strands of RNA whose function is unknown.
Researchers at Harvard School of Public Health discovered that cells move in a group, propelled by forces from within and nearby cells, to fill spaces. This phenomenon, dubbed 'kenotaxis,' could improve understanding of disease mechanisms and inform potential drug targets.
Researchers at Scripps Research Institute receive $1.4 million from the National Cancer Institute to create a potential new drug targeting malignant cells in CLL, while sparing normal tissues. The study aims to deliver cytotoxic drugs with specific targeting using cell surface receptor TOSO and receptor tyrosine kinase ROR1.
Researchers at UT Dallas discovered that lung cancer cells consume more oxygen and synthesize a critical chemical called heme, which can be exploited to inhibit cancer growth. Inhibiting heme synthesis affects lung cancer cells' ability to proliferate and migrate.
A study by UCSD researchers reveals that MCL-1 promotes normal heart function, but its absence leads to rapid heart failure and cell death. The protein's role in cancer treatment and potential cardiac toxicity are also explored.
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.
Researchers used advanced mathematical modelling to devise strategies for making cancer cells exquisitely sensitive to virus infection, killing them without affecting normal cells. The models were remarkably accurate, predicting experimental outcomes in a mouse model of the disease and creating a useful framework for further research.
Researchers at Uni Basel have discovered Sox4 as a key player in cancer metastasis, triggering the epithelial-mesenchymal transition (EMT) process. The study found that Sox4 promotes the expression of genes involved in EMT and metastasis, leading to changes in gene expression and cell behavior.
Researchers at the University of Copenhagen have discovered a new way cells communicate with each other using antennae-like structures called primary cilia. This breakthrough sheds light on the causes of debilitating diseases such as heart defects and birth defects, highlighting the importance of TGFβ signalling in fetal development.
Researchers at UCLA have isolated a new population of pluripotent stem cells, called Multi-lineage Stress-Enduring (Muse-AT) cells, from fat tissue that can differentiate into virtually every cell type in the human body. These cells are stress-resistant and may even be activated by severe stress, making them potentially superior source...
Researchers at the University of California, San Diego School of Medicine discovered a novel mechanism that suppresses tumor growth by stabilizing heterochromatin, a form of chromosomal DNA. This finding suggests a potential new approach to inhibit cancer gene expression and may represent a new class of tumor suppressors.
Researchers have captured the first three-dimensional crystalline snapshot of the initial step in actin filament formation, crucial for understanding cell shape and cancer. The study's dual-mutant approach helped overcome challenges in forming crystals, revealing critical contacts involved in nucleation.
Researchers at Monash University have identified a sub-group of cells that can contribute to prostate cancer recurrence, opening up new treatment options. These previously unidentified cells are potential targets for future therapies and may be targeted before the cancer reaches an incurable stage.
Researchers developed a novel approach to make ovarian cancer cells susceptible to an antitumor drug, potentially improving treatment outcomes. The strategy targets telomeres and shows promise in treating other epithelial cancers.
Researchers have identified two ruthenium-based complexes that target cancer cells more effectively and are less toxic than current chemotherapies. The complexes, which seem to target cells in hypoxic states, could complement widely used platinum-based therapies like cisplatin.
Researchers at the University of Montreal have discovered how rapamycin prevents cells from dividing, potentially slowing cancer progression and other diseases of abnormal growth. The study reveals that TOR sends a signal to shut down B cyclin production through an intermediary protein.
Researchers at LMU discover how cellular respiration generates reactive oxygen species that can cause DNA mutations, leading to cell dysfunction and cancer. The study highlights the importance of improving treatment options for cancer by inhibiting DNA repair processes in tumor cells.
Researchers successfully targeted doxorubicin to mitochondria, killing cancer cells even those with developed pumps. The study suggests this approach could work with other nucleus-targeting anti-cancer drugs.
Mayo Clinic researchers found that positively charged gold nanoparticles can be effective against ovarian cancer cells when their cellular stress is increased. This is achieved by inhibiting calcium uptake into the mitochondria, which helps to make the nanoparticles more effective in destroying cancer cells.
Scientists discovered that a molecule called BRD4 recognizes a specific amino acid on NF-kappa B and activates it, preventing its degradation in cancer cells. This interaction is critical in the development of cancer, and blocking it may lead to new cancer treatments.
A new computational method called viSNE enables scientists to analyze high-dimensional cancer data, revealing distinct cell subpopulations and detecting minimal residual disease. This breakthrough technology has the potential to improve cancer diagnosis and treatment.
Researchers at Memorial Sloan-Kettering Cancer Center have discovered that expression of TRAIL in transplanted hematopoietic stem cells is critical for an effective anti-tumor response. This finding has led to the development of new therapeutic strategies to suppress graft-versus-host disease while maintaining anti-tumor activity.
Researchers at MIT have identified ALKBH7 as a key protein involved in programmed necrosis, a cell death pathway that can help prevent cancer cells from surviving DNA damage. By mimicking the effects of this protein, drugs may be able to induce necrosis in resistant cancer cells, providing a new potential target for cancer treatment.
A team of researchers at NYU School of Medicine has made a breakthrough in understanding how pancreatic tumor cells feed themselves. By identifying the role of macropinocytosis in delivering nutrients to Ras-transformed cancer cells, they have uncovered a potential new target for treating this lethal disease.
A new study reveals distinct characteristics between inducible and natural IL17-producing T cells, with different signals required for cytokine production. The findings suggest a specific role of Akt protein complex in regulating cytokine production by these cell types.
A University of Colorado Boulder study suggests that a tumor suppressor gene helps cells fend off stress and survive under starvation conditions. The research found that the Rb gene regulates the expression of multiple genes to help organisms survive longer when encountering starvation.
Researchers at Walter and Eliza Hall Institute discover that p53 protein can prevent cancer formation even without regulating cell death or division after DNA damage. The study sheds new light on the complex functions of p53, which was previously believed to have a straightforward role in preventing cancer.
Researchers found that the egg genome is reprogrammed to match sperm DNA with or without paternal contribution. The mother's genes undergo extensive changes to prepare for differentiation.
Researchers at Stanford University School of Medicine developed a new technique to visualize cell interactions in living mice, pinpointing metastatic cancer cells' locations after breaking off from initial tumor sites. The method uses light-emitting proteins and has potential applications in studying various cell interactions.
Researchers developed powerful data-sifting algorithms to assemble the most complete genetic profile of acute myeloid leukemia, an aggressive form of blood cancer. The work aims to lead to new AML treatments based on the genetics of each patient's disease.
Researchers found that a combination of chemoradiation therapy and surgery improves overall survival in stage 3 non-small cell lung cancer patients. Five-year survival rates were twice as high for those who received chemoradiation followed by surgery compared to those who only had chemoradiation.
Researchers at Karolinska Institutet have obtained detailed images of how the transport protein GLUT transports sugars into cells. The study's findings could lead to new strategies to fight cancer cells by blocking fuel pumps that introduce sugars and other nutrients required for cell metabolism.
Researchers at Mount Sinai identified new targets for abnormal cell division, finding that blocking CDK7 can inhibit the activity of other critical enzymes CDK4 and CDK6. This discovery suggests turning off these enzymes may be an effective therapeutic target for preventing cancer cell proliferation.
CNIO researchers have successfully mapped the proteins involved in human DNA replication, a process targeted by many chemotherapeutic agents. The study provides new insights into the mechanisms underlying cancer cell division and holds promise for developing new therapeutic strategies.
Researchers used high-quality video imaging to investigate why a particular cancer drug is effective at killing cells. The study found that the drug creates a cluster of protein molecules on one side of the cell, making it easier for natural killer cells to kill it.
A Northwestern University study has developed a pioneering biophotonics technology to detect ovarian cancer by analyzing cells from the cervix or uterus. The partial wave spectroscopic microscopy technique shows diagnostic changes in these cells even when they appear normal under a microscope, offering a potential breakthrough in early...
Scientists have developed a new chemical compound, WEHI-539, that inhibits BCL-XL protein in cancer cells. This could lead to the design of potential anti-cancer agents that restore cell death and improve treatment outcomes for patients with various types of cancer.
Researchers have discovered that protein machines that copy DNA pause frequently during the process, creating potential for dangerous mutations. Efficient repair of these breakdowns is crucial to prevent corruption of the genetic code.
Scientists at NIH and Pitt School of Medicine discovered a method to grow large numbers of stem cells by blocking CD47 membrane protein, increasing expression of four genes essential for iPS cell formation and allowing directed differentiation into various tissue types.
Researchers at the University of Helsinki discovered that the Myc oncoprotein makes cancer cells vulnerable to cell death by activating AMPK, a biochemical sensor. This leads to the activation of tumor suppressor protein p53, which promotes apoptosis in cancer cells.
Scientists have developed GUMBOS-based materials with targeted properties for medical use, such as selectively toxic to cancer cells and non-toxic to normal cells. The technology also has potential uses in solar cells and biomedical imaging.
The Myc oncogene can disrupt the 24-hour internal rhythm in cancer cells, suggesting potential for improved cancer treatments. By promoting the expression of Rev-erbα and NAMPT, Myc upregulates genes that suppress circadian oscillations, leading to altered metabolism and potentially increased replication rates in cancer cells.
New research reveals chemotherapy activates the body's immune system to target and destroy cancer cells. The treatment converts dying tumors into therapeutic vaccines, boosting the host's immune response against cancer.
Researchers envision cell-based therapeutics as a promising approach to treat critical diseases. Cells can adapt and respond better than small-molecule drugs, offering a more predictable treatment option.
A new form of radiation therapy, BNCT, has been developed by University of Missouri researchers, putting cancer into remission in mice without harmful side effects. The technique targets cancer cells by delivering boron chemicals that shatter and destroy cancer cells from the inside out.