Articles tagged with Cancer Cells
Researchers at the University of Pennsylvania School of Medicine have demonstrated that injured pancreatic cells readily regenerate back into healthy acinar cells. This finding holds promise for treating cancer and inflammation of the pancreas, while shifting focus from regenerating insulin-producing beta cells.
A recent study found that reducing calorie intake later in life can induce health and longevity benefits similar to lifelong calorie reduction. The researchers discovered that certain drugs mimic this effect, which may lead to the development of new
Scientists discovered a protein that enables cells to bypass damaged DNA during replication, averting cell suicide. However, this protein also makes errors that may contribute to the development of cancer.
A new procedure, anal cytology, detected abnormal cell changes in 244 HIV-positive patients, leading to subsequent biopsy confirmations. Abnormal results prompt further investigation and management.
Scientists at Dana-Farber Cancer Institute mapped the structures of small molecules and mutated protein receptors in non-small cell lung cancer cells. They found that two inhibitors bind more tightly to specific mutations, potentially leading to more effective treatments.
A study published in Cancer Cell reveals that a specific sequence of genetic mutations determines the behavior of cystic pancreatic cancer, which has a 50% long-term survival rate. The research found that cells with this mutation are resistant to TGFb's tumor-promoting properties, contributing to their improved survival.
Researchers found that vitamin A derivative ATRA increases levels of miRNA-15b and miRNA-16-1, which inhibit Bcl-2 gene activity. This helps explain how the drug works by regulating genes that need to be silenced for cell differentiation.
Researchers identified 50 genes that interfere with genetic activities of genes causing uncontrolled cell division. These genes work by producing proteins that directly attach to cell-division genes, hindering their activity.
Research by Cold Spring Harbor Laboratory finds that harmless viruses can cause cancer through chromosomal instability, potentially leading to cancer progression. Protecting against these viruses may decrease cancer incidence.
Researchers used a microfluidic chip to study the mating habits of yeast cells, revealing that a second MAPK plays a crucial role in the process. The findings shed new light on how cells send and receive signals from one another and from their environment.
Researchers identified a new route to cancer treatment by exploiting mutations that control cell movement. Understanding the collaboration between Ras and p53 genes may lead to novel therapeutic targets like Rho proteins.
Robert C. von Borstel presents cancer as an invasive process similar to species evolution, with mutations and selection driving its progression. He hopes his work will help people re-examine cancer in a new light.
Researchers at TRIUMF are developing custom radioisotopes to target cancer cells more efficiently. They aim to create tailor-made treatment programs for each patient, reducing radiation doses and treatment sessions.
Researchers have found a way to deliver a messenger into cancer cells that forces them to respond to death signals using an HIV protein. This approach has shown promise in killing cancer cells and could provide new treatment options for patients with deadly cancers.
A new study finds that p38-alpha MAPK inhibits tumor formation by sensing oxidative stress and triggering apoptosis. Cancer cells may evade this mechanism by desensitizing p38-alpha to ROS, highlighting potential therapeutic targets for cancer treatment.
A new medical technique using microsecond electrical pulses has been shown to create permanent nanoscale holes in target cell membranes without harming surrounding tissue. This technique, called irreversible electroporation (IRE), has the potential to revolutionize minimally invasive surgical treatments for tumors.
Purdue University researchers use dendrimers to label specific proteins in living cells, allowing them to determine protein functions and diagnose diseases. This new method provides a more reliable alternative to existing methods, which require small sample amounts and damage the natural environment.
Researchers developed a small-molecule inhibitor of Plk1, a key kinase controlling cell division. The compound BI 2536 effectively halts cancerous cell growth in culture and in animal models, causing cell death and tumor regression. This discovery has therapeutic potential for patients with locally advanced or metastatic cancers.
Researchers at Oncolytics Biotech have developed a harmless virus that not only kills tumor cells but also primes the immune system to mount a powerful defense against cancer. Studies have shown that reovirus exposure can activate dendritic cells, which then educate natural killer cells and T cells to attack the tumor.
Researchers at Brown University have identified GABP as a critical transcription factor that restarts cell division, a process fundamental to development, renewal, and cancer growth. Disrupting GABP may lead to new cancer treatments.
Scientists have linked telomere loss to both cancer and aging by visualizing chromosomes of cells from patients with Werner Syndrome. Rebuilding structures called telomeres significantly blocks genetic damage seen in cells of patients with Werner Syndrome.
Researchers discovered that ceramide helps stem cells organize into primitive ectoderm, which further differentiates into embryo tissues. The lipid's presence is essential for cell polarity and differentiation.
Researchers at University of California, San Diego found a molecular link between chronic inflammation and cancer development. The protein p100 enables communication between inflammatory response and normal cell growth, but excessive levels may overactivate developmental pathways, leading to cancer.
A new strategy for fighting cancer aims to make its genes get lost in translation, silencing oncogenes by targeting weak messenger RNAs. The researchers discovered a small molecule that effectively inhibits the translation of these weak mRNAs, leading to the decline of cancer-promoting proteins.
A new test developed by Dana-Farber Cancer Institute scientists identifies malignant blood cells that are highly vulnerable to an experimental cancer drug. The drug works by neutralizing the Bcl-2 action, unleashing molecules that trigger suicide in the cancer cells.
Researchers have made a breakthrough in molecular technology that could help deliver life-saving drugs directly to cancer-ridden cells. The discovery involves attaching therapeutic drugs to molecules using tiny molecules that can travel through the bloodstream.
Researchers at Rice University have developed a novel way to deliver drugs directly into cancer cells using buckyball nanoparticles as passkeys. The technique, which mimics viral proteins, shows promise in penetrating the defenses of liver and neuroblastoma cancer cells, two types often difficult to treat.
Researchers found that the p53 gene's ability to direct a damaged cell to stop growing or commit suicide depends on turning on separate groups of target genes. Alterations in an amino acid, lysine 120, can influence this decision, potentially leading to new strategies in chemotherapy drug development.
Researchers at Johns Hopkins University have developed a hybrid molecule that combines a sugar with a short-chain fatty acid to kill cancer cells in lab tests. The molecule triggers cellular suicide and orchestrates the expression of genes responsible for halting uncontrolled growth.
The study found that AVN944 significantly inhibited the IMPDH enzyme and induced biomarkers associated with cancer cell death. The gene HspA1A marker was elevated even at low doses of the drug, indicating potential for tumor cell apoptosis.
Scientists discovered that higher body mass, not lifespan, increases the risk of cancer due to telomerase expression. Rodents from various species showed a correlation between body size and telomerase activity, while human's don't express it in somatic cells, suggesting evolution prioritized cancer prevention over healing.
A new technology allows users to record and store massive amounts of data onto a single disc, such as the Smithsonian National Air and Space Museum's entire collection or 500 movies, maintaining excellent quality without damage. The UCF team's Two-Photon 3-D Optical Data Storage system uses lasers to compact information onto a DVD.
Researchers at Children's Hospital Oakland Research Institute identified a specific enzyme called sphingosine phosphate lyase (SPL) that can cause the death of cancer cells. The study found that SPL makes cancer cells more vulnerable to chemotherapy, while removing the enzyme makes the cells more resistant to treatment.
Researchers at the Salk Institute reveal how cellular repair proteins recruit a second machinery to create a protective structure at chromosome ends, maintaining chromosomal stability. Telomeres exist to prevent damage and ensure cell division integrity.
Researchers suggest repairing abnormal blood vessels in retinopathy using adult bone marrow–derived myeloid progenitor cells. Dendritic cells form part of granuloma walls containing Listeria monocytogenes, maintaining integrity through immunosuppressive protein IDO.
ABT-737, a BH3 mimetic, targets Bcl-2 proteins to induce apoptosis in cancer cells. The treatment has shown effectiveness against acute myeloid leukemia (AML) cells and can be combined with MCL-1 inhibitors for improved results.
The ACE experiment found that antiprotons are four times more effective at terminating live cells than protons, with the potential to reduce damage to healthy tissue. Researchers plan further tests to assess the effectiveness of antiprotons for cancer therapy and ensure minimal harm to surrounding tissues.
Researchers found that white blood cells in cancer-resistant mice can sense and kill cancer cells through a multi-step process, involving migration, recognition, and physical contact. The discovery suggests that some cancers may share common characteristics that make them vulnerable to this type of immune response.
Researchers at Max Planck Institute for Molecular Genetics in Berlin have explained the molecular principles of cell division control mechanisms. The study found that checkpoint kinases interact with a different category of proteins involved in developing the cell division spindle.
Researchers at the University of Manchester have made a breakthrough in developing a new class of cancer drugs that target the Aurora B enzyme, which helps cells divide and can lead to uncontrolled cell growth in cancer. Early clinical trials suggest the drug's toxicity is mild, offering a revolutionary new way to treat cancer.
A team of researchers identified a protein, Lck, that plays a crucial role in stimulating immune cells to recall past encounters with pathogens, enabling quick responses to reinfection. This discovery may aid in the development of vaccines against diseases like AIDS and autoimmune disorders.
A study found that grape seed extract significantly inhibits the growth of colorectal tumors in both human cells and mice. The extract works by increasing the availability of a critical protein called Cip1/p21, which freezes the cell cycle and often pushes cancer cells to self-destruct.
Researchers at VCU University have identified a new therapeutic target for asthma, allergies, and cancer by uncovering the transport mechanism of bioactive molecule S1P out of mast cells. The study may lead to the development of new treatments for these conditions.
Cells use a molecular signature to distinguish their own RNA from viral RNA, triggering an immune response and cell suicide. This discovery opens up new possibilities for therapy, including using triphosphate-end RNAs to trigger anti-viral responses and gene therapy.
Researchers at Mayo Clinic have discovered a protein pair that could be used to prevent tumors. The study found that CDK2 modifies FOXO1 in damaged cells, triggering apoptosis and potentially halting cancer cell growth. This breakthrough provides new hope for the development of targeted anti-tumor therapies.
A new technique called multi-isotope imaging mass spectrometry (MIMS) allows researchers to image and quantify molecules at a subcellular level. This enables the tracking of individual donor cells after transplantation and the measurement of cancer treatment drug efficacy within cells.
Researchers at the University of Illinois Chicago have identified an antibiotic that specifically targets the FoxM1 gene, which is responsible for cancer cell proliferation. The antibiotic, siomycin A, was found to induce cancer cells to commit suicide in a process called apoptosis, with no effect on normal cells.
Researchers have unveiled a new systematic approach to drug discovery that matches diseases with potential treatments using gene signatures. The 'Human Connectivity Map' allows scientists to compare disease signatures with those of treated cells, identifying effective treatments for cancer, obesity and Alzheimer's disease.
The University of Virginia School of Medicine has received a $35.7 million grant renewal from the National Institute of General Medical Sciences to continue its Cell Migration Consortium research. The consortium, comprising nearly 40 researchers globally, aims to understand cell migration and its role in diseases like cancer.
Researchers at Mayo Clinic found that the protein p120 catenin can both suppress and promote metastasis, depending on its interaction with cadherin proteins. The study suggests that a future designer drug could block the beginning of metastasis or stop it once it starts.
Researchers at The Wistar Institute have determined the three-dimensional structure of a key two-molecule complex involved in long-term gene storage, primarily in non-growing cells. This discovery provides important insights into how cells protect genes that could trigger cancers and other disorders.
Newly discovered behavior in cancer cells reveals a toggle switch that enables them to morph into highly mobile cells, invade other tissues, and adapt comfortably. This understanding could lead to finding ways to stop metastasis, the most deadly trait of cancer.
Researchers discovered that viruses can infect cells more efficiently by attaching to different carbohydrates on the cell surface. This finding helps explain how flu and other viruses evade the immune system and may be useful for developing gene therapies for cancer and brain diseases.
Researchers successfully exploited oxidative stress in cancer cells to preferentially kill malignant cells while exhibiting minimal toxicity in normal cells. The study found that a naturally occurring compound called PEITC can be used to achieve such activity.
Researchers at Salk Institute discover that cancer cells use NF-kB survival factor to stay alive when attacked by chemotherapeutic drugs. This finding suggests a strategy to enhance the effectiveness of rapamycin-based therapies by inhibiting NF-kB signaling.
A Purdue University researcher has shed light on the details of one mechanism by which targeted drug therapy is achieved. The understanding of how to deliver and unload a cancer drug can be extrapolated to other diseased cells, including those involved in arthritis, multiple sclerosis, and Crohn's disease.
Scientists have found a way to get purine nucleoside phosphorylase (PNP) into the cells of mice lacking the enzyme, which could lead to a treatment for individuals with PNP deficiency. The PTD-PNP fusion protein corrected most immune defects in Pnp-deficient mice.
Researchers at the University of Illinois Chicago discovered a molecular motor that helps cells determine which way is up by transporting a key lipid. This process is essential for maintaining cell polarity and preventing cancerous metastasis. The study sheds light on the trafficking and disposition of polarity determinants.
Researchers identify small synthetic molecule PAC-1 that directly activates procaspase-3 and induces apoptosis in cancer cells. This discovery offers a promising approach for personalized anti-cancer therapy by bypassing the broken signaling pathway in cancer cells.
Human cells exposed to high-energy protons and then iron or titanium particles showed a significant increase in anchorage-independent growth, a characteristic of early cancer development. The timing of the particle exposure was critical, with cells responding more strongly when hit by protons first.