Articles tagged with Cancer Cells
A collaborative study between UNC and Duke scientists reveals that disruptions in protein signals can lead to improper mitochondrial distribution during cell division, resulting in reduced ATP levels. This finding has implications for diseases such as cancer and neurodegenerative disorders.
Researchers have discovered a compound that attacks cancer cells by depriving them of glucose, a process found in most rapidly dividing cells. The team tested the compound on kidney cancer cells and found it nearly halved glucose uptake and slowed tumor growth, with minimal side effects.
The UBC device allows scientists to analyze individual cells rapidly and cost-effectively, accelerating genetic research and cancer diagnosis. By analyzing isolated cells, researchers can distinguish between normal and cancer cells, leading to more accurate treatments.
Researchers at Ohio State University designed a nanocarrier that maximizes gene silencing by targeting equivalent highways for entry into cells. The carrier, called SPANosome, reduces protein production by 95% compared to traditional carriers.
Cancer researcher Peter Duesberg suggests that cancer is a form of speciation, where tumors are new species that operate independently and can grow without host control. This theory could lead to new insights into cancer growth and metastasis, as well as new approaches to therapy.
A research team led by Bradley Davidson discovered that specialized structures in sea squirt cells, called invadopodia, may help cancer cells evade elimination processes. In contrast to cancer cells, sea squirt cells use these structures to pick up chemical signals for development, not invasion.
Researchers at the University of Maryland School of Medicine have found a complex molecular relationship between ERK and CHK2 proteins, which could lead to new treatments for diffuse large B-cell lymphoma. The study showed that inhibiting both proteins simultaneously killed more cancer cells than treating them separately.
Researchers developed a new mouse model to test cancer drugs by simulating gene inhibition, preventing rapid cell division in cancer cells while leaving healthy cells unaffected. The study published in Nature Communications validates the preclinical relevance and predictive value of the inducible RNAi-based mouse model.
Researchers at Hebrew University identified the molecular basis for DNA breakage, a key feature of cancer development. The study sheds light on how DNA replication stress leads to breaks, providing new insights into cancer development and potential therapeutic approaches.
The LuCED test uses 3D imaging to accurately detect cancer cells in sputum samples from high-risk individuals. This approach can significantly lower the number of false positive cases, making mass screening programs more feasible and cost-effective.
Researchers at Johns Hopkins have identified two genes, ATRX and DAXX, that contribute to the lengthening of telomeres in cancer cells. The study found a correlation between mutations in these genes and alternative lengthening of telomeres in various types of tumors.
Researchers at Salk Institute find that a short segment of p53 regulates activity in blood-forming stem cells, affecting their survival and proliferation after DNA damage. The study suggests that targeting this regulatory mechanism with drugs could reduce unwanted tissue damage from chemotherapy or radiation treatment.
A new study by UCSF researchers reveals that complex mutations in genes like TP53 occur earlier in skin and ovarian cancers than previously thought. The findings could help doctors develop new diagnostics for early cancer detection.
Researchers at Columbia University developed a new technique to evaluate human stem cells using cell micropatterning, enabling the study of developmental processes and disease diagnosis. The technique reveals directional motion patterns in cells, which can distinguish between normal and pathological behaviors.
Research reveals that leftover embryonic cells found in all adults may be precursors of deadly esophageal cancers, including Barrett's esophagus. The study suggests targeting these precursor cells as a potential strategy for stopping the disease before it starts.
Researchers discovered that Barrett's esophagus, a precursor to esophageal cancer, arises from a small group of leftover embryonic cells present in all adults. This finding opens up new avenues for therapeutic intervention to prevent the progression of cancer. The study used mouse models and identified specific cell surface markers to ...
Researchers developed a novel approach to cancer therapy by creating a drug that inhibits the mobility of cancer-promoting proteins within cells. The treatment uses a 'glue' molecule that binds to these proteins, forcing them to the cell membrane and making cancer cells more vulnerable to chemotherapy.
Using Archimedes' principle, MIT scientists have devised a method to measure the density of individual cells, which could provide biophysical insight into fundamental cellular processes. The new device rapidly exchanges fluids, allowing for rapid measurement and potentially screening potential cancer drugs.
Researchers have found that ovarian cancer cells use brute force to invade surrounding tissues and organs. The study identified key proteins involved in this process, providing a potential target for future treatments.
A new study by NIH researchers reveals the interaction between telomeres and a toxic protein called progerin that triggers both premature aging syndrome and normal cellular aging. Shortened telomeres lead to increased production of progerin, causing cell damage and activation of programmed aging.
Researchers at the IRCM have made a significant breakthrough in understanding the Sonic Hedgehog protein's role in cancer development. The team found that specific receptors play a crucial role in transmitting signals from the protein, which could lead to new avenues for treating diseases such as cancer.
Scientists discovered that a single amino acid prevents perforin from killing host cells, protecting cytotoxic lymphocytes from destruction. The findings shed light on the immune system's ability to regulate cell death and disease.
Researchers at University of Western Ontario discovered how biochemical pathways can be rewired in cancer cells to resist apoptosis, a key process in normal cell turnover. This 'rewiring' allows cancer cells to ignore death signals and potentially evade therapy.
Researchers have discovered that cancer cells use specific chemokines to create a survival niche in the lymph nodes and spleen, allowing them to grow and develop. This niche is created by the interaction between cancer cells and stromal cells, which secrete increased quantities of chemokines CCL19/CCL21.
Cancer cells exploit a unique metabolic pathway fueled by sugar consumption to survive. Researchers identified HIF-1 as controlling gene expression in low-oxygen conditions, with PKM2 playing a crucial role in this process.
Researchers found that a specific section of the AKAP12 gene responds to retinoid treatment, reducing vascular cell growth. The study suggests that this gene could be a target for treating vascular diseases and potentially other cancers.
Researchers at Uppsala University have developed a new method to study signal systems in individual cells, revealing the molecular effect of drugs and facilitating the discovery of targeted pharmaceuticals for cancer treatment. This tool provides insight into how cancer cells communicate with normal cells and exploit their functions.
Researchers discovered a hyperactive Wnt signaling pathway in human sarcoma cells, which increases cell growth and proliferation by increasing CDC25A gene expression. This suggests that medications targeting the Wnt pathway may be effective in treating human sarcomas.
Scientists at Harvard School of Public Health discovered that cells exert forces on their neighbors, leading to a cooperative yet chaotic migration. The study found that collective cellular migration is not a smooth process, but rather an 'organized chaos' with pushing and pulling in all directions.
Researchers at UCSF have identified BCL6, a protein that leukemia cells use to survive treatment, as the basis for drug resistance. Targeting this protein may lead to more powerful cancer drugs and improved cure rates for children with leukemia.
Researchers discovered a link between cell rigidity and proteins associated with cancer activity, using innovative collaboration between physics and cell biology. Exerting mechanical force on cells activates Rho GEF proteins, leading to tumor growth and metastasis.
Researchers at Wake Forest Baptist Medical Center found a specific mutation in the FLT3 receptor makes cells resistant to standard chemotherapy treatment for acute myeloid leukemia (AML). The study suggests a need for personalized approaches in treatment and may lead to new therapeutic research.
A study suggests that evaluating gene expression changes in nasal cells can serve as a non-invasive approach for early detection of lung cancer. The researchers identified 170 genes that were differentially expressed between patients with and without lung cancer, including genes linked to colon cancer and tumor suppression.
Researchers at UT Southwestern Medical Center have discovered a protein that guides blood vessel development and may lead to a treatment to starve cancer cells of nutrients. The protein, Rasip1, is specific to blood vessels and essential for their formation, making it a potential target for blocking tumor growth.
Researchers at Hebrew University discovered that insufficient building blocks in cancer cells lead to DNA damage. External supply of DNA building blocks can reactivate normal DNA synthesis and reduce cancerous features.
Researchers discovered that lopinavir selectively kills HPV-infected non-cancerous cells while leaving healthy cells relatively unaffected. The study suggests a potential treatment for HPV-related cervical cancer using locally applied lopinavir cream or pessary.
Researchers have found that over-expression of motor protein km23-1 can block human ovarian tumor growth, leading to eventual cancer cell death. This discovery offers promise for new therapies to treat ovarian cancer, a disease affecting U.S. women with an estimated 21,880 new cases and 13,850 deaths in 2010.
Cancer cells survive by ignoring signals to become senescent and continuing to make copies of themselves at will. Researchers discovered a molecular switch required for entry into quiescence and senescence, which may provide new targets for cancer treatment and help develop neurons in infants with Down syndrome.
A study by Fred Hutchinson Cancer Center researchers reveals a signaling protein called Reelin helps brain cells navigate during development. This finding may hold clues to understanding how cancer cells migrate within the body.
Researchers at the Salk Institute have uncovered a new structural beacon, called the C-tail, which is found in half of all telomeres in alternative lengthening of telomeres (ALT) tumors. This unique feature may be a key to understanding cancer cell immortality and developing effective treatments.
Researchers discovered a worm protein controlling growth factor secretion, which is linked to human cancers. The study proposes that abnormal growth factor secretion may stimulate cancer formation and offers a potential targeted treatment approach.
Researchers have created nanoparticles that can store large amounts of drugs, allowing for a millionfold increase in efficiency over comparable methods. The 'protocells' can target specific cancer cells while restricting toxic chemotherapy drugs from leaking into the system, mitigating side effects.
Researchers at The Wistar Institute have identified a connection between Merlin and angiomotin, two proteins involved in cell signaling pathways. This discovery may lead to a new therapeutic approach for NF2 by targeting tumor cells directly and starving them of nutrients.
Researchers at UT Southwestern Medical Center found that Klotho, an anti-aging hormone, suppresses renal fibrosis and cancer growth in mice. This discovery offers a potential new treatment for patients with chronic kidney disease and acute kidney injury.
The TET1 enzyme controls gene activity during fetal development, preventing genes from being turned off at critical stages. By modifying methyl groups, TET1 acts as a safeguard to ensure normal cell growth and development.
Researchers study sea squirts' simple body structure to unravel complex mechanisms of heart formation, shedding light on GATA's role in congenital heart defects. Disrupting GATA function independently in the developing gut preserves heart cell identity, while disrupting it in heart precursor cells causes limbo-like state.
A Wayne State University study found that soy isoflavones can sensitize cancer cells to radiation while protecting normal tissue. The study demonstrated that soy isoflavones can block DNA repair mechanisms in cancer cells, leading to increased killing of lung cancer cells by radiation
Researchers unveiled groundbreaking cellular analysis tools, drug-delivery methods, and novel approaches to high-throughput drug discovery. The session highlighted advances in imaging and simultaneous identification of biological compounds, as well as the use of peptides as potential drugs and biological probes.
Scientists at the University of Hull have identified a cellular mechanism controlling tissue factor inclusion in endothelial microparticles, which may help treat cardiovascular disease and cancer. The on-off switch, involving tandem amino acids, regulates phosphate molecule addition to control tissue factor release.
Researchers from UPCI and Pitt will present over 80 posters, talks, and tutorials on various cancer studies, including the effects of immunomodulatory derivatives on blood cell production pathways and the role of inflammatory mediators in immune system dysfunction. Additionally, they will discuss the development of vaccines targeting p...
A new study finds that vismodegib, a hedgehog pathway inhibitor, prevents the development of advanced basal cell carcinomas in patients with basal cell nevus syndrome. The treatment also shows promise for patients with an inherited predisposition to basal cell carcinoma.
Cancer cells that reign during leukemia relapses have distinct DNA profiles compared to those at diagnosis. These mutated cells exhibit aggressive behavior in mice, suggesting a possible link between human and mouse models.
A new hedgehog pathway inhibitor, GDC-0449, demonstrated efficacy in preventing and treating basal cell cancer among patients with basal cell nevus syndrome. The drug reduced the development of new lesions and decreased tumor size, offering a promising treatment option for these patients.
Forced splicing of p21Cip1 gene leads to its down-regulation and induction of programmed cell death in cancer cells. This finding suggests new approaches to enhance chemotherapeutic drug efficacy by inhibiting splicing.
PBS-Bio presents two abstracts at the AACR conference, showing how drugs UNBS1450 and NDC-1308 affect cancer cells. The technology allows real-time measurement of cellular responses to drugs, identifying potential biomarkers for patient selection and drug development.
A recent study published in the Journal of Thoracic Oncology found that soy isoflavones can sensitize cancer cells to radiation, increasing killing efficiency while protecting normal lung tissue from damage. Researchers used a soy mixture consisting of genistein, daidzein and glycitein to demonstrate this effect.
Researchers at Dana-Farber Cancer Institute have developed a targeted therapy strategy that slows the progression of NUT midline carcinoma in children. The approach uses an HDAC inhibitor to distract cancer proteins from their usual activity, causing cells to behave like normal cells.
A study identified three critical steps to transform normal blood cells into leukaemic ones, each subverting a different cellular process. The researchers found that NPM1 mutation is a key event in acute myeloid leukaemia development and can cooperate with other mutations to cause the disease.
Researchers at LSU Health Sciences Center have identified a protein called c-MYC oncoprotein that enables cancer cells to resist DNA-damaging agents like cisplatin. The study suggests that inhibiting this protein may provide a novel strategy for cancer therapy in combination with DNA-damaging agents.
Researchers created a computational model that describes how intestinal cells in mice respond to TNF, revealing the importance of location and protein interactions in cell fate. The study demonstrates the power of systems biology in modeling complex biological systems and predicting disease outcomes.