Articles tagged with Tumor Cells
A new study shows that tumor blood vessels develop from precancerous stem cells, a type of cell that can become malignant. The findings suggest that screening anti-angiogenic drugs should include these cells to improve their effectiveness in blocking tumor growth.
Scientists discovered that metastatic pancreatic cancer cells produce enough of the protein IDO to evade detection by the immune system, allowing them to spread in the body. This finding may lead to new ways to detect pancreatic cancer spreading to lymph nodes and enhance tumor immune therapy strategies.
Immune cells can detect prostate cancer using a specific receptor on T cells, which recognizes the cancerous tumor. The molecular signpost is histone H4, a protein found in all cells but displayed only on the surface of tumor cells.
Researchers studied yeast cells to understand actin network regulation, which is crucial for cell movement. The study found that Arp2/3 regulatory proteins have distinct roles in actin assembly and endocytosis, shedding light on the immune system's ability to target disease-causing invaders and cancer cells' migration.
Researchers developed a novel approach to gauge disease progress in adult T-cell lymphoma and leukemia, using firefly genes to detect cancer cells. The study found that combining PS-341 and zoledronic acid effectively killed 95% of ATLL cells, while also reducing bone resorption and calcium buildup.
Researchers designed a technique that uses the body's own cells and a virus to destroy cancer cells, which could lead to a new cancer vaccine. The study shows promising results in treating melanoma, lung cancer, and colorectal cancer by targeting tumor cells in the lymph nodes.
Researchers at CSHL have identified and repressed breast cancer stem cells in mouse tissue by manipulating microRNAs, suggesting a potential therapeutic target for breast cancer treatment. The study found that the delivery of the microRNA let-7 to breast-tissue cells can help distinguish stem-like tumor-initiating cells from other cells.
Researchers found that bortezomib selectively inhibits melanoma tumor cells by overactivating the cancer-promoting gene c-MYC, leading to increased production of NOXA and promoting cell death. The study suggests a novel treatment strategy for various types of cancer.
Researchers at Ohio State University have found that stress hormone norepinephrine promotes tumor cell growth and metastasis in certain types of blood cancer. The study suggests that blocking norepinephrine receptors may slow disease progression and improve treatment outcomes.
New compounds that target Inhibitor-of-Apoptosis (IAP) proteins have been shown to induce apoptosis in tumor cells. The IAP antagonists block the anti-death proteins and engage other players that lead to cell death, with little effect on healthy cells.
Scientists at Washington University School of Medicine have identified an enzyme called MOF that is essential for tumor development and growth. By manipulating MOF in tumor cells, researchers hope to make them more sensitive to radiation therapy, which could lead to improved cancer treatment outcomes.
GSK923295A, a first-in-class targeted therapy, demonstrates broad activity and potential for enhanced tolerability in preclinical studies. The experimental drug inhibits the mitotic kinesin CENP-E, leading to apoptosis and misaligned chromosomes in cancer cells.
Researchers at UMass Medical School have identified a new pathway for cancer cell growth and survival, providing a blueprint for the design of novel anticancer agents. The study found that targeting the Hsp90 chaperone in the mitochondria can induce massive tumor cell death while sparing normal cells.
Scientists have created a method to target and destroy tumor cells by attaching folate to gold nanorods, which then burst through the membrane upon near-infrared light exposure. This triggers a complex biochemical mechanism leading to cell death.
Researchers found that certain existing drugs can target and inhibit the growth of brain tumors by modifying key signaling molecules. The study suggests that these drugs may be repurposed for treatment of brain tumors.
Scientists at Johns Hopkins Medicine have developed a novel way to fight colorectal cancer using tiny molecules to deliver potent radiation inside cancer cells. The new system proved able to specifically target colon cancer cells, reducing unwanted side effects.
Scientists identify EphB2 and EphB3 receptors as key players in limiting tumor cell growth to confined compartments. This mechanism prevents tumors from invading other tissue areas.
Researchers found that a heat-shock response mechanism helps cancer cells survive and thrive, but inhibiting this process may lead to a new cancer treatment. The discovery also sheds light on the complex relationship between aging, longevity, and cancer risk.
Researchers have developed a customized virus, Delta-24-RGD, that targets and eliminates brain tumor stem cells. In lab experiments and human brain cancer in mice, the virus shows promise in killing glioblastoma multiforme tumors, which are resistant to radiation and chemotherapy.
Researchers at Purdue University have developed a new technology that detects cancer cells in the bloodstream by scanning surface veins. This non-invasive method allows for earlier diagnosis and more accurate monitoring of disease progression, enabling personalized treatment.
A novel 3D cell culture model has been developed to study the selective uptake of nanoparticles in brain tumors. The model uses a combination of tumor aggregates and normal brain tissue slices, allowing researchers to investigate tumor cell invasion into brain tissue.
Researchers have created cancer stem cells in a Petri dish from human breast tissue, which can initiate tumors and metastasize. The new study provides clues about the trajectory of cancer cells and offers a boon to researchers studying these elusive cells.
Researchers at Duke University found that high-intensity focused ultrasound can activate the immune system to attack cancer cells, including those that have spread through the bloodstream. The treatment uses mechanical vibration to break apart tumor cells, releasing toxic substances that alert the immune system to cancer threats.
A study in mice shows that switching off a single malfunctioning gene can halt the growth of tumor cells and turn them back to their normal life cycle. The researchers found that cancer cells retained the ability to undergo senescence, a natural mechanism that causes cells to die when they become old or dysfunctional.
Scientists have discovered that cancer cells eliminate the enzyme protein kinase G (PKG), leading to uncontrolled cell proliferation. Reintroducing PKG into cancer cells has been shown to inhibit tumor growth and angiogenesis, suggesting a potential new avenue for targeted cancer treatment.
Researchers developed a new treatment for liver cancer using a monoclonal antibody targeting PDGFRá. The antibody significantly reduced tumor cell proliferation and increased programmed cell death in human and mouse liver cancer cell lines.
Researchers at Virginia Tech and UC Berkeley developed irreversible electroporation (IRE) to target cancer cells, successfully abling tissue in rat livers. IRE preserves vessel architecture and kills cells with minimal damage to surrounding healthy tissue.
Researchers have identified a synthetic version of a frog-derived molecule that could provide a new treatment option for brain tumors. The molecule, known as Amphinase, targets the sugary coating on tumor cells and inactivates RNA within them, causing the tumor to die.
Researchers at the University of Chicago discovered a new genetic marker called let-7, which appears to define different stages of cancer. The study found that high levels of let-7 expression are associated with less aggressive cancer, while low levels are linked to poor prognosis.
Researchers at UT Southwestern Medical Center have discovered how the compound beta-lapachone kills certain cancer cells, leading to a new paradigm for treating non-small cell lung cancer. Beta-lapachone interacts with an enzyme called NQO1, present in high levels in non-small cell lung cancer and other solid tumors.
A breast cancer cell line has been found to behave like cancer stem cells, allowing researchers to study the dynamics of cancer stem cells in tissue. This breakthrough could lead to targeted treatments for breast cancer by specifically targeting cancer stem cells for destruction while leaving normal stem cells intact.
Researchers at EPFL discovered how tumor cells exploit slow fluid flow in the lymphatic system to migrate to functional vessels. The study highlights the importance of biophysical environment and continuous slow flow in tumor cell migration.
Researchers have found that a combination of radiation treatment and angiogenesis inhibitors can overcome tumor radioresistance by inducing apoptosis in tumor cells. This dual therapy approach shows promise in treating tumors resistant to radiation, offering a new potential treatment strategy.
Researchers suggest targeting beta1-integrin to treat cancer by reducing tumour cell proliferation and inducing cellular senescence, potentially preventing metastases. Blocking this protein function in transgenic mice with pancreatic insulinomas resulted in tumour cells becoming senescent and unable to form new tumours.
Researchers at Cold Spring Harbor Laboratory identified a family of micro RNAs (miRNAs) that enable the p53 pathway to fight cancer growth. By comparing levels of miRNAs in cells with various pre-cancerous genetic lesions, they found a connection between changes in the p53 pathway and the loss of specific miRNAs, such as miR-34.
Researchers used embryonic stem cells to investigate how some tumours migrate to other parts of the body, making treatment more difficult. They found that a crucial change in cell behavior, known as epithelial-mesenchymal transition, allows cancer cells to move and spread.
Research by Dr. Eileen White and colleagues suggests that autophagy can protect genome integrity during starvation, but its loss can accelerate tumor progression. The normal function of autophagy sustains cells while limiting genome damage.
A study by Dr. Mary J.C. Hendrix found that inhibiting Nodal signaling in aggressive melanoma cells can reverse their invasiveness and tumor formation, reverting them to a more benign skin cell type. This discovery provides a promising new target for regulating tumor progression and metastasis.
Research suggests that phytochemicals in cruciferous vegetables, such as broccoli and watercress, can stop human prostate cancer cells from growing and inhibit the formation of blood vessels that feed tumors. This study provides promising preliminary evidence for the potential anti-cancer properties of these vegetables.
A study by Dana-Farber Cancer Institute researchers found that inhibiting the ATM protein can kill tumor cells with dysfunctional DNA repair pathways. Individuals with one mutant copy of a key gene are also at increased risk of developing cancer, as their remaining gene becomes mutated in specific cell types.
A study found that inhibiting the protein ATM can kill cancer cells with dysfunctional DNA repair pathways, offering hope for a new treatment. Additionally, researchers discovered that inhibiting the protein CaMKII can drive leukemic cells to mature and die, providing an alternative strategy for treating acute promyleocytic leukemia.
Aging cells with dysfunctional telomeres can promote tumorigenesis, but p53-mediated senescence may suppress spontaneous cancer development. Activating the senescence pathway is sufficient to prevent tumorigenesis in mutant mice with dysfunctional telomeres.
Researchers developed a new tumor targeting strategy that leverages one of the body's natural antibodies and immune responses. The approach recognizes and kills only cancer cells displaying high levels of integrins, reducing the risk of harming healthy cells.
Researchers discovered that Src activates PMR1, a protein that destroys specific messenger RNAs, leading to halted production of tumor-suppressor proteins. This mechanism could contribute to cancer development.
Scientists have discovered a new type of cell that plays a role in cancer development, which can either remain benign or become malignant depending on environmental cues. The finding may help define the role of cancer stem cells in tumor growth and recurrence.
Researchers challenge the cancer stem cell hypothesis, suggesting that tumors arise from normal cells and genetic variation rather than a single abnormal stem cell. The study identifies two distinct populations of cancer cells that can be targeted with experimental drugs.
Researchers have discovered a peptide that can free the protein p73, which induces tumor cell death, and effectively kills both p53-sufficient and p53-deficient human tumor cell lines. The study suggests targeting the p73-mediated pathway could provide a new avenue for developing anticancer therapeutics.
Researchers used two-photon microscopy to visualize T lymphocyte infiltration into solid tumours in real-time. T lymphocytes target tumour cells by recognizing the antigen and binding with enzymes, ultimately leading to cell death.
New research by Rockefeller University shows that bortezomib can kill multiple myeloma cells in a way that elicits an immune response, potentially enhancing patients' immunity to tumors. The treatment works by exposing heat shock proteins on dying cells, which then activate dendritic cells to present antigens to memory and killer T cells.
Researchers found that tumor tissue has random mutation rates up to 100 times higher than normal tissue from the same patient. This may explain why cells in a tumor have so many genetic mutations and could lead to ineffective chemotherapy treatments.
Researchers found that an excess of SF2/ASF, a critical protein in RNA splicing, can cause cancer. The study identified specific genes whose patterns of splicing were altered by this factor, including a gene encoding a protein kinase required to maintain tumor cells in a cancerous state.
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.
Cold Spring Harbor Laboratory scientists have identified a new tumor suppressor gene, CHD5, which prevents multiple types of cancer. The gene's role in regulating the tumor-preventing power in cells suggests that modulation of its activity may provide novel strategies for better design of more effective cancer therapies.
A new study has discovered a potential link between an approved obesity drug and cancer treatment. Researchers found that the drug Orlistat can block fatty acid synthase, an enzyme crucial for tumor cell growth, promoting cell death instead.
Researchers have discovered a new way to fight colorectal cancer by targeting the 'skeletons' of cancer cells, which enable them to reproduce and spread. High-dose PPARgamma inhibitors destroy cancer cell microtubules, reducing their ability to grow and metastasize.
Researchers identified human pancreatic cancer stem cells, which can produce tumors in half of mice tested. These stem cells are highly tumorigenic and resistant to traditional therapy, making them a promising target for new treatments.
Researchers successfully reactivate p53 in mice, causing tumors to self-destruct through senescence and apoptosis. This breakthrough offers potential new strategies for cancer treatment.
Researchers at MIT have shown that re-activating the tumor suppressor gene p53 can cause tumors to shrink or disappear in mice. The study offers critical genetic evidence that continuous repression of p53 is required for a tumor to survive.
Scientists at Oxford University have identified a surprising way to switch off a gene involved in cell division using a previously unknown type of RNA. This discovery could lead to new anti-cancer treatments by inhibiting the production of an enzyme that controls thymine production.
Researchers found that tumor cells treated with agents inducing apoptosis were more likely to undergo autophagy when p53 expression was inhibited. Inhibiting autophagy increased the effectiveness of chemotherapy and delayed tumor recurrence in mouse models.