Articles tagged with Tumor Cells
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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 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.
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.
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.
A study shows that SH2B1 in the brain regulates body weight and fat content, implicating it as a potential target for treating obesity and type II diabetes. Additionally, researchers have found that autophagy represents a survival mechanism for tumor cells treated with agents that initiate tumor cell death.
Researchers at U-M Comprehensive Cancer Center and Stanford University have identified a stem cell marker in head and neck tumors, which may help develop targeted therapies. The study found that cells expressing the CD44 marker can grow into new tumors, suggesting a potential target for cancer treatment.
Researchers have discovered a potential new treatment for breast cancer by inhibiting the protease enzyme TACE, which is strongly present in aggressive forms of the disease. Inhibition of TACE blocks shedding of growth factor proteins, resulting in inhibition of cell division and reversion of malignant characteristics.
Researchers found that regulatory T cells (Treg) are impaired in the absence of WASp, leading to systemic autoimmune disease. However, a spontaneous revertant mutation in a patient's Treg cells improved their function, suggesting that a defect in Treg function contributes to the autoimmunity associated with WASp deficiency.
Researchers have identified a new key step in how the Polo kinase enzyme functions, confirming its potential as a target for anti-cancer drug development. The study sheds light on how the enzyme helps cells divide and multiply in an uncontrolled manner to form tumors.
Researchers at Cedars-Sinai Medical Center identified genes that make brain cancer-causing stem cells resistant to chemotherapy and other treatments. The study found that these cells can regenerate and become even more aggressive after treatment, highlighting a potential target for new therapies.
Research suggests that T-beta-RIII can suppress breast cancer progression by blocking TGF-beta signaling. Low levels of T-beta-RIII are associated with decreased recurrence-free survival in patients with breast cancer.
Researchers discovered that changes in expression of one component of the TGF-beta receptor, T-beta-RIII, might provide a mechanism for the distinct effects of TGF-beta at different stages of breast cancer. Additionally, analysis of RB functionality could help clinicians determine the most effective therapy for their patients.
A new computer simulation of tumor growth sets the stage for individualized cancer treatment. The model suggests that the microenvironment around tumor cells determines the tumor's ultimate cellular makeup and invasive potential.
Researchers used advanced microscopy techniques to visualize T cells actively migrating through and killing tumor cells in real-time. The study provides new insights into the mechanisms of interaction between T cells and tumor cells, with the presence of antigen determining migration and interaction.
Researchers propose that natural selection drives the evolution of cancer, with tumor cells constantly evolving through mutation and selection. This understanding could lead to new therapeutic strategies, such as targeting benign cells to outcompete malignant ones.
New research suggests stress hormones can stimulate tumor cells to produce compounds breaking down tissue and facilitating metastasis. Beta-blocker drugs may slow cancer growth by blocking receptors.
A pioneering study has found that the tumor suppressor gene p53 plays a crucial role in regulating communication between tumor cells and their surrounding stroma. The study identified 111 secreted proteins, 39 of which were enhanced and 21 inhibited by wt-p53 expression.
WEHI researchers will investigate impaired apoptosis and differentiation in tumourigenesis and therapy, as well as molecular regulation of blood cell production and function. The funding may lead to new approaches for cancer treatment and novel therapeutic strategies for blood disorders.
Researchers at Johns Hopkins have found that lung cancer cells exploit the NRF2 gene to detoxify chemicals, including chemotherapy agents, rendering them ineffective. This discovery may lead to new treatment strategies by blocking NRF2 activity, potentially improving standard chemotherapy drug efficacy.
Researchers found that nearly all tumor cells in the bone marrow of early-stage breast cancer patients have a putative breast cancer stem cell phenotype, increasing the risk of disease progression. This study provides evidence that these stem cells may be responsible for metastases and has significant implications for cancer treatment.
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 discover a three-drug combo that inhibits the growth of aggressive prostate tumors by targeting neural signaling molecules and energy sources. The combination, using diuretic amiloride, Parkinson's disease medication carbidopa, and sedative-reversal drug flumazenil, shows promise for potential therapeutic applications.
Researchers have created a method to release substances into tumor cells using microcapsules and laser light, which could lead to more targeted cancer treatments. The technique involves heating the polymer shell of the capsule with infrared laser light, causing it to open and releasing its contents.
A new study finds that drinking carbonated soft drinks is not linked to esophageal cancer or cardia adenocarcinoma. Additionally, bortezomib has been shown to inhibit the growth of neuroblastoma cells, a childhood tumor type.
Researchers found that a form of cancer affecting dogs is spread through the transmission of tumor cells, with evidence pointing to its origins in wolves or closely related ancient dog breeds. The disease has been transmitted among dogs for at least two centuries and has adapted to evade immune responses.
Researchers discovered that malignant melanoma cells secrete Nodal, a protein essential for proper embryo development, inducing abnormal skull and backbone formation in zebrafish embryos. Blocking Nodal signaling reduced melanoma cell invasiveness and promoted reversion to normal skin cells.
Researchers at Massachusetts General Hospital have identified potential ovarian cancer stem cells, which may be responsible for tumor recurrence and resistance to chemotherapy. These stem-like cells were found in mouse and human ovarian cancer lines, and were sensitive to certain treatment approaches.
Researchers have found that nicotine stimulates cell proliferation and progression of tumors already initiated by tobacco carcinogens. The presence of nicotinic acetylcholine receptors on bronchial cells and lung cancer cells is key to this process, suggesting a new mechanism in lung cancer development.
Researchers found that pancreatic tumors surround themselves with regulatory T cells to avoid detection by the immune system. Depleting these cells slowed tumor growth and increased survival time in mice. The study suggests a potential way to block tumor recruitment of regulatory T cells and revive cancer immunotherapy.
Researchers at the University of Pennsylvania School of Medicine discovered that the loss of menin protein leads to proliferation of pancreatic islet cells, which secrete insulin. This finding has implications for treating Type 1 diabetes and could lead to new treatments.
Researchers at The Hebrew University of Jerusalem isolated malignant tumor cells from their nutritional and oxygen supplies, inhibiting growth and stopping metastases. Actibind, a protein found in black mold, was shown to bind actin in human and animal cells, halting cell growth and reducing the ability of cancer cells to form new tumors.