Research on the biology of tumor cells. Covers tumor spread, cell-particle diagnostics, new anti-tumor molecules, and cancer-killing immune 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.
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.
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 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.
Researchers successfully reactivate p53 in mice, causing tumors to self-destruct through senescence and apoptosis. This breakthrough offers potential new strategies for cancer treatment.
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.
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 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.
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 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 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 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.
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.
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.
A study by USC researchers identified a protein called EphB4 that protects tumor cells from the immune system. Turning off this protein could make cancer cells more vulnerable to attack, and future therapies may aim to block its function.
MIT researchers have discovered that tumor cells become aneuploid due to subtle errors in microtubule attachment. The study sheds light on the role of checkpoint proteins and their interaction with APC and EB1 molecules in maintaining normal cell division.
Blocking the conversion of glucose to lactate in mammary tumor cells impaired mitochondrial function and hindered tumor cell proliferation in low oxygen conditions. Alterations in glucose metabolism are linked with changes in mitochondrial physiology, highlighting LDH-A's critical role in tumor growth.
Apo2L/TRAIL, a new cancer drug, has shown activity in treating advanced cancers with minimal side effects. The agent selectively induces programmed cell death in cancer cells while sparing normal cells, offering hope for targeted treatment options.
A team of researchers from Munich discovered a cellular mechanism that protects against tumours by controlling the Bcl-3 oncogene. The study identified Cyld as a potential tumour suppressor, which can accumulate around the nucleus and prevent Bcl-3 from entering it.
The study found that pro-inflammatory cytokines increase positive regulators of IFNg production while shutting down negative regulators like TGFb, which lowers IFNg levels. This fine balance ensures healthy NK cell activity and prevents autoimmune diseases and cancer.
A team of researchers discovered that CYLD has a second role in controlling tumor growth by modifying the cancer-promoting protein Bcl-3. Mice lacking CYLD developed significantly more and larger skin tumors than normal mice, suggesting that CYLD plays a crucial role as a tumor suppressor.
The study found a triple interaction between CD44, hyaluronan, and LARG that initiates two molecular pathways causing tumor cell growth and migration. The complex can be used as a marker for potentially aggressive head-neck tumors and may lead to new therapeutic strategies targeting the PDZ domain of LARG.
Research suggests that a genetic mutation in the Arf gene can cause leukemias to resist Gleevec treatment, leading to aggressive disease progression. This finding may lead to new treatments that re-sensitize tumor cells to Gleevec therapies.
Researchers at St. Jude Children's Research Hospital found that a combination of the Bcr-Abl mutation and loss of both Arf genes in bone marrow cells triggers an aggressive form of ALL. Inactivating both Arf genes enables leukemic cells to multiply despite imatinib treatment, highlighting potential strategies for overcoming resistance.
Researchers find that growth factor SCF promotes tumor angiogenesis by interacting with normal neurons, leading to worsened prognosis in patients. Decreased SCF expression improves survival in mouse glioma models, highlighting the importance of considering normal cells in cancer treatment.
The Mayo Clinic research identifies a signaling mechanism by which natural killer cells initiate a toxic response against cancers and viruses. The discovery provides crucial information for designing therapies to stop, reverse or protect against cancer.
Researchers found that low-intensity electrical stimulation increased the uptake of doxorubicin in cancer cells, causing them to die even at low concentrations. This novel strategy could bypass multidrug resistance and enhance the efficacy of existing chemotherapeutic treatments.
A new molecule, ARC, has shown promise as a potential anticancer drug that selectively kills tumor cells without harming normal cells. The compound inhibits RNA synthesis in normal cells but induces cell death in cancer cells by blocking the cell cycle, making it an attractive alternative to existing drugs that can harm healthy tissue.
Researchers found that cells adapt to low oxygen conditions by inhibiting mitochondrial function and increasing the conversion of glucose to lactate. This active process, mediated by hypoxia-inducible factor-1 (HIF-1), helps protect tumor cells from death and may be targeted by cancer therapies.
Xencor's engineered antibody Fc variants show enhanced effector functions, killing tumor cells 10 times more toxic than conventional treatments. These advancements hold promise for developing next-generation antibody therapeutics.
Robert A. Weinberg's work on human oncogenes led to understanding cancer's mechanisms of invasion and progression. Angela M. Hartley Brodie developed aromatase inhibitors to prevent breast cancer recurrence in postmenopausal women.
Researchers have successfully used a gene therapy approach to deliver telomerase, an enzyme that lengthens cell lifespan, without causing tumors in human patients. The technique allows for the growth of blood vessels in patients with vascular disease, offering new treatment options.
A new MRI drug, mangafodipir, has been found to improve the effectiveness of chemotherapy by increasing antitumoral activity while protecting normal cells from damage. The study suggests that mangafodipir may enhance the therapeutic index of anticancer agents and supports investigation into its use in cancer patients.
Researchers discovered that elastin fragments in mice lungs trigger emphysema. Additionally, a study found that pericyte dysfunction allows tumors to spread by forming leaky blood vessels. Another study identified female mice lacking IBP protein, which makes their T cells resistant to death and contributes to lupus-like disease.
UF researchers identified a gene called focal adhesion kinase (FAK) that produces an enzyme creating a protective barrier for cancer cells. Blocking this interaction with protein VEGFR-3 kills malignant cells. The findings open new avenues for improved cancer therapies.
The Tumor-Host Genomics project aims to understand the molecular and cellular interactions between tumor cells and their microenvironment. By developing advanced functional genomics instruments and technologies, researchers hope to identify new targets for anti-cancer therapy.