Brain tumours: Artificial stimulation of the immune system could mean less aggressive treatment. Brain metastases are common secondary complications of other types of cancer, particularly lung, breast and skin cancer. The body's own immune response in the brain is rendered powerless in the fight against these metastases by inflammatory reactions. Researchers at the MedUni Vienna have now, for the first time, precisely characterised the brain's immune response to infiltrating metastases. This could pave the way to the development of new, less aggressive treatment options. "The active phagocytes are quite literally overwhelmed by the tumour and even the white blood cells are too weak to fight off these metastases on their own; they have to be stimulated before they can have any effect," explains oncologist Matthias Preusser from the University Department of Internal Medicine I and the Comprehensive Cancer Center (CCC), a joint institution operated by the MedUni Vienna and the Vienna General Hospital.
Cannabinoid may treat brain cancer. Researchers at University of California, San Diego Moores Cancer Center are evaluating the safety and tolerability of a synthetic cannabinoid called dexanabinol (ETS2101). Delivered as a weekly intravenous infusion, the drug is being tested in patients with all forms of brain cancer, both primary and metastatic. "In this Phase I study, we are examining the safety of multiple doses of dexanabinol, extent of penetration into the brain, and suitability for future trials," said Santosh Kesari, MD, PhD, principal investigator, and director of neuro-oncology, UC San Diego Moores Cancer Center.
"What we hope to determine is the safe and optimal dose of drug in the brain. " Dexanabinol is a cannabinoid derivative that causes no psychotropic effects. It was tested previously as a neuroprotective in patients with traumatic brain injury. During these trials the drug was found to cross the blood-brain barrier. Tumor cell growth does not follow a master plan. Scientists at Charité -- Universitätsmedizin Berlin could explain a yet unknown regulatory network that controls the growth of tumor cells. Understanding such networks is an important task in molecular tumor biology in order to decode the relationships between the determinants defining which molecules are produced and in what quantities, in both normal and tumor cells. The study is published in the journal Molecular Systems Biology. The growth of a tumor and its reaction to specifically targeted therapy is dictated by changes in its genetic material (mutations) encoding special signal molecules.
These molecules activate the genetic program of tumor cells via branched signaling pathways and influence all processes needed for cell division, the mobility of cells and metastasis. Significant steering elements of these tumor-specific programs are called transcription factors. Fasting makes brain tumors more vulnerable to radiation therapy. A new study from USC researchers is the first to show that controlled fasting improves the effectiveness of radiation therapy in cancer treatments, extending life expectancy in mice with aggressive brain tumors. Prior work by USC professor of gerontology and biological sciences Valter Longo, corresponding author on the study and director of the Longevity Institute at the USC Davis School of Gerontology, has shown that short-term fasting protects healthy cells while leaving cancer cells vulnerable to the toxic effects of chemotherapy.
The latest study, which appears in the online journal PLoS ONE, is the first to show that periods of fasting appear to have the same augmenting effect on radiation therapy in treating gliomas, the most commonly diagnosed brain tumor. Gliomas have a median survival of less than two years. "With our initial research on chemotherapy, we looked at how to protect patients against toxicity. Chemotherapy-resistant cancer stem cell could be 'Achilles' heel' of cancer. Scientists at Mount Sinai School of Medicine have discovered a subpopulation of cells that display cancer stem cell properties and resistance to chemotherapy, and participate in tumor progression. This breakthrough could lead to the development of new tests for early cancer diagnosis, prognostic tests, and innovative therapeutic strategies, as reported in Cancer Cell.
Resistance to chemotherapy is a frequent and devastating phenomenon that occurs in cancer patients during certain treatments. Unfortunately, tumors that initially respond to chemotherapy eventually become resistant to it, contributing to tumor progression and death. The study reveals that these new cancer "stem" cells, which have not been differentiated into more specific cell types, are capable of multiplying despite being exposed to chemotherapy, while differentiated cells die.
Ongoing studies suggest that this new cell type exist in other tumor types such as breast cancer, colon cancer, bladder cancer and lung cancer. Genetic link to prostate cancer risk in African Americans found. Prostate cancer in African-American men is associated with specific changes in the IL-16 gene, according to researchers at the University of Illinois at Chicago College of Medicine. The study, published online in the journal Cancer Epidemiology, Biomarkers & Prevention, establishes the association of IL-16 with prostate cancer in men of both African and European descent.
"This provides us with a new potential biomarker for prostate cancer," says principal investigator Rick Kittles, UIC associate professor of medicine in hematology/oncology. Previously identified changes in the gene for IL-16, an immune system protein, were associated with prostate cancer in men of European descent. But the same changes in the gene's coded sequence -- called "polymorphisms" -- did not confer the same risk in African Americans.
Polymorphisms result from DNA mutations and emerge in the ancestral history of different populations. Enlisting the AIDS virus to fight cancer. Can HIV be transformed into a biotechnological tool for improving human health? According to a CNRS team at the Architecture et Réactivité de l'ARN (RNA Architecture and Reactivity) laboratory, the answer is yes.
Taking advantage of the HIV replication machinery, the researchers have been able to select a specific mutant protein. Added to a culture of tumor cells in combination with an anticancer drug, this protein improves the effectiveness of the treatment at 1/300 the normal dosage levels. Published in PLoS Genetics on 23 August 2012, these findings could lead to long-term therapeutic applications in the treatment of cancer and other pathologies. The human immunodeficiency virus (HIV), which causes AIDS, uses human cell material to multiply, primarily by inserting its genetic material into the host cells' genome. One advantage of this experimental technique is that the mutant proteins were tested directly on cells in culture.