Posts tagged cancer
Articles and news from the latest research reports.
Scientists Identify New Stem Cells with Therapeutic Potential
The discovery, published in the journal PLOS Biology, offers new opportunities in the treatment of cardiovascular diseases, cancer and many other diseases.
The growth of new blood vessels – angiogenesis – occurs during the repair of damaged tissue and organs in adults. However, malignant tumors also grow new blood vessels in order to receive oxygen and nutrients. As such, angiogenesis is both beneficial and detrimental to health, depending on the context, requiring therapeutic approaches that can either help to stimulate or prevent it. Therapeutics that aim to prevent the growth of new blood vessels are already in use, but the results are often more modest than predicted.
For more than a decade, Prof Petri Salvén of the University of Helsinki and his colleagues have studied the mechanisms of angiogenesis to discover how blood vessel growth could be prevented or accelerated effectively.
“We succeeded in isolating endothelial cells with a high rate of division in the blood vessel walls of mice. We found these same cells in human blood vessels and blood vessels growing in malignant tumors in humans. These cells are known as vascular endothelial stem cells. In a cell culture, one such cell is capable of producing tens of millions of new blood vessel wall cells,” Prof Salvén said.
From their studies in mice, the team was able to show that the growth of new blood vessels weakens, and the growth of malignant tumors slows, if the amount of these cells is below normal. Conversely, new blood vessels form where these stem cells are implanted.
Scientists discover novel diabetes and obesity therapy, and potential cause of major side effects from hedgehog inhibitors used as a cancer treatment
Cancer, diabetes, and excess body weight have one thing in common: they alter cellular metabolism. Scientists from the Max Planck Institute of Immunobiology and Epigenetics in Freiburg and the Medical University of Vienna together with an international research team have jointly resolved a new molecular circuit controlling cellular metabolism. The previously unknown signalling pathway, acting downstream of the hedgehog protein enables muscle cells and brown fat cells to absorb sugars without relying on insulin. Substances that selectively activate the signalling pathway could thus be utilized in the treatment of diabetes and obesity. With their results, the researchers are also able to explain why various new anti-cancer agents have induced mysterious pronounced side effects in the clinics.
The first detailed and complete picture of a protein complex that is tied to human birth defects as well as the progression of many forms of cancer has been obtained by an international team of researchers led by scientists with the U.S. Department of Energy (DOE)’s Lawrence Berkeley National Laboratory (Berkeley Lab). Knowing the architecture of this protein, PRC2, for Polycomb Repressive Complex 2, should be a boon to its future use in the development of new and improved therapeutic drugs.
Most experimental cancer drugs never make it to market because they don’t help enough people in early clinical trials. But even in “failed” drug trials, researchers may find that a few patients see their tumors shrink dramatically. Since it’s not clear why some respond but most don’t, researchers typically shake their heads and move on. But researchers today report that by sequencing the entire genome of one outlier patient’s tumor, they learned why her cancer disappeared when she took an experimental drug that didn’t help others. That drug now has a new lease on life for this cancer, and such testing may help revive other cancer drugs that showed promise in lab studies but initially failed in clinical testing.
Cancer May Result From Wrong Number of Genes
When a young person develops cancer, doctors most often assume that genetics are the reason, because the patient hasn’t lived long enough to accumulate environmental damage. But it’s been hard to find the faulty DNA behind many tumors. Now, using new genomic technology, scientists have discovered a novel explanation for some testicular cancers, the most common cause of cancer in men under 35. Rather than being triggered by a single gene mutation, the tumors are caused by too many or too few copies of a gene in a person’s cells. These “copy number variations” have been linked to other conditions such as autism, but never before to cancer.
Can bacteria fight brain cancer?
The thinking behind an approach that has caused trouble in California.
Last week, the Sacramento Bee reported that two neurosurgeons at the University of California, Davis, had been banned from research on humans after deliberately infecting three terminally ill cancer patients with pathogenic bacteria in an attempt to treat them. All three died, two showing complications from the infection. Nature explores what happened and the science behind it.
Building a human on a chip, organ by organ
Human “organs on chips” could be linked to make the ideal guinea pig, revolutionising the way drugs are tested and cancer is treated
Such organs on chips can be used to model how human organs function and respond to drugs, says Ingber. He thinks that they even have the potential to eliminate the use of animals in drug testing. “Animal testing is expensive and time-consuming, and animals are not always representative of humans.”
Still, Ingber points out that the chips can perform some roles that animal studies cannot. For instance, they could be personalised by building them from an individual’s own cells. In theory, a doctor could send tissue samples to a lab to test a potentially harmful therapy on such a chip before handing out a prescription. This would be especially useful for people with cancer, as the various therapies available can have very different effects on different people, Ingber says. “You could get a quick yes-or-no answer to whether a drug would work or not,” he says.
Personalised chips might also speed up clinical trials. “Someday it might be possible to shortcut clinical trials by using chips containing cells from different human populations that are known to respond differently to specific drug classes,” Ingber says.
Most Commonly Mutated Gene in Cancer May Have a Role in Stroke
ScienceDaily (June 22, 2012) — The gene p53 is the most commonly mutated gene in cancer. p53 is dubbed the “guardian of the genome” because it blocks cells with damaged DNA from propagating and eventually becoming cancerous. However, new research led by Ute M. Moll, M.D., Professor of Pathology at Stony Brook University School of Medicine, and colleagues, uncovers a novel role for p53 beyond cancer in the development of ischemic stroke. The research team identified an unexpected critical function of p53 in activating necrosis, an irreversible form of tissue death, triggered during oxidative stress and ischemia.
Dr. Ute Moll, Professor of Pathology, has uncovered a novel role for p53 in the development of ischemic stroke. (Credit: Image courtesy of Stony Brook Medicine)
The findings are detailed online in Cell.
Ischemia-associated oxidative damage leads to irreversible necrosis which is a major cause of catastrophic tissue loss. Elucidating its signaling mechanism is of paramount importance. p53 is a central cellular stress sensor that responds to multiple insults including oxidative stress and is known to orchestrate apoptotic and autophagic types of cell death. However, it was previously unknown whether p53 can also activate oxidative stress-induced necrosis, a regulated form of cell death that depends on the mitochondrial permeability transition pore (PTP) pore.
"We identified an unexpected and critical function of p53 in activating necrosis: In response to oxidative stress in normal healthy cells, p53 accumulates in the mitochondrial matrix and triggers the opening of the PTP pore at the inner mitochondrial membrane, leading to collapse of the electrochemical gradient and cell necrosis," explains Dr. Moll. "p53 acts via physical interaction with the critical PTP regulator Cyclophylin D (CypD). This p53 action occurs in cultured cells and in ischemic stroke in mice. "
Of note, they found in their model that when the destructive p53-CypD complex is blocked from forming by using Cyclosporine-A type inhibitors, the brain tissue is strongly protected from necrosis and stroke is prevented.
"The findings fundamentally expand our understanding of p53-mediated cell death networks," says Dr. Moll. "The data also suggest that acute temporary blockade of the destructive p53-CypD complex with clinically well-tolerated Cyclosporine A-type inhibitors may lead to a therapeutic strategy to limit the extent of an ischemic stroke in patients."
"p53 is one of the most important genes in cancer and by far the most studied," says Yusuf A. Hannun, M.D., Director of the Stony Brook University Cancer Center, Vice Dean for Cancer Medicine, and the Joel Kenny Professor of Medicine at Stony Brook. "Therefore, this discovery by Dr. Moll and her colleagues in defining the mechanism of a new p53 function and its importance in necrotic injury and stoke is truly spectacular."
Dr. Moll has studied p53 for 20 years in her Stony Brook laboratory. Her research has led to numerous discoveries about the function of p53 and two related genes. For example, previous to this latest finding regarding p53 and stroke, Dr. Moll identified that p73, a cousin to p53, steps in as a tumor suppressor gene when p53 is lost and can stabilize the genome. She found that p73 plays a major developmental role in maintaining the neural stem cell pool during brain formation and adult learning. Her work also helped to identify that another p53 cousin, called p63, has a critical surveillance function in the male germ line and likely contributed to the evolution of humans and great apes, enabling their long reproductive periods.
Source: Science Daily