Nearly one in six deaths from prostate cancer could be prevented if targeted screening was introduced for men at a higher genetic risk of the disease, according to a new UCL-led computer modelling study.
Prostate cancer is the most common form of cancer in men with around 130 new cases diagnosed in the UK every day and more than 10,000 men a year dying as a result of the disease. However, unlike breast and cervical cancer there is currently no national screening programme for this disease in the UK.
A blood test that detects raised levels of the prostate-specific antigen (PSA) can be used to screen for prostate cancer. However, this test is not a reliable indicator as it does not accurately distinguish between dangerous cancers from harmless ones—leading to both unnecessary operations and missed cancers that are harmful.
P53 is the most famous cancer gene, not least because it’s involved in causing over 50% of all cancers. When a cell loses its p53 gene—when the gene becomes mutated—it unleashes many processes that lead to the uncontrolled cell growth and refusal to die, which are hallmarks of cancer growth. But there are some cancers, like kidney cancer, that that had few p53 mutations. In order to understand whether the inactivation of the p53 pathway might contribute to kidney cancer development, Haifang Yang, Ph.D., a researcher with the Sidney Kimmel Cancer Center—Jefferson Health probed kidney cancer’s genes for interactions with p53.
Earlier work found that PBRM1—the second most mutated gene in kidney cancer—could interact with p53. However, other researchers were unable to definitively show that it was truly an important mechanism in kidney cancer.
Rather than looking at the p53 protein itself, first author Weijia Cai a postdoc in Dr. Yang’s lab and other collaborators looked at an activated version of p53, one that is studded with an additional chemical marker—an acetyl group—at many specific spots.
From the beginning of time, humankind has searched for the secret to a long life. Now science may have found an answer, in the form of molecular augury. The pattern of chemical chains that attach to the DNA in your cells—on-off switches known as epigenetic markers—can reveal how swiftly you are aging, and perhaps even how much longer you will live. While genetic testing might tell you where you came from, epigenetics promises a glimpse into the future. Now, a handful of companies are offering commercial blood or saliva tests based on the science of epigenetics—a chance to find out how old you truly are.
Companies claim they can now easily calculate your biological age. Should you take them up on it?
To that end, Fields decided to ask a Florida judge to grant him a warrant that would override the new policy, allowing him to search GEDmatch’s entire database, including users who hadn’t opted in — and Judge Patricia Strowbridge did just that, the detective announced at a recent police convention, according to the NYT.
Legal experts told the NYT that this appears to be the first time a judge has approved a DNA website warrant this broad, with New York University law professor Erin Murphy calling it “a huge game-changer.”
“The company made a decision to keep law enforcement out, and that’s been overridden by a court,” Murphy told the newspaper. “It’s a signal that no genetic information can be safe.”
Quite a number of readily understandable reviews were published this month, along with an X10 episode on epigenetic alterations; if you’re new to the biology of aging or want to introduce someone else to the topic with new material, this is a great time to start.
LEAF News
We will be returning to New York in 2020 for our third conference focused on aging research, investment, and biotech business. Judy Campisi, Aubrey de Grey, Hanadie Yousef, Steve Horvath, Andrei Gudkov, and Polina Mamoshina are among the speakers confirmed so far. Join the conference mailing list to stay informed as more details are announced.
Researchers have found a woman with a rare genetic mutation that has protected her from dementia even though her brain has developed major neurological features of the disease.
Half of people who live to 85 will develop Alzheimer’s disease — a disturbing statistic. But research into a family in South America has revealed a gene mutation that appears to afford protection, and may lead to a way to treat or possibly even prevent the disease.
Scientists have developed a new gene-therapy technique by transforming human cells into mass producers of tiny nano-sized particles full of genetic material that has the potential to reverse disease processes.
Though the research was intended as a proof of concept, the experimental therapy slowed tumor growth and prolonged survival in mice with gliomas, which constitute about 80 percent of malignant brain tumors in humans.
The technique takes advantage of exosomes, fluid-filled sacs that cells release as a way to communicate with other cells.
Optogenetics, a tool for controlling neurons with light, has given neuroscientists the ability to flip brain cells on and off more or less at will, revolutionizing neuroscience.
Yet the technique faces a fundamental challenge: To study all but the outermost part of the brain, researchers need to implant fiber optics or other invasive devices to deliver light deep into the brain.
Now, in Proceedings of the National Academy of Sciences, Stanford researchers report that they’ve found a less invasive way to do so: injectable nanoparticles that convert sound waves, which can easily penetrate into the brain, into light.
The answer is essentially yes … in the short term.
If you’re an apparently healthy person who wants to learn about your genetic disease risks, you can send a saliva sample and a hundred bucks or so to an array-based direct-to-consumer genetic testing company and get some trait information and selected health risks, plus details about your genetic ancestry. But as the direct-to-consumer (DTC) companies themselves will tell you, this is only a fraction of the medical value that may be hidden in your genome. Many of the experts in both ancestry and medical genomics will suggest that since consumer facing genomics are not as comprehensive as those meeting medical standards, it is quite OK for consumers to pay for these products out of their own pockets.
But when it comes to health care, people expect products and services that are medically beneficial to be available to more than just those people who can pay for them. As medical science increasingly demonstrates the life altering value of genomics, the notion that these services must be paid for out of pocket, making it inaccessible to some, does not seem appropriate or fair.
We recently launched the Brigham Preventive Genomics Clinic, the first academic clinic in the world to offer comprehensive, high quality genome sequencing and in-depth interpretation to apparently healthy adults and their children. Over the past two years of planning this clinic, we have struggled with the reality that there is no health insurance coverage for preventive genomic testing, and our patients must therefore pay out of pocket. This is a troubling feature for a clinic at Brigham and Women’s Hospital, which is known for its ties to communities in Boston with diverse ethnic and socioeconomic backgrounds. One must ask: Is a service like this further widening the inequities in our health care system?
