Lifeboat Foundation

New cancer immunotherapies involve extracting a patient’s T cells and genetically engineering them so they will recognize and attack tumors. This technique is a true medical breakthrough, with an increasing number of leukemia and lymphoma patients experiencing complete remissions since CAR T therapy was FDA approved in 2017.

This type of therapy is not without challenges, however. Engineering a patient’s T cells is laborious and expensive. And when successful, the alterations to the immune system immediately make patients very sick for a short period of time, with symptoms including fever, nausea and neurological effects.

Now, University of Pennsylvania researchers have demonstrated a new engineering technique that, because it is less toxic to the T cells, could enable a different mechanism for altering the way they recognize cancer.

Duchenne muscular dystrophy (DMD) is one of the most common and most devastating muscular diseases, greatly reducing patients’ quality of life and life expectancy. Now, researchers in Germany have managed to use the CRISPR gene-editing tool to correct the condition in pigs, bringing the treatment ever closer to human trials.

A protein called dystrophin is necessary for muscles to regenerate themselves, but people with DMD have a genetic mutation that removes the gene that produces dystrophin. That means that affected children usually begin to show symptoms of muscle weakness by age five, lose the ability to walk by about age 12, and rarely live through their 30s as their heart muscles give out.

Because it’s a genetic condition, DMD is a prime target for treatment with the gene-editing tool CRISPR. This system is prized for its ability to cut out problematic genes and replace them with more beneficial ones, and has been put to work treating cancer, HIV and forms of blindness.

We are delighted to announce that Dr. Brian Kennedy, a Distinguished Professor in the Department of Biochemistry and Physiology at the National University of Singapore (NUS) will be joining the LEAF scientific advisory board.

Professor Kennedy is an important figure in the research community, as he is internationally recognized for his research and efforts to translate those findings into therapies that could potentially slow, delay, or even prevent age-related diseases. He previously served as the President of the Buck Institute, where he still remains as a Professor.

At the NUS, he is developing therapeutic interventions that directly target human aging along with biomarkers that can validate if a therapy has worked or not. Professor Kennedy and his team have been exploring the epigenetic clock, a biomarker that measures methylation of the human genome to determine biological age. They are also investigating inflammatory biomarkers of aging using metabolomics, the study of chemical processes involving metabolites, the intermediates and products of metabolism.

A new study from Washington University School of Medicine in St. Louis suggests that bone marrow — or blood stem cells — from healthy donors can harbor extremely rare mutations that can cause health problems for the cancer patients who receive them.

A stem cell transplant — also called a bone marrow transplant — is a common treatment for blood cancers, such as acute myeloid leukemia (AML). Such treatment can cure blood cancers but also can lead to life-threatening complications, including heart problems and graft-versus-host disease, in which new immune cells from the donor attack a patient’s healthy tissues.

A new study from Washington University School of Medicine in St. Louis suggests that extremely rare, harmful genetic mutations present in healthy donors’ stem cells — though not causing health problems in the donors — may be passed on to cancer patients receiving stem cell transplants. The intense chemo- and radiation therapy prior to transplant and the immunosuppression given after allow cells with these rare mutations the opportunity to quickly replicate, potentially creating health problems for the patients who receive them, suggests the research, published Jan. 15 in the journal Science Translational Medicine.

Continue reading “Mutations in donors’ stem cells may cause problems for cancer patients” »

Analyses of the viral genome are already providing clues to the origins of the outbreak and even possible ways to treat the infection, a need that is becoming more urgent by the day: Early on Saturday in China, health officials reported 15 new fatalities in a single day, bringing the death toll to 41. There are now nearly 1,100 confirmed cases there.

Reading the genome (which is made of RNA, not DNA) also allows researchers to monitor how 2019-nCoV is changing and provides a roadmap for developing a diagnostic test and a vaccine.

“The genetics can tell us the true timing of the first cases” and whether they occurred earlier than officials realized, said molecular biologist Kristian Andersen of Scripps Research, an expert on viral genomes. “It can also tell us how the outbreak started — from a single event of a virus jumping from an infected animal to a person or from a lot of animals being infected. And the genetics can tell us what’s sustaining the outbreak — new introductions from animals or human-to-human transmission.”

Grey hair seems to be driven by stem cell exhaustion, one of the suggested reasons we age. One researcher believes we can turn back the clock on greying hair.

Melissa Harris’s research points to a new paradigm for hair graying. “We thought that once you go gray the stem cells are all lost — there’s no going back,” Harris said. “But presumably they can be reactivated.”

Continue reading “Going gray isn’t a one-way trip? UAB researcher exploring ways to ‘rejuvenate’ gray hairs” »

If you are interested in superlongevity, I have a spectacular book for you: Lifespan — Why We Age and Why We Don’t Have To, by David Sinclair PhD.

Sinclair has written a book about all the various ways in which humans can extend their lifespan and their healthspan.

One of the best aspects of this book is that Sinclair has a way of writing that is clear and insightful. It is so rare for me to read a book about scientific experiments in which it is easy to follow the methodology, but it is unique to also have an explanation of the application of the results that is crystal clear. Sinclair does both simply and easily.

Continue reading “Lifespan: Why We Age—and Why We Don’t Have To” »

CHICAGO/LONDON (Reuters) — When a newly organized vaccine research group at the U.S. National Institutes of Health (NIH) met for the first time this week, its members had expected to be able to ease into their work. But their mandate is to conduct human trials for emerging health threats — and their first assignment came at shocking speed.

To better understand the dynamics of bats and potential threats to human health, Goldberg and his colleagues explored the relationship of an African forest bat, a novel virus and a parasite. Their work, described in a report published July 13 in Nature Scientific Reports, identifies all three players as potentially new species, at least at the molecular level as determined by their genetic sequences.

Many viral pathogens often have more than one or two hosts or intermediate hosts needed to complete their life cycles. The role of bat parasites in maintaining chains of viral infection is little studied, and the new Wisconsin study serves up some intriguing insights into how viruses co-opt parasites to help do the dirty work of disease transmission.

The parasite in the current study is an eyeless, wingless fly, technically an ectoparasite. It depends on the bat to be both its eyes and wings. And it plays host to a virus, as the current study shows. For the virus, the fly plays the role of chauffeur. “From a virus’s perspective, an ectoparasite is like Uber. It’s a great way to get around — from animal to animal — at minimal expense and effort,” Goldberg explains.