A protein famed among scientists and clinicians for its ability to suppress the development of many types of tumors may just be moonlighting as a cancer fighter, a recent study by researchers at Stanford Medicine found. The study, conducted in laboratory mice, suggests that the protein, p53, instead evolved to promote the repair of tissues and cells after injury.

The surprising finding is like learning that your favorite bit actor is actually an Oscar-winning director who dabbles in performance on the weekends.

“This turns what we thought we knew about p53 on its head,” said Laura Attardi, Ph.D., professor of radiation oncology and of genetics. “We need to consider that p53’s role as a tumor suppressor may be secondary to a more basic role in repairing damage to tissues.”

The transfer of a neurotransmitter from one type of skin cell to another (melanocytes to keratinocytes) altered electrical activity and promoted melanoma initiation in preclinical models, according to results published in Cancer Discovery, a journal of the American Association for Cancer Research.

Melanoma is a deadly form of skin cancer that develops in melanin-containing skin cells known as melanocytes. An intrinsic feature of melanocytes is their ability to secrete melanin-containing vesicles to surrounding skin cells called keratinocytes to give skin its color.

While approximately half of all melanomas harbor mutations in the BRAF gene, these mutations are present in many benign skin lesions as well.

There are many microbes in our environment; many are harmless, some perform important functions, and some may pose a threat. Aspergillus fumigatus, for example, is a fungus that can be often be found in soil, as well as decaying organic matter; it has a crucial role in recycling carbon and nitrogen on our planet. A. fumigatus is also widely distributed in the air, so on average, people probably inhale a few hundred spores of A. fumigatus every day. This fungus is highly adaptive, and it can also evade weakened immune defenses in immunocompromised individuals to cause lung infections, called Aspergillosis. There are limited treatment options for this disease, and it’s difficult to treat effectively.

Scientists have now analyzed genetic data from about 250 strains of this fungus, and data from 40 Aspergillosis patients that characterized the lung microbiomes of these individuals. This showed that when people are infected with A. fumigatus, the composition of their lung microbiome begins to change dramatically. The findings have been reported in Nature Communications.

Study explores perspectives on the applications of somatic genome editing.

Cellular therapies like chimeric antigen receptor (CAR) T cells could represent a promising new avenue by which to treat autoimmune diseases, according to a recent review article. The authors cautioned, however, that most of the research testing CAR-based therapies has been in very early-stage trials.

CAR T cells are human cells that have been genetically modified to express a synthetic receptor, The cells have been used successfully as a therapy in several types of cancer, such as large B-cell lymphoma and multiple myeloma.

Manipulating T cells to target cancer cells has worked to treat some cancers. Researchers are investigating whether the same approach might be used to curb the dysregulated immune response that underlies autoimmune disease.

Malaria is a possibly fatal disease caused by a parasite transferred by mosquitos to humans. Common symptoms include fever, chills, and flu-like traits. According to the Centers for Disease Control (CDC), around 2,000 cases of malaria are diagnosed in the United States per year. The diagnosis is common in individuals coming back from Africa or Asia. On a global scale, about 700,000 people die from malaria, and most are children. However, death from malaria can usually be prevented with early detection and proper medical care. Researchers are trying to proactively target malaria by developing a new vaccine using genetic material.

Researchers from the Victoria University of Wellington’s Ferrier Research Institute, the Malaghan Institute of Medical Research, and the Peter Doherty Institute for Infection and Immunity have all worked together to develop a vaccine that can effectively stimulate cells in the immune system against malaria-causing parasite, Plasmodium. The vaccine, described in Nature Immunology, is designed to generate resident memory cells in the liver to combat Plasmodium. Resident memory cells are a type of immune cell that reside in tissues throughout the body to target invading pathogens that enter those tissues.

The vaccine is made with messenger ribonucleic acid (mRNA), as opposed to peptides or proteins. The difference between the two is the type of material delivered by the vaccine. Peptide-based vaccines use peptides from the virus to elicit an immune response. Alternatively, mRNA vaccines use mRNA extracted from the virus. In this study, the researchers originally used a peptide-based vaccine but recently found mRNA improves the activation of resident immune cells to kill malaria-based pathogens. The treatment result was significant between the two types of vaccines because the peptide-based vaccine had small fragments of protein and could not stimulate the immune system effectively, while the mRNA could encode for an entire malaria protein.

It’s now easier for scientists to create gene-edited insects thanks to a new technique called “direct parental CRISPR.”