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The animal looked and barked like a dog—albeit one with long, pointed, foxlike ears—but it also climbed bushes, a behavior more typical of the local Pampas fox, and it refused common dog food, preferring to eat rats.

Caretakers began to wonder if it might be a hybrid—a mixture of domestic dog and some local wild canid. They contacted geneticists Thales Renato Ochotorena de Freitas from the Universidade Federal do Rio Grande do Sul and Rafael Kretschmer from the Universidade Federal de Pelotas who, last month, published a study confirming the animal was the world’s first documented fox-dog. The finding excited and intrigued experts in animal genetics.

“What a strange hybrid beast!” wrote Roland Kays, a biologist with North Carolina State University and the North Carolina Museum of Natural Sciences, on X (formerly Twitter), alongside a photo of the creature and link to the study.

Philosophers have wrestled with the question of whether we are truly free to decide on our actions for centuries. Now, insights from genetics, neuroscience and evolutionary biology are shedding fresh light on the issue.

By Clare Wilson

A genetically engineered marine microorganism is shown to break down polyethylene terephthalate (PET) in saltwater. This plastic, used in everything from water bottles to clothing, is a significant contributor to microplastic pollution in oceans.

“This is exciting because we need to address plastic pollution in marine environments,” says Nathan Crook, corresponding author of a paper on the work and an assistant professor of chemical and biomolecular engineering at North Carolina State University.

And the answers point to a profound reality: We have far more in common with our extinct cousins than we ever thought.

Neanderthals within us

Until recently, the genetic legacy from ancient humans was invisible because scientists were limited to what they could glean from the shape and size of bones. But there has been a steady stream of discoveries from ancient DNA, an area of study pioneered by Nobel Prize winner Svante Paabo who first pieced together a Neanderthal genome.

A new artificial intelligence program is helping scientists speedily sift through thousands of data sets and millions of papers to home in on genes that underly disease, drastically condensing a search process that once took months.

Using computer software, scientists can scan entire genomes, or an organism’s full set of DNA, of mice that model human diseases. The goal: to identify genetic mutations that cause those diseases and open new doors for scientists to better harness genetics to develop disease treatments, said Gary Peltz, MD, PhD, professor of anesthesiology, perioperative and pain medicine at Stanford Medicine.

But to do that, scientists must search through massive sets of genomic data, which yields more false positives than researchers care to admit. It’s also time intensive. Peltz wanted to make the genetic discovery process easier, faster and more accurate.

The genetic code of a rare form of kidney cancer, called reninoma, has been studied for the first time. In a paper, published in Nature Communications, researchers at the Wellcome Sanger Institute, Great Ormond Street Hospital and The Royal Free Hospital also revealed a new drug target that could serve as an alternative treatment if surgery is not recommended.

There are around 100 cases of reninoma reported to date worldwide, and it is among the rarest of tumors in humans. Although it can usually be cured with surgery, it can cause severe hypertension or it can spread and develop into metastases. There are no existing medical treatments for reninoma and management involves surgery alone. Until now, it had been unknown what genetic error causes reninoma.

In the new study, a collaboration between the Wellcome Sanger Institute and Great Ormond Street Hospital and The Royal Free Hospital, researchers found that there is a specific error in the genetic code of a known cancer gene, NOTCH1, that is behind the development of this rare cancer.

Researchers at the Francis Crick Institute, the University of Cambridge, Imperial College London, the University of Liverpool, the University of Cape Town and UKHSA have uncovered a link between an antiviral drug for COVID-19 infections called molnupiravir and a pattern of mutations in the SARS-CoV-2 virus.

Molnupiravir works by inducing mutations in the virus’s genetic information, or genome, during replication. Many of these mutations will damage or kill the virus, reducing viral load in the body. It was one of the first antivirals available on the market during the COVID-19 pandemic and was widely adopted by many countries.

In research published in Nature, the scientists used global sequencing databases to map mutations in the SARS-CoV-2 virus over time. They analyzed a family tree of 15 million SARS-CoV-2 sequences so that at each point in each virus’s evolutionary history they could see which mutations had occurred.

There are many therapies that target cancer. The most well-known is chemotherapy, which is a toxic chemical that is directed at a tumor to kill the cells. This is currently the standard of care for most types of cancer. However, as science advances, less toxic and more direct therapies are discovered. The most recently discovered therapy is known as ‘immunotherapy’, which redirects the immune system to kill the tumor. There are many successful treatments with immunotherapy among different types of cancers, including melanoma and lung cancer. Unfortunately, immunotherapy is limited in many solid tumors due to the immunosuppressive tumor microenvironment (TME). The TME is a pro-tumor environment that the cancer has made by releasing specific proteins that allow it to progress. In this environment the tumor can remain undetected from the immune system and progress throughout the body. Different immune cells in the TME become polarized and alter their functions to help the tumor proliferate and grow. It is now becoming more common to pair therapies together including immunotherapy with chemotherapy. Scientists are still trying to find ways to improve treatment and completely eradicate the tumor.

In San Francisco, California, a group of scientists, led by Dr. Alex Marson, are working to modify gene expression to reprogram or change immune cells in the TME to attack cancer. There has been some success, but this immunotherapy does not help treat all patients. In addition, the screening process to determine genetic changes to determine which cells would result in the greatest treatment efficacy is a long, arduous process. A group at the Gladstone Institutes has worked with Marson at University of California San Francisco (UCSF) to develop a strategy that helps pair different genetic combinations in a faster amount of time to determine the most beneficial treatment outcomes. This screening technique is called Pooled Knockin Screening (ModPoKI). ModPoKI finds the best genetic modifications to express in immune cells that will have prolonged anti-tumor efficacy.

The study that demonstrated ModPoKI was published recently in Cell, which demonstrates our ability to now understand how to combine genetic programs. ModPoKI combines genes into long lines of DNA to generate roughly 10,000 combinations to match with a genetically engineered immune cell known as a T cells are major immune cells that primarily target foreign antigens, like cancer cells, and kill them. Once the optimal gene modification is found, it is put into the engineered immune cells that are polarized to kill cancer. After further investigation, the combinations made by ModPoKI resulted in the most polarized anti-tumor T cells.

Two drugs from a class new to HIV medicine called BH3 mimetics were unveiled at July’s 12th International AIDS Society Conference on HIV Science (IAS 2023) in Brisbane. They may contribute to a cure for HIV by killing off long-lived cells that contain HIV genes in their DNA. Notably, venetoclax (Venclexta) and obatoclax only killed off cells containing intact DNA, capable of giving rise to new viruses, and did not delete cells containing defective, harmless DNA.

A number of drugs and treatments from the anti-cancer arsenal have been investigated as HIV cure research such as HDAC inhibitors, PD-1 inhibitors and therapeutic vaccines. (And, of course, the six successful cures so far have used the radical cancer therapy of a stem cell (bone marrow) transplant.)

This is not coincidental: cancer and AIDS are both the end result of mutations in the DNA of some of our cells. In the case of cancer they arise in the host DNA and in HIV infection they are introduced by a virus, but both are the result of ‘rogue genes’ (some other viruses, such as HPV, directly cause cancers).