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This could give more immunity to viruses with the gene they found helped people survive the black death.


“We all think that COVID-19 was insane and completely changed the world and our societies,” Barreiro says. “COVID has a mortality rate of about 0.05% – something like that. Now try to project – if it’s even possible – a scenario where 30 to 50% of the population dies.”

Now a new study, published Wednesday in the journal Nature, shows that the Black Death altered more than society: It also likely altered the evolution of the European people’s genome.

In the study, Barreiro and his colleagues found that Black Death survivors in London and Denmark had an edge in their genes – mutations that helped protect against the plague pathogen, Yersinia pestis. Survivors passed those mutations onto their descendants, and many Europeans still carry those mutations today.

The gene-silencing complex HUSH might be involved in complex disorders affecting the brain and neurons. However, its mechanism of action remains unclear. Researchers from the Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA) now uncover the in vivo targets and physiological functions of a component of the HUSH gene-silencing complex and one of its associated proteins.

The work, conducted in laboratory mouse models and human organoids, links the HUSH complex to normal , neuronal individuality and connectivity, as well as mouse behavior. The findings are published in Science Advances.

The human silencing hub (HUSH) complex was recently identified to be of key importance for silencing repetitive genetic elements including transposons in mammals. The HUSH complex contains MPP8, a protein that binds the histone modification mark H3K9me3. Additionally, HUSH is known to recruit other proteins including the zinc finger protein MORC2.

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Cancer research – and its impact on patient care – has made some significant strides in just the last 10 years. For example, the availability and affordability of sequencing genetic information has improved greatly – meaning researchers and doctors are now better able to get information about a person’s risk for certain cancers as well as what drugs might work best for cancer patients. Another major leap forward came with the approval of vaccines that help prevent infections from the human papilloma virus (HPV) that cause cervical cancers. Many other advances have occurred in the areas of targeted therapy, immunotherapy, and cancer screening technology.

Still, cancer remains a massive health problem that researchers across the United States and elsewhere are working tirelessly to solve. Many experts are hopeful that they can build on decades of learning and recent advances to move even more rapidly toward reducing the cancer burden.

We invited 10 American Cancer Society Research Professors to share their perspectives and predictions for how cancer research will evolve over the next 10 years – and what this might mean for patients. These 10 experts are among the very best in their field; the Society’s Research Professor grants are awards that go to a select group – researchers and doctors who have made seminal contributions that have changed the direction of basic, clinical, psychosocial, behavioral, health policy or epidemiologic cancer research.

The lone volunteer in a unique study involving a gene-editing technique has died, and those behind the trial are now trying to figure out what killed him.

Terry Horgan, a 27-year-old who had Duchenne muscular dystrophy, died last month, according to Cure Rare Disease, a Connecticut-based nonprofit founded by his brother, Rich, to try and save him from the fatal condition.

Although little is known about how he died, his death occurred during one of the first studies to test a gene editing treatment built for one person. It’s raising questions about the overall prospect of such therapies, which have buoyed hopes among many families facing rare and devastating diseases.

With inherited gene mutations from both parents, a woman in Spain is battling with 12 tumors in her body.

As stated by the Spanish National Cancer Research Centre (CNIO), the woman first developed a tumor when still a baby and other tumors followed it within five years. 36 year-old-patient has developed twelve tumors, at least five of them malignant in her life. Each one has been of a unique kind and has affected a different area of the body.

“We still don’t understand how this individual could have formed during the embryonic stage, nor could have overcome all these pathologies,” says Marcos Malumbres, director of the Cell Division and Cancer Group at the Spanish National Cancer Research Centre (CNIO).

Genetic engineering is a rapidly progressing scientific discipline, with tremendous current application and future potential. It’s a bit dizzying for a science communicator who is not directly involved in genetics research to keep up. I do have some graduate level training in genetics so at least I understand the language enough to try to translate the latest research for a general audience.

Many readers have by now heard of CRISPR – a powerful method of altering or silencing genes that brings down the cost and complexity so that almost any genetics lab can use this technique. CRISPR is actually just the latest of several powerful gene-altering techniques, such as TALEN. CRISPR is essentially a way to target a specific sequence of the DNA, and then deliver a package which does something, like splice the DNA. But you also need to target the correct cells. In a petri dish, this is simple. But in living organism, this is a huge challenge. We have developed several viral vectors that can be targeted to specific cell types in order to deliver the CRIPR (or TALEN), which then targets the specific DNA.

Now I would like to present a different technique I have not previously written about here – alternative splicing. A recent study presents what seems like a significant advance in this technology, so it’s a good time to review it. “Alternative splicing” refers to a natural phenomenon of genetics. Genes are composed of introns and exons. I always thought the nomenclature was counterintuitive, but the exons are actually the part of the gene that gets expressed into a protein. The introns are the part that is not expressed, so they are cut out of the gene when it is being converted into mRNA, and the exons are stitched together to form the sequence that is translated into a protein. Alternative splicing refers to the fact that the way in which the introns are removed and the exons stitched together can vary, creating alternative forms of the resulting protein.