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HiDEF-seq advances cancer treatment:


HiDEF-seq technique could further help develop or advance new prevention approaches or develop treatments for genetic diseases and even cancer.

Gilad Evrony, senior study author and a core member of the Center for Human Genetics & Genomics at NYU Grossman School of Medicine told Science Direct:

The reason targeted treatment for non-small cell lung cancer fails to work for some patients, particularly those who have never smoked, has been discovered by researchers from UCL, the Francis Crick Institute and AstraZeneca.

The study, published in Nature Communications, shows that lung cancer cells with two particular genetic mutations are more likely to double their genome, which helps them to withstand treatment and develop resistance to it.

In the UK, lung cancer is the third most common type of cancer and the leading cause of cancer death. Around 85% of patients with lung cancer have (NSCLC), and this is the most common type found in patients who have never smoked. Considered separately, “never smoked” lung cancer is the fifth-most common cause of cancer death in the world.

New research shows that ferroptosis, a form of cell death, occurs in severe COVID-19 patient lungs. Stopping it improves outcomes. In some severe cases of COVID-19, the lungs undergo extreme damage, resulting in a range of life-threatening conditions like pneumonia, inflammation, and acute respiratory distress syndrome. The root cause of those wide-ranging reactions in the lungs has until now remained unclear.

A new study by researchers at Columbia and the Columbia University Irving Medical Center sheds light on this mystery.

The study found that ferroptosis, a form of cell death first named and identified at Columbia in 2012, is the major cell death mechanism that underlies COVID-19 lung disease.

The gene-editing technique employs prime editors along with advanced enzymes known as recombinases. This method has the potential to lead to universal gene therapies that are effective for conditions like cystic fibrosis.

Researchers at the Broad Institute of MIT and Harvard have enhanced a gene-editing technology that can now efficiently insert or replace entire genes in human cell genomes, potentially making it suitable for therapeutic uses.

The advance, from the lab of Broad core institute member David Liu, could one day help researchers develop a single gene therapy for diseases such as cystic fibrosis that are caused by one of hundreds or thousands of different mutations in a gene. Using this new approach, they would insert a healthy copy of the gene at its native location in the genome, rather than having to create a different gene therapy to correct each mutation using other gene-editing approaches that make smaller edits.

Exhibit apparent links that we will examine in this review. The null hypothesis that aging and cancer coincide because both are driven by time, irrespective of the precise causes, can be confronted with the idea that aging and cancer share common mechanistic grounds that are referred to as ‘hallmarks’. Indeed, several hallmarks of aging also contribute to carcinogenesis and tumor progression, but some of the molecular and cellular characteristics of aging may also reduce the probability of developing lethal cancer, perhaps explaining why very old age ( 90 years) is accompanied by a reduced incidence of neoplastic diseases. We will also discuss the possibility that the aging process itself causes cancer, meaning that the time-dependent degradation of cellular and supracellular functions that accompanies aging produces cancer as a byproduct or ‘age-associated disease’

Karleigh Fry pioneers robotic neurosurgery:


An 8-year-old girl from Oklahoma has become the world’s first pediatric patient to undergo robotic deep brain stimulation (DBS).

The announcement was made by two collaborating hospitals, Oklahoma Children’s Hospital OU Health and Bethany Children’s Health Center.