Medical Bulletin 11/April/2023

Here are the top medical news for the day:

Cellular identity discovery has potential to impact cancer treatments: Study

A puzzle regarding PRC2 has intrigued the Bracken lab and other scientists in the field for years: two forms (PRC2.1 and PRC2.2) exist in the cell but the Bracken lab previously showed that the two forms of PRC2 target the same regions of DNA and do the same job. So why do we need two versions?

A team of scientists led by those in Trinity College Dublin has discovered new mechanisms involved in establishing cellular identity, a process that ensures the billions of different cells in our bodies do the correct job. This new discovery in stem cells - a result so surprising that the team initially believed it to be an error in the lab - has potential translational impacts in cancer biology and associated targeted treatments.

Reference:

TRINITY COLLEGE DUBLIN,Molecular Cell

Study finds ‘Beige fat’ could hold key to age-related metabolism change

Mammals, including humans, have two main types of fat: white adipose tissue (WAT), which stores energy from excess calorie intake, and brown adipose tissue (BAT), which burns calories to produce heat to maintain body temperature.

By stimulating the production of a certain type of fat cells, the effects of a slowing metabolism could be reversed, according to a new study by researchers in Cornell’s Division of Nutritional Sciences, which is housed in the College of Human Ecology and the College of Agriculture and Life Sciences.

The study, published March 31 in Nature Communications, shows therapeutic promise in a third type of fat, a subtype of WAT: beige fat. Beige fat has the same cellular precursors as white fat and the same thermogenic properties as brown fat, which means it helps to reduce blood sugar and the fatty acids that cause hardening of the arteries and heart disease.

Reference:

Abigail Benvie et al,Nature Communications,doi 10.1038/s41467-023-37386-z

Protein with novel anti-tumoral activities identified

The tumor suppressor gene called TP53 effectively restricts the development and growth of many different tumor types across the human body, and it is the most frequently mutated tumor suppressor gene in human cancers. This gene encodes a protein called p53, which is both a potent inhibitor of cell proliferation and an inducer of apoptosis.

Understanding how cancer develops is critical for designing effective, personalized cancer therapies. Researchers have known for years that cancer begins with mutations in certain types of genes. One of these types of cancer genes are so-called “tumor suppressors.” When functioning normally, tumor suppressor genes can stop malignant cells from undergoing uncontrolled cell proliferation and initiate a process of cell elimination called apoptosis, a form of cell death. Mutations in tumor suppressor genes can cause these genes to lose their functionality, eventually contributing to the development of cancer.

Reference:

FAM193A is a positive regulator of p53 activity,Cell Reports,doi10.1016/j.cellrep.2023.112230