Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: genetics – Page 396

BioViva warmly welcomes Dr de Magalhaes to our Scientific Advisory Board!

Dr de Magalhaes graduated in Microbiology in 1999 from the Escola Superior de Biotecnologia in his hometown of Porto, Portugal, and then obtained his PhD in 2004 from the University of Namur in Belgium. Following a postdoc with genomics pioneer Prof George Church at Harvard Medical School, in 2008 Dr de Magalhaes was recruited to the University of Liverpool. He now leads the Integrative Genomics of Ageing Group (http://pcwww.liv.ac.uk/~aging/) which focuses on understanding the genetic, cellular, and molecular mechanisms of ageing. Dr de Magalhaes has authored over 100 publications and given over 100 invited talks, including three TEDx talks.

Read more

Continuing from Motherboard, “In an email to Motherboard, a DARPA spokesperson said that four research teams have received allotments of the $45 million funding from the agency as a part of Insect Allies, and that all teams have now entered phase two. The teams include researchers from Penn State University, the University of Texas, and Ohio State University.”

It isn’t difficult to tell what opinion this article represents. Do we need this, or want to trust people with placing genetically modified viruses in the crops that become our grocery store produce?

Read more

The cells of most patients’ cancers are resistant to a class of drugs, called proteasome inhibitors, that should kill them. When studied in the lab, these drugs are highly effective, yet hundreds of clinical trials testing proteasome inhibitors have failed. Now scientists may have solved the mystery of these cells’ surprising hardiness. The key: Resistant cancer cells have shifted how and where they generate their energy. Using this new insight, researchers have identified a drug that resensitizes cancer cells to proteasome inhibitors and pinpointed a gene that is crucial for that susceptibility.

As develop, they accrue multiple genetic alterations that allow the cells to quickly reproduce, spread and survive in distant parts of the body, and recruit surrounding cells and tissues to support the growing tumor. To perform these functions, cancer cells must produce high volumes of the proteins that support these processes. The increased production and numerous mutated proteins of cancer cells make them particularly dependent on the proteasome, which is the cell’s protein degradation machine. These huge protein complexes act as recycling machines, gobbling up unwanted proteins and dicing them into their amino acid building blocks, which can be reused for the production of other proteins.

Previously, researchers exploited cancer cells’ increased dependency on their proteasomes to develop anti-cancer therapies that inhibit the proteasomes’ function. Several distinct proteasome inhibitors have been developed, and when used in the lab, these proteasome inhibitor drugs are indeed highly effective at eradicating tumor cells. However, when administered to animal models or patients with cancer, such as multiple myeloma, proteasome inhibitors have limited efficacy and even initially vulnerable cancer cells quickly develop resistance to them. How do cancer cells so adroitly sidestep drugs that should kill them?

Read more

Helicobacter pylori, a globally distributed gastric bacterium, is genetically highly adaptable. Microbiologists at LMU have now characterized its population structure in individual patients, demonstrating an important role of antibiotics for its within-patient evolution.

The cosmopolitan bacterium Helicobacter pylori is responsible for one of the most prevalent chronic infections found in humans. Although the infection often provokes no definable symptoms, it can result in a range of gastrointestinal tract pathologies, ranging from inflammation of the lining of the stomach to gastric and duodenal tumors. Approximately 1 percent of all those infected eventually develop stomach cancer, and the World Health Organization has classified H. pylori as a carcinogen. One of Helicobacter pylori’s most striking traits is its genetic diversity and adaptability. Researchers led by microbiologist Sebastian Suerbaum (Chair of Medical Microbiology and Hospital Epidemiology at LMU’s Max von Pettenkofer Institute have now examined the genetic diversity of the species in the stomachs of 16 patients, and identified specific adaptations that enable the bacterium to colonize particular regions of the stomach.

Read more

Many mutations in DNA that contribute to disease are not in actual genes but instead lie in the 99% of the genome once considered “junk.” Even though scientists have recently come to understand that these vast stretches of DNA do in fact play critical roles, deciphering these effects on a wide scale has been impossible until now.

Using artificial intelligence, a Princeton University-led team has decoded the functional impact of such mutations in people with . The researchers believe this powerful method is generally applicable to discovering such genetic contributions to any disease.

Publishing May 27 in the journal Nature Genetics, the researchers analyzed the genomes of 1,790 families in which one child has but other members do not. The method sorted among 120,000 mutations to find those that affect the behavior of genes in people with autism. Although the results do not reveal exact causes of cases of autism, they reveal thousands of possible contributors for researchers to study.

Read more