“Fifty years after the show aired, Star Trek’s fictional tricorder is far from becoming a reality. But a $10 million prize from the XPRIZE Foundation is hoping to motivate inventors to create one quickly.”
“Fifty years after the show aired, Star Trek’s fictional tricorder is far from becoming a reality. But a $10 million prize from the XPRIZE Foundation is hoping to motivate inventors to create one quickly.”
Cancer thrives when mutated cells undergo frequent division. Most anti-cancer drugs work by inserting themselves in between the DNA base pairs that encode our genetic information. This process is known as intercalation, and it can result in subtle changes to the DNA molecule’s geometric shape or tertiary structure. These structural changes interfere with the DNA’s transcription and a cell’s replication process, ultimately resulting in cell death.
While intercalating agents used in chemotherapy drugs are highly effective in fighting cancer, they also may kill important cells in the body and lead to other complications such as heart failure. Therefore, researchers are always searching for faster, cheaper and more accurate tools to aid in the design of next-generation anti-cancer drugs with reduced side effects.
A paper published in ACS Nano, one of the top nanotechnology journals in the world, explores this topic. “Modeling and Analysis of Intercalant Effects on Circular DNA Conformation,” (LINK TO http://pubs.acs.org/doi/abs/10.1021/acsnano.6b04876) focuses on the effect of the intercalating agent ethidium bromide (a mimic for many chemotherapy drugs) on the tertiary structure of DNA.
Experts may reassure us that artificial intelligence won’t take over the world anytime soon – but they just might invade the multiplex.
At least that’s the plot developing at IBM, where the Watson artificial-intelligence team programmed a computer to come up with a scary trailer for “Morgan,” a thriller about a genetically modified, AI-enhanced super-human.
It’s an add-on for CRISPR.
Researchers have created a new genome editing technique called Target-AID, which induces point mutations instead of cutting DNA
Gene editing technology has fantastic potential, but there are remaining issues and questions over safety and specificity. The major contender is currently CRISPR-Cas9, but this induces a double stranded break in DNA which is a slightly riskier approach — particularly if it cuts in other locations too that you don’t want it to. Research teams across the world are both optimising and customising the CRISPR system; creating more accurate versions or versions that regulate gene expression as opposed to editing it. One such team has now built an add-on to CRISPR, Target-AID.
From selective breeding to genetic modification, our understanding of biology is now merging with the principles of engineering to bring us synthetic biology.
Written, animated and directed by James Hutson, Bridge8.
Transcript can be found here:
http://technyou.edu.au/fun-stuff/videos/video-transcripts/
Dr Haroldo Silva from SENS talks about ALT cancer in this short film.
As normal cells divide, the ends of their chromosomes (telomeres) progressively shorten until eventually the cells reach senescence or undergo apoptosis. Cancers, which disproportionally kill more individuals in the 65 years or above age group, often overcome this built-in replication limit by expressing the enzyme telomerase.
However, about 10–15% cancers do not use telomerase and at least a major subset of these exhibit hallmarks of Alternative Lengthening of Telomeres (ALT) activity, including long and heterogeneous telomere lengths, presence of ALT-associated PML nuclear bodies (APBs), and generation of high-levels of C-rich circular telomeric DNA repeats (C-circles). Although there are many telomerase-based anti-cancer therapies in clinical development at the moment, research on ALT has not produced any promising therapies so far. This lag is due in part to a lack of assays that are reliable and amenable to high-content/high-throughput (HTS) screens.
The OncoSENS team has made significant progress toward making some of these key ALT assays compatible with the HTS format, which should not only speed up the development of ALT-based anti-cancer therapies but also broaden the amount of research performed on ALT. Our team has already begun applying the assays above to test the involvement of several genes in the ALT pathway and the progress on that front will also be showcased. Undoubtedly, successfully shutting down both ALT- and telomerase-based pathways of telomere maintenance in cancers will move the field forward towards realizing the goal of a complete eradication of one of the main age-related fatal diseases burdening society.
Visit www.sens.org/videos to view the rest of our SENS6 videos.
Many lower organisms retain the miraculous ability to regenerate form and function of almost any tissue after injury. Humans share many of our genes with these organisms, but our capacity for regeneration is limited. Scientists at the MDI Biological Laboratory in Bar Harbor, Maine, are studying the genetics of these organisms to find out how regenerative mechanisms might be activated in humans.
The ability of animals to regenerate body parts has fascinated scientists since the time of Aristotle. But until the advent of sophisticated tools for genetic and computational analysis, scientists had no way of studying the genetic machinery that enables regeneration. Using such tools, scientists at the MDI Biological Laboratory have identified genetic regulators governing regeneration that are common across species.
In a paper published in the journal PLOS ONE, MDI Biological Laboratory scientistsBenjamin L. King, Ph.D., and Voot P. Yin, Ph.D., identified these common genetic regulators in three regenerative species: the zebrafish, a common aquarium fish originally from India; the axolotl, a salamander native to the lakes of Mexico; and the bichir, a ray-finned fish from Africa.
#CRISPR can be used to alter the genes of not only one organism, but an entire species, through a method of inheritance known as a gene drive. But what happens if something goes awry?