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Genes, Genomics & Genetics In Medicine / Medical Applications



I used to say that if you could turn genes on and off then you could turn cancer cells on and off.

I was not the only one who wondered about this, as this article in New Scientist seems to suggest;

How to get your genes switched on

16 November 2006
From New Scientist Print Edition. Subscribe and get 4 free issues.

The latest twist on the Nobel prizewinning method of RNA interference, or RNAi, could prove to be a real turn-on. Whereas standard RNAi silences a target gene, switching protein production off, the new technique boosts gene activity, providing a genetic "on" switch...

...Although the exact mechanism remains unclear, Li's team has already found that it requires a protein called Ago2, which is also involved in the standard RNAi process. Li believes RNA activation could find widespread use, for example in treating cancer by boosting the activity of tumour suppressor genes.

From issue 2578 of New Scientist magazine, 16 November 2006, page 20

New Scientist article

Could be cool...no need for taking stem cells from a place anymore perhaps.

What do you think?


I am a meat popsicle
Sep 18, 2001
Inside a starship, watching puny humans from afar
I think I'd agree with this basic concept, although I'm no scientist.
Massively simplifying things, I think DNA/genes etc. work in a similar manner to DIP switches. Turn some genes on and some off, and you get a particular result. Do a different combination of the same genes, and you'll get a different result. And so on ad infinitum.


Aug 19, 2003
Selfish genes may drive out diseases
Genetic elements that select for their own survival could establish disease-resistance genes in insect populations

[Published 29th March 2007 07:02 PM GMT]


Researchers have come up with a new way to establish desirable genes in insect populations, according to an online Science report this week. The authors created a synthetic selfish genetic element that propagates rapidly through Drosophila populations -- an approach they say could also help drive malaria-resistance genes into mosquito populations.

The approach "looks very convincing" for establishing disease-resistance genes in insect populations, said Marcelo Jacobs-Lorena of Johns Hopkins Bloomberg School of Public Health in Baltimore, who was not involved in the study. "If it works in Drosophila, I think the chances that it would work in insects of medical importance is quite high."

Researchers have identified and created mosquitoes that carry genetic elements preventing them from transmitting malaria or dengue; last week, Jacobs-Lorena and his colleagues showed that one type of malaria-resistant mosquito can outcompete normal mosquitoes when feeding on infected blood, although this advantage may not be enough to establish the resistance gene in a mosquito population. Consequently, researchers are searching for ways to ensure that such resistance genes become ubiquitous throughout an insect population, said study senior author Bruce Hay of the California Institute of Technology in Pasadena.

Led by Chun-Hong Chen, also of Caltech, the researchers created a synthetic genetic element based on Medea(maternal-effect dominant embryonic arrest) elements. These selfish genetic elements are thought to select for their own survival through a toxin-antidote system, Hay said. The mother's Medea element causes toxin release into all of her oocytes, and only those progeny that inherit the Medea element themselves can produce an antidote.

The researchers constructed a transposable element vector containing both a toxin and an antidote. The "toxin" consists of two microRNAs that silence expression of a crucial development gene called myd88. When myd88 is silenced in ooctyes, embryos suffer ventral patterning defects and fail to hatch. The antidote consists of a myd88 replacement. "The toxin is a loss of an essential function, and the antidote is the restoration of that function," Hay explained.

The transposable element worked as expected: When female flies containing the element mated with wild-type males, about half of the progeny suffered patterning defects and died. The other half inherited the embryonic antidote and survived. To see if this element could establish itself in a population, the researchers performed cage experiments. When 25% of the flies started out with the genetic element, all flies contained at least one copy of the element after 10-12 generations.

"The next step will be to add an effector gene" to the vector, such as a gene that induces resistance to malaria, according to Frederic Tripet of Keele University in Staffordshire, UK, who was not involved in the work. That way, the vector could be used to propagate this gene through an insect population, ideally mosquitoes that can carry the virus.

Currently, for the mosquito, scientists still know very little about the genes and promoters in oogenesis and early embryogenesis that would have to be involved in spreading the disease-resistant genes, Hay said. But, according to Tripet, "this is just a question of time, not a major difficulty."

One potential obstacle for establishing this genetic element in the wild is that mosquito populations can be reproductively isolated from one another, Tripet told The Scientist. "It is likely that the more we study those populations, the more reproductive barriers we will find that can locally prevent or slow down the spread of introduced transgenes."

Genetically altered mosquitoes will have to be released in large numbers into affected areas in order for introduced genes to establish themselves, Hay said, but previous efforts to release sterile mosquitoes have shown that this is feasible. "Getting the numbers up will always be a challenge... but we know that it can be done."

Melissa Lee Phillips
[email protected]

Links within this article

C.-H. Chen et al., "A Synthetic Maternal-Effect Selfish Genetic Element Drives Population Replacement in Drosophila," Science, published online March 29, 2007.

A.A. James, "Gene drive systems in mosquitoes: rules of the road," Trends in Parasitology, February 2005.

J. Weitzman, "Molecular make-up of a malaria mosquito," The Scientist, October 3, 2002.

Marcelo Jacobs-Lorena

K.D. Vernick et al., "Molecular genetics of mosquito resistance to malaria parasites," Current Topics in Microbiology and Immunology, 2005.

S. Sanides, "The malaria hut," The Scientist, August 1, 2006.

M.L. Phillips, "Anti-malaria genes give mosquitoes an edge," The Scientist, March 20, 2007.

R.W. Beeman et al., "Maternal-effect selfish genes in flour beetles," Science, April 3, 1992.

Frederic Tripet

G. Davidson, "The five mating types of the Anopheles gambiae complex," Rivista di Malariologia, December 1964.

F. Gould, P. Schliekelman, "Population genetics of autocidal control and strain replacement,"
Annual Review of Entomology, 2004.

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C'thuluan Balloon Animal
Nov 25, 2002
link to Stuff

For the first time, scientists have pinned down a molecular process in the brain that helps to trigger schizophrenia. The researchers involved in the landmark study, which was published Wednesday in the journal Nature, say the discovery of this new genetic pathway likely reveals what goes wrong neurologically in a young person diagnosed with the devastating disorder.

The study marks a watershed moment, with the potential for early detection and new treatments that were unthinkable just a year ago, according to Steven Hyman, director of the Stanley Centre for Psychiatric Research at the Broad Institute at the Massachusetts Institute of Technology. Hyman, a former director of the National Institute of Mental Health, calls it "the most significant mechanistic study about schizophrenia ever."


tart of darkness
Jan 3, 2009
Great news! Hopefully this will be the thing that finally opens the door to effective treatments, with fewer unpleasant side-effects. I've known some people who really struggled with this seemingly hopeless disease, or diecided not to have children because there was schizophrenia somewhere in their family tree.

We were just talking last night about the synapse-pruning theory, but with the idea that not enough synapses were removed. This seems to prove the exact opposite - it's too many synapses pruned instead.

Comfortably Numb

Aug 7, 2018
A fundamental discovery about how gene activity is regulated

Source: phys.org/Johns Hopkins University Bloomberg School of Public Health

Researchers at Johns Hopkins Bloomberg School of Public Health have discovered a fundamental mechanism that regulates gene activity in cells. The newly discovered mechanism targets RNA, or ribonucleic acid, a close cousin of DNA that plays an important role in cellular activity.

The discovery, detailed in a paper published February 3 in the journal Molecular Cell, is a significant addition to the foundational understanding of how gene activity is regulated, and may ultimately lead to powerful new medical treatments.

The newly discovered mechanism effectively silences or dials down certain active genes as a basic cellular regulatory or quality-control system. It may even act as a defense against viruses. When genes are active, they are copied out into strands of RNA. These RNA strands perform cellular functions on their own or are translated into proteins. The new mechanism destroys RNA strands that have excessively folded over and stuck to themselves to form knots, hairpins, and other structures. These highly structured RNAs can occur during normal processing but could possibly also be caused by misfolding.

The finding is likely to have implications for medical research because many human disorders, including cancers and neurodegenerative diseases, such as ALS (Amyotrophic Lateral Sclerosis) and Huntington disease-like syndromes, involve failures of normal RNA regulation and/or the accumulation of abnormally folded or tangled RNA in affected cells



Dec 5, 2003
Looks like the Big EgoBoo to me.

They already have FOUR kids!

And they wanted something new...and old...and lets face it risky.