https://soundcloud.com/a16z/a16z-podcast-techs-big-ideas-and…andreessen
Category: biotech/medical – Page 2814
If cancer is predominantly a random process, then why don’t organisms with thousands of times more cells suffer more from cancer? Large species like whales and elephants generally live longer, not shorter lives, so how are they protected against the threat of cancer?
While we have a great deal more to learn when it comes to cancer biology, the general belief is that it arises first from mutation. It’s becoming clear it’s actually an incredibly complicated process, requiring a range of variable factors such as mutation, epigenetic alteration and local environment change (like inflammation). While some students may have spent sleepless nights wondering how many mutated cells they contain after learning the fallibility of our replication mechanisms, the reality is that with such an error rate we should all be ridden with cancer in childhood — but we’re not. Our canine companions sadly often succumb around their 1st decade, but humans are actually comparatively good at dealing with cancer. We live a relatively long time in the mammal kingdom for our size and even in a modern environment, it’s predominantly an age-related disease.
While evolution may have honed replication accuracy, life itself requires ‘imperfection’ to evolve. We needed those occasional errors in germ cells to allow evolution. If keeping the odd error is either preferable or essentially not worth the energy tackling when you’re dealing with tens of trillions of cells, then clearly there is more to the story than mutation. In order to maintain a multi-cellular organism for a long enough period, considering that errors are essentially inevitable, other mechanisms must be in place to remove or quarantine problematic cells.
Tony Wyss-Coray studies the impact of aging on the human body and brain. In this eye-opening talk, he shares new research from his Stanford lab and other teams which shows that a solution for some of the less great aspects of old age might actually lie within us all.
Scientists at Ohio State University say they’ve grown the first near-complete human brain in a lab.
The brain organoid, if licensed for commercial lab use, could help speed research for neurological diseases and disorders, like Alzheimer’s and autism, Rene Anand, an Ohio State professor who worked on the project, said in a statement Tuesday.
“We will have a more precise prediction of efficacy of therapy and possible side effects before we do clinical trials,” Anand told The Huffington Post via email, explaining how his model is a more ethical alternative to trials that use rodent specimens. Anand said reducing the use of animals improves research as they’re “not as likely to predict clinical outcomes as human brain models.”
A lab-grown brain is the most complete ever developed, equivalent to the brain maturity of a five-week-old foetus.
Cancer requires extensive and fast division in order to become a serious threat, but this feature also renders it vulnerable, allowing certain growth pathways to be targeted. A new drug candidate has emerged which exploits this weakness, overstimulating proteins required for growth — tipping cellular stress in virulent cancer cells over the edge.
“No prior drug has been previously developed or proposed that actually stimulates an oncogene to promote therapy. Our prototype drug works in multiple types of cancers and encourages us that this could be a more general addition to the cancer drug arsenal.”
Many types of cancer require specific mutations in genes related to growth, and one particular target is the steroid receptor coactivator (SRC) family of oncogenes. These lie at the centre of signalling pathways used to grow rapidly, and conventional research has focused on inhibiting them to prevent tumour growth. Instead of inhibiting, this new strategy aims to upregulate their activity, overstimulating them to an extent that destroys the host cell. In their search for a suitable molecule which might cause such stimulation, researchers stumbled across a compound labeled MCB-613.
Lifespan.io is running a SENS fundraiser to aid research into Mitochondrial repair. This is a new fundraiser platform to help get important regenerative medicine research funded and underway. Let us hope this is the start of how research could be funded and that it opens up faster progress.
Engineering backup copies of mitochondrial genes to place in the nucleus of the cell, aiming to prevent age-related damage and restore lost mitochondrial function.
EchoPixel uses virtual reality to help doctors visualize each patient’s unique anatomy and internal structure in a floating 3D image.
Meanwhile there is something important going on in the fight against baldness.
As in the majority of tissues, the hair follicle has stem cells. There are two types of stem cells that are responsible for the continuous renewal of the follicles. The first type is called active stem cells and they start dividing quite easily. Stem cells of the second type are called quiescent and in case of the new hair growth they don’t start dividing as easily. At the same time, the new hair is based primarily on quiescent cells, which attracted close attention of researchers to these cells. At first people thought that baldness was due to this type of cells.
However, recent studies showed that bald men did have those quiescent cells in their follicles. The problem was that they didn’t divide at all and didn’t contribute to forming new hairs.
This means that even a bald person still has the potential to grow new hair, but because of lack of some regulatory factors quiescent cells can’t start replicating.
Elaine Fuchs was able to identify these regulatory factors in her study published in Cell. Apparently, it’s all about the transit-amplifying cells that are the progeny of the active stem cells.
BioViva
Posted in biotech/medical, life extension
An interesting little Bioviva clip about their upcoming gene therapy work.
CEO Liz Parrish discusses BioViva and gene therapy…. Diseases of aging beware.