Lifeboat Foundation

You may have heard of precision medicine in the news, but what actually is it, and what could it mean for the future of healthcare?

In the past, medicine was geared for the masses and was applied to large numbers of people, on the basis of average effectiveness. If a particular substance was ineffective on 10% of the population, it could still pass through and be prescribed anyway. Before genomics, it was tricky to understand or postulate why people had such varied responses to medication, but now we have the right tools — things are changing.

While all humans have extremely similar genes in percentage terms, there are distinct differences in each of us that create our particular vulnerabilities and characteristics. We also respond differently to many treatments; a cure for one might be mediocre for another. This is particularly true for cancer. With the Precision Medicine Initiative taking off, taking into account genetics, lifestyle and environment is beginning to give us an edge — making medicine more accurate and effective.

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California researchers opened the world’s largest publicly available stem cell bank Tuesday, which will aid in the search for cures for genetic diseases such as Alzheimer’s, epilepsy and autism.

Universities from around the state will contribute adult skin samples to the bank, while the Buck Institute for Research in Novato will store the material.

The Stem Cell Bank is funded through a $32 million grant awarded in 2013 by the California Institute for Regenerative Medicine, which itself was established in 2004 through voter approval of Proposition 71. That measure provided an initial $3 billion in state bonds to the institute.

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A key mystery of the DNA replication process has been unraveled by researchers from King Abdullah University of Science and Technology (KAUST).

Before a bacterium can divide, it must make a copy of its genetic material, the circular DNA molecules that resemble bunched rubber bands, through a process called DNA replication. In this process, the two strands of DNA making up the circular DNA molecule unwind and separate to become templates for generating new strands.

To ensure the process is well regulated, the bacterium has set a number of “roadblocks,” or termination sites on the DNA, to ensure the permanent stoppage of replication forks, Y-shaped structures formed between the strands as the DNA molecule splits.

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THE genome is written in an alphabet of just four letters. Being able to read, study and compare DNA sequences for humans, and thousands of other species, has become routine. A new technology promises to make it possible to edit genetic information quickly and cheaply. This could correct terrible genetic defects that blight lives. It also heralds the distant prospect of parents building their children to order.

The technology is known as CRISPR-Cas9, or just CRISPR. It involves a piece of RNA, a chemical messenger, designed to target a section of DNA; and an enzyme, called a nuclease, that can snip unwanted genes out and paste new ones in. Other ways of editing DNA exist, but CRISPR holds the promise of doing so with unprecedented simplicity, speed and precision.

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Cancerous melanoma cells, shown with their cell bodies (green) and nuclei (blue), are nestled in tiny hollow lumens (tubes) within the cryogel (red) structure. (credits: Thomas Ferrante, Sidi A. Bencherif / Wyss Institute at Harvard University)

A new biologically inspired “injectable cryogel whole-cell cancer vaccine” combines patient-specific harvested cancer cells and immune-stimulating chemicals or biological molecules to help the body attack cancer. It has been developed by scientists at Harvard’s Wyss Institute and Dana-Farber Cancer Institute.

This new approach is simpler and more economical than other cancer cell transplantation therapies, which harvest tumor cells and then genetically engineer them to trigger immune responses once they are transplanted back into the patient’s body, the researchers say.

Continue reading “Anti-cancer vaccine uses patient’s own cancer cells to trigger immune responses” »

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.

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The left-brain hemisphere of a normal mouse shows the normal level and cellular distribution of the Pax6 gene expression in the developing neocortex. The right-brain hemisphere shows a sustained, primate-like Pax6 expression pattern in the neocortex of a double transgenic mouse embryo. These animals have more Pax6-positive progenitor cells and a higher Pax6 expression level in the germinal layer close to the ventricle in the right hemisphere. (credit: © MPI of Molecular Cell Biology & Genetics)

Researchers at the Max Planck Institute of Molecular Cell Biology and Genetics have created a transgenic mouse in which a gene called Pax6, during embryonic development, is highly expressed in a specific group of brain cortical cells called neural progenitor stem cells (the cells that generate all cells that make up the brain).

The resulting mouse brain generated more neurons than normal and exhibited primate-like features — notably those in the top layer, a characteristic feature of an expanded neocortex.

Continue reading “How to create a genius mouse” »

Wyss Institute scientists believe that synthetic gene drives, if researched responsibly, might be used in the future to render mosquito populations unable to transmit malaria (credit: CDC)

An international group of 26 experts, including prominent genetic engineers and fruit fly geneticists, has unanimously recommended a series of preemptive measures to safeguard gene drive research from accidental (or intentional) release from laboratories.

RNA-guided gene drives are genetic elements — found naturally in the genomes of most of the world’s organisms — that increase the chance of the gene they carry being passed on to all offspring. So they can quickly spread through populations if not controlled.

Continue reading “Move over, autonomous AI weapons, there’s a new risk in town: ‘gene drives’” »

Professor Hyun-Gyu Park of the Department of Chemical and Biomolecular Engineering at Korea Advanced Institute of Science and Technology (KAIST) has developed a technique to analyze various target DNAs using an aptamer, a DNA fragment that can recognize and bind to a specific protein or enzyme. This technique will allow the development of affordable genetic diagnosis for new bacteria or virus, such as Middle Ease Respiratory Syndrome (MERS). The research findings were published in the June issue of Chemical Communications, issued by the Royal Society of Chemistry in the United Kingdom. The paper was selected as a lead article of the journal.

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