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Category: biotech/medical

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.

The research, headed by Wyss Core Faculty member David Mooney, Ph.D., was reported online in an open-access paper in Nature Communications on August 12.

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An interesting paper that uses ALA to shore up telomerase activity, loss of telomeres inhibition of P53 expression and mitochondrial dysfunction in one go. They use ALA (alpha lipoic acid) to induce PGC-1α in this case though PGC1-alpha seems to be a potential target for intervention as I understand that ALA is difficult to deliver to cells. In this case this involves the vascular system and atherosclerosis.

http://www.cell.com/cell-reports/abstract/S2211-1247(15)00825-6

Short telomeres and Mitochondrial dysfunction are increasingly implicated as being closely linked as this 2012 Dephino paper demonstrates in the aging heart:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3718635/

“On a mechanistic level, recent reports linking telomere dysfunction to metabolic and mitochondrial compromise provide a novel mechanism as to how dysfunctional telomeres can compromise cardiac function. This telomere-p53-PGC-mitochondrial axis aligns with many changes seen in aged hearts: impaired OXPHOS, decreased ATP generation, and increased ROS levels”

PGC-1α Deficiency Augments Vascular Aging and Atherosclerosis, Coinciding with Telomere Dysfunction and Shortening and DNA Damage through TERT Downregulation.

(A) The aortas from PGC-1α+/+ApoE−/− and PGC-1α−/−ApoE−/− mice (18-month-old males, standard diet, n = 5) were excised for SA-βG staining.

(B) The aortic arch from PGC-1α−/−ApoE−/− and control mice (18-month-old males, n = 5) was dissected for examination of atherosclerotic lesion formation.

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Most cancer-busting strategies focus on removing cancerous cells. While this approach has proved extremely effective on many patients, most treatments have unpleasant side effects and there are many strains which prove extremely challenging to remove. An alternative model to this is to alter instead of remove — fixing cancerous behaviour by ‘reprogramming’ cells that go rogue; essentially swiss finishing school for cellular miscreants. A study published in Nature Cell Biology now provides hope that this tactic could in fact work in many cancers.

Researchers from Mayo Clinic’s Florida campus have found that adhesion proteins, which act like a glue sticking cells together, actually interact with a cell’s ‘microprocessor’. This processor creates molecules called miRNAs, which regulate multiple genes and essentially activate or de-activate different behavioural programs (like commands in computer programming). When healthy cells bump into a neighbour and begin to glue together, these adhesion proteins normally influence both cells — tuning down growth pathways. In cancer, the lab found this adhesion is perturbed; de-regulating miRNA production and enabling rampant growth. When scientists corrected these miRNA levels, the growth was arrested.

“The study brings together two so-far unrelated research fields — cell-to-cell adhesion and miRNA biology — to resolve a long-standing problem about the role of adhesion proteins in cell behavior that was baffling scientists. Most significantly, it uncovers a new strategy for cancer therapy”

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After a wide analysis of evidence, researchers have come up with a number of factors that appear to have the strongest influence on the development of Alzheimer’s disease.

Nearly 17,000 studies, released from 1968 to 2014, were scrutinized and 323 were chosen — covering 93 different risk factors. After collecting the data and grading factors according to their impact strength, researchers came up with a number that had a Grade 1 impact.

So what are they?

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As regenerative medicine expands, our ability to engineer organs is growing with it. Researchers can now grow a number of so called ‘organoids’ — mini-organs which can teach us more about developmental biology and enable vastly improved testing. In the latest addition to the bunch, a team from Ohio State University has successfully engineered the most complete model yet of a human brain, with a similar maturity to a 5 week old fetus.

Containing 99% of the genes present in the human fetal brain, and about the size of an eraser, the organoid was developed from transformed adult human skin. This method could allow more ethical and precise clinical trials, both speeding up and enabling more rigorous, personalized testing. As animal testing frequently fails to predict varied human responses, these organoid models offer an alternative approach which could revolutionize clinical trial methodology.

“It not only looks like the developing brain, its diverse cell types express nearly all genes like a brain. We’ve struggled for a long time trying to solve complex brain disease problems that cause tremendous pain and suffering. The power of this brain model bodes very well for human health because it gives us better and more relevant options to test and develop therapeutics other than rodents.”

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Checkout the latest Longevity Reporter Newsletter (22nd August, 2015), covering this week’s top news in health, aging, longevity.

This week: An Entire Nervous System Captured On Film; 10 Enduring Health Myths, Debunked By Science; Peto’s Paradox: Why Don’t Larger Animals Get Cancer More Often?; Antioxidants: Separating Myth From Reality; And more.

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While billions have now been spent on researching dementia in its various forms, progress is still limited and the underlying triggers are still not clear. The majority of research over the past 30 years has revolved around targeting the amyloid plaques that build up in the disease, but this has resulted in limited success. Is it time to focus resources on other hypotheses instead?

The real problem with tackling these conditions is the sheer complexity of the brain and biology. Research is usually a trial and error process filled with intelligent guesswork, but this means it can often take a great deal of time to establish what’s actually going wrong. The cause or effect conundrum is a significant roadblock in research and working out which aspects drive a disease and which are a result of another malfunction can take serious resources and time. When researchers first began analysing Alzheimer’s patients, perhaps the most obvious feature was the now famous amyloid plaque, but while amyloid may seem like a clear culprit because it’s so clearly out of place, it could easily be a smokescreen; the reason why it appears at all may be far more relevant than the plaque itself.

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