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A new cancer therapy developed by Purdue University researchers attacks tumors by tricking cancer cells into absorbing a snippet of RNA that naturally blocks cell division. As reported in Oncogene, tumors treated with the new therapy did not increase in size over the course of a 21-day study, while untreated tumors tripled in size over the same time period. The paper is tiled “A first-in-class fully modified version of miR-34a with outstanding stability, activity, and anti-tumor efficacy.”

Cancer can begin almost anywhere in the human body. It is characterized by cells that divide uncontrollably and that may be able to ignore signals to die or stop dividing, and even evade the immune system. The therapy, tested in mouse models, combines a delivery system that targets cancer cells with a specially modified version of microRNA-34a, a molecule that acts “like the brakes on a car,” slowing or stopping cell division, said Andrea Kasinski, lead author and the William and Patty Miller Associate Professor of biological sciences at Purdue University.

In addition to slowing or reversing tumor growth, the targeted microRNA-34a strongly suppressed the activity of at least three genes—MET, CD44 and AXL—known to drive cancer and resistance to other cancer therapies, for at least 120 hours. The results indicate that the patent-pending therapy, the newest iteration in more than 15 years of work targeting microRNA to destroy cancer, could be effective on its own and in combination with existing drugs when used against cancers that have built drug resistance.

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More remarkably, the advent of artificial intelligence (AI) and machine learning-based computers in the next century may alter how we relate to ourselves.

Continue reading “Artificial Intelligence: Transforming Healthcare, Cybersecurity, and Communications” »

Applying deep learning to large-scale genomic data of species or populations is providing new opportunities to understand the evolutionary forces that drive genetic diversity. This Review introduces common deep learning architectures and provides comprehensive guidelines to implement deep learning models for population genetic inference. The authors also discuss current opportunities and challenges for deep learning in population genetics.

Strategy using genetically engineered T cells would attack cancer while sparing healthy blood stem cells.

A new technique analysing modern genetic data suggests that pre-humans survived in a group of only 1,280 individuals.

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Naked mole rats are rodents that are about the size of a mouse with a key difference, aside from having no fur — they’re extremely long-lived — reaching ages of around 40 years old. For comparison, lab mice live an average of about three and a half years. To explain their extensive lifespans, researchers have sought to pinpoint how naked mole rats evade the onset of age-related diseases like cancer. In doing so, they’ve identified a form of gelatinous substance called hyaluronan, which has anti-inflammatory and anticancer properties. Now, the question of whether the benefits of the naked mole rat’s abundant levels of this form of hyaluronan — called high molecular mass hyaluronic acid (HMM-HA) — can be exported to other species has recently drawn attention.

Published in Nature, Gorbunova and colleagues from the University of Rochester show that genetically modifying mice to harbor an enzyme that produces HMM-HA extends their lifespan. The researchers go on to show that increasing HMM-HA reduces the prevalence of cancer. Additionally, the nmrHAS2 gene improves the healthspan of mice by countering physiological dysfunction, as measured with a frailty score. These findings provide the first evidence that genes from long-lived species can be exported to other species, perhaps conferring benefits to humans one day.

Plants possess the unique ability to completely regenerate from a somatic cell, i.e., an ordinary cell that does not typically participate in reproduction. This process involves the de novo (or new) formation of a shoot apical meristem (SAM) that gives rise to lateral organs, which are key for the plant’s reconstruction.

On a cellular scale, the formation of SAM is meticulously controlled by either positive or negative regulators (genes/protein molecules) that may induce or restrict shoot regeneration, respectively. But which molecules are involved? Are there other regulatory layers that are yet to be uncovered?

To seek answers to the above questions, a research group led by Nara Institute of Science and Technology (NAIST), Japan studied the process in Arabidopsis, a plant commonly used in genetic research.

In this article, the fourth installment of our five-part series on different pathways of aging, we look at the rejuvenation of cells, tissues, and stem cells, a topic that has been gaining increasing popularity thanks to remarkable advancements in the field of epigenetic reprogramming. Recent research suggests that despite the accumulation of molecular damage over time, cells and tissues can indeed undergo rejuvenation. We’ll be exploring key subjects such as Epigenetic reprogramming, PGC1a and GSK3β, Telomerase (TERT), as well as Apoptosis and senescence. Join us on this enlightening journey as we uncover the groundbreaking discoveries that are shaping the future of aging research.

The idea for reprogramming was simple yet beautiful. Children are born young, even though their parents are old, because they have undergone a process of cellular reprogramming that leads to rejuvenation.