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Feature Rescuing the guardian of the genome

P53 is a protein that plays a critical role in preventing cells with DNA damage or other cellular insults from turning cancerous. The protein is mutated in about half of all human cancers. When that happens p53 is unable to fold up into its normal 3D shape, which prevents it from latching onto DNA and sounding the cellular alarm in response to damage. Researchers have long tried to combat cancer by boosting the number of copies of healthy p53 in cells, and a number of drugs that do that remain in human trials. But none has yet made it to market. Now, researchers are making headway on a new approach, finding drugs that prop up mutated p53 and restore its proper shape so that it can once again bind DNA and signal for help. One such drug has already passed an initial human trial and others are on the way. If any succeed, they could change the landscape of cancer therapy and perhaps pave the way for other protein-rescuing drugs to combat protein-misfolding diseases such as Alzheimer's and Parkinson's. Author: Robert F. Service
Source: ScienceNOW - Category: Science Authors: Source Type: news

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Fight Aging! provides a weekly digest of news and commentary for thousands of subscribers interested in the latest longevity science: progress towards the medical control of aging in order to prevent age-related frailty, suffering, and disease, as well as improvements in the present understanding of what works and what doesn't work when it comes to extending healthy life. Expect to see summaries of recent advances in medical research, news from the scientific community, advocacy and fundraising initiatives to help speed work on the repair and reversal of aging, links to online resources, and much more. This content is...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Discussion of advocacy for the cause is a usual feature of our community, as we try things and attempt to make progress in persuading the world that rejuvenation research is plausible, practical, and necessary. There are more people engaged in advocacy now than at any time in the past decade, and so discussions of strategy come up often. New ventures kicked off in 2017 include the Geroscience online magazine, and among the existing ventures the LEAF / Lifespan.io volunteers seem to be hitting their stride. The mainstream media continues to be as much a hindrance as a help, and where it is a help you will usually find Aubre...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Japanese scientist Yoshinori Ohsumi, 71, won the 2016 Nobel Prize on Monday for his research on autophagy ― a metabolic recycling process in which cells eat parts of themselves to survive and stay healthy. His initial work, first started in 1992, focused on the genes behind the autophagy process in yeast cells. Autophagy, however, has implications for several human diseases, including cancer, neurodegenerative diseases, infectious diseases and diabetes. Now drugs that can target the process are being tested in early-stage clinical trials in human beings, which could fundamentally change everything from the way ...
Source: Science - The Huffington Post - Category: Science Source Type: news
In conclusion, our results demonstrate that circulating GDF11 levels are reduced in our mouse model of premature aging, which shares most of the symptoms that occur in normal aging. However, GDF11 protein administration is not sufficient to extend longevity in these progeroid mice. Although accelerated-aging mouse models can serve as powerful tools to test and develop anti-aging therapies common to both physiological and pathological aging, the existence of certain differences between the two processes implies that further investigation is still required to determine whether long-term GDF11 administration has a pro-surviva...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
In conclusion, hTERT expression strictly limits telomerase activation in most of somatic cells, whereas mTERT expression is detectable in most of mouse tissue cells. The interspecies differences between human and mice suggest an improved mouse line, in which both telomerase regulation and telomere length controls are humanized, would considerably benefit the studies of human aging and cancer using mouse models. ON CELLULAR REPROGRAMMING AND CELLULAR REJUVENATION https://www.fightaging.org/archives/2016/07/on-cellular-reprogramming-and-cellular-rejuvenation/ The commentary linked below takes a look at some rece...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
In conclusion, we showed for the first time that 7-KC induces oxidative stress via lysosomal dysfunction, resulting in exacerbation of calcification. CHIMERIC ANTIGEN RECEPTOR CANCER THERAPIES CAN NOW TARGET SOLID TUMORS https://www.fightaging.org/archives/2016/06/chimeric-antigen-receptor-cancer-therapies-can-now-target-solid-tumors/ If the research community is to win in the fight to cure cancer, and win soon enough to matter for all of us, then the focus must be on technology platforms that can be easily and cheaply adapted to many different types of cancer. The biggest strategic problem in the field is tha...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
We examined the engraftment and differentiation of alkaline phosphatase-positive NSCs expanded from the postnatal subventricular zone (SVZ), 3 months after grafting into the intact young or aged rat hippocampus. Graft-derived cells engrafted robustly into both young and aged hippocampi. Although most graft-derived cells pervasively migrated into different hippocampal layers, the graft cores endured and contained graft-derived neurons. The results demonstrate that advanced age of the host at the time of grafting has no major adverse effects on engraftment, migration, and differentiation of grafted subventricular zone...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
This study teaches us that poor wound healing and wrinkling and sagging that occur in aging skin share similar mechanisms." Reduced cell cohesiveness of outgrowths from eccrine sweat glands delays wound closure in elderly skin Human skin heals more slowly in aged vs. young adults, but the mechanism for this delay is unclear. In humans, eccrine sweat glands (ESGs) and hair follicles underlying wounds generate cohesive keratinocyte outgrowths that expand to form the new epidermis. Our results confirm that the outgrowth of cells from ESGs is a major feature of repair in young skin. Strikingly, in aged s...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
This study is the first CAR T-cell trial to infuse patients with an even mixture of two types of T cells (helper and killer cells, which work together to kill cancer). With the assurance that each patient gets the same mixture of cells, the researchers were able to come to conclusions about the effects of administering different doses of cells. In 27 of 29 participants whose responses were evaluated a few weeks after the infusion, a high-sensitivity test could detect no trace of their cancer in their bone marrow. The CAR T cells eliminated cancers anywhere in the body they appeared. Of the two participants who did n...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Thalidomide and its close analogs (lenalidomide and pomalidomide) are widely used to treat a variety of diseases, such as multiple myeloma and other cancers as well as the symptoms of several inflammatory disorders. However, thalidomide is known for its teratogenic adverse effects when first clinically introduced in the 1950s, and is associated with drowsiness and peripheral neuropathy. Hence, there is intense interest to synthesize, identify and develop safer analogs.Researchers at the National Institute on Aging’s Drug Design and Development Section synthesized novel thalidomide analogs that demonstrate clinical po...
Source: NIH OTT Licensing Opportunities - Category: Research Authors: Source Type: research
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