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Category: life extension – Page 675

Entering the Final Days of the SENS Universal Cancer Treatment Fundraiser

For cancer research, meanwhile, the situation is more akin to an economic revolution, or disruptive advance in technology. Because all cancers must lengthen their telomeres, and because telomere lengthening is governed by a small number of processes, there is the opportunity to change the focus of cancer research from an endless procession of expensive new therapies, each targeting a tiny number of the hundreds of subtypes of cancer, to one single therapy that can effectively suppress all cancers.

The last few days have arrived for this year’s SENS Research Foundation crowdfunding campaign, focused on important groundwork to establish a universal therapy for all types of cancer. There are still a few thousand dollars left in the matching fund, so donations are still being matched. Cancer is just as much a part of aging that must be ended, brought completely under control, as all of the other line items in the SENS rejuvenation research portfolio, and this year is the first time that the SENS Research Foundation has run a fundraiser for this program.

Hopefully there is no need to remind the audience here that the SENS Research Foundation, and important ally the Methuselah Foundation, have in recent years achieved great progress in the field of rejuvenation research on the basis of our donations and our support. Some of the high points you’ll find mentioned here and there at Fight Aging!: support and ongoing expansion of the mitochondrial repair technologies now under development at Gensight; seed funding Oisin Biotechnologies for senescent cell clearance; unblocking efforts to clear glucosepane cross-links that stiffen tissues; running the lauded Rejuvenation Biotechnology conferences; and many more. If only all charities produced as great an impact with as few resources — and if only we were further along in the bootstrapping of an industry focused on the development of rejuvenation therapies.

An Investigation of How Telomerase Cancers can Switch to Become ALT Cancers

Traditional cancer research is well funded but ALT cancers are not. SENS Research is aiming to raise funds to address this vital gap in our scientific knowledge. Most scary thing of all is that some regular cancers that abuse telomerase can switch to this ALT method to keep growing when telomerase blocking therapies are used.

The paper I’ll point out today is a timely one, given that the SENS Research Foundation’s fundraiser for early stage work on a therapy for alternative lengthening of telomeres (ALT) cancers is nearing its close. There are still thousands of dollars left in the matching fund, so give it some thought if you haven’t yet donated. The search for ways to safely sabotage ALT is a useful, important line of research because blocking telomere lengthening is a path to a universal cancer therapy, those research groups presently working on it are all looking to achieve this goal by interfering in the activities of telomerase, cancers can switch from using telomerase to using ALT, and next to no-one is working on ways to suppress ALT mechanisms. It seems fairly clear based on the evidence to date that the universal cancer therapy that lies ahead, built by inhibiting telomere lengthening, must involve a blockade of both telomerase and ALT. The open access paper below reinforces this point, the authors investigating how exactly cancers switch from telomerase to ALT to maintain their dangerous growth.

Cancer research today has a grand strategy problem. There is only so much funding and only so many researchers, but hundreds of subtypes of cancer. Therapies tend to be highly specific to the peculiarities of one type of cancer or a small class of cancers, meaning that great expense and time leads to a treatment that is only applicable for a fraction of cancer patients, all too often a tiny fraction. Further, since tumors evolve at great speed, any one individual patient’s cancer may find its way out from under the hammer by changing its signature and mode of operation. All is not doom and gloom, however. Consider that the research community could build a therapy applicable to all cancers with little to no modification, where the cost of development would be no greater than any one of the highly specific therapies presently in use and under development. That therapy would be, of course, based on the blockade of telomere lengthening.

Google’s Antiaging company Calico will use Computational Biology and Machine Learning

Calico, a company focused on aging research and therapeutics, today announced that Daphne Koller, Ph.D., is joining the company as Chief Computing Officer. In this newly created position, Dr. Koller will lead the company’s computational biology efforts. She will build a team focused on developing powerful computational and machine learning tools for analyzing biological and medical data sets. She and her team will work closely with the biological scientists at Calico to design experiments and construct data sets that could provide a deeper understanding into the science of longevity and support the development of new interventions to extend healthy lifespan.

Calico will try to use machine learning to understand the complex biological processes involved in aging.

The Golden Age

I HIGHLY recommend reading this novel, as well as it sequels! It’s a beautiful, smart, and occasionally frightening exploration of what our civilization will look like post singularity, what WE will look like as posthumans, and where we might go from there.

The Golden Age is Grand Space Opera, a large-scale SF adventure novel in the tradition of A. E. Van vogt and Roger Zelazny, with perhaps a bit of Cordwainer Smith enriching the style. It is an astounding story of super science, a thrilling wonder story that recaptures the excitements of SF’s golden age writers.

The Golden Age takes place 10,000 years in the future in our solar system, an interplanetary utopian society filled with immortal humans. Within the frame of a traditional tale-the one rebel who is unhappy in utopia-Wright spins an elaborate plot web filled with suspense and passion.

Phaethon, of Radamanthus House, is attending a glorious party at his family mansion to celebrate the thousand-year anniversary of the High Transcendence. There he meets first an old man who accuses him of being an impostor and then a being from Neptune who claims to be an old friend. The Neptunian tells him that essential parts of his memory were removed and stored by the very government that Phaethon believes to be wholly honorable. It shakes his faith. He is an exile from himself.

Elena Milova speaking in support of OncoSENS crowdfunding campaign

The MMTP has recorded this film in support of SENS Research and their quest to find solutions to ALT cancer.

To support OncoSENS project with a donation click the link:

https://www.lifespan.io/campaigns/sens-control-alt-delete-cancer/

Telomere shortening acts as a biological mechanism for limiting cellular life span. Most cancer cells bypass this failsafe by synthesizing new telomeres using the enzyme telomerase.

Several therapies targeting this well-described telomerase-based pathway are in the advanced stages of clinical development, but as with any cancer therapy there is the potential for development of resistance against telomerase-based strategies to defeat cancer. Studies using mice and human cancer cell lines have demonstrated that cancer can overcome the loss of telomerase by using a telomerase-independent mechanism called Alternative Lengthening of Telomeres (ALT).

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Could an algorithm help to save people’s eyesight? Google thinks so

Google’s artificial intelligence research lab DeepMind is exploring whether its technology could be used to identify early signs of eye diseases that ophthalmologists might not spot.

DeepMind, which was acquired by Google in 2014, has struck an agreement with Moorfields Eye Hospital in London that gives it access to about a million anonymous retinal scans, which it will feed into its artificial intelligence software.

The algorithm will target two of the most common eye diseases: age-related macular degeneration and diabetic retinopathy, which affect more than 100 million people around the world.

Safer Gene Editing Without Cleaving DNA

It’s an add-on for CRISPR.

Researchers have created a new genome editing technique called Target-AID, which induces point mutations instead of cutting DNA

Gene editing technology has fantastic potential, but there are remaining issues and questions over safety and specificity. The major contender is currently CRISPR-Cas9, but this induces a double stranded break in DNA which is a slightly riskier approach — particularly if it cuts in other locations too that you don’t want it to. Research teams across the world are both optimising and customising the CRISPR system; creating more accurate versions or versions that regulate gene expression as opposed to editing it. One such team has now built an add-on to CRISPR, Target-AID.

Uncovering the genetic basis of ALT (Alternative Lengthening of Telomeres) — Harold Silva

Dr Haroldo Silva from SENS talks about ALT cancer in this short film.

As normal cells divide, the ends of their chromosomes (telomeres) progressively shorten until eventually the cells reach senescence or undergo apoptosis. Cancers, which disproportionally kill more individuals in the 65 years or above age group, often overcome this built-in replication limit by expressing the enzyme telomerase.

However, about 10–15% cancers do not use telomerase and at least a major subset of these exhibit hallmarks of Alternative Lengthening of Telomeres (ALT) activity, including long and heterogeneous telomere lengths, presence of ALT-associated PML nuclear bodies (APBs), and generation of high-levels of C-rich circular telomeric DNA repeats (C-circles). Although there are many telomerase-based anti-cancer therapies in clinical development at the moment, research on ALT has not produced any promising therapies so far. This lag is due in part to a lack of assays that are reliable and amenable to high-content/high-throughput (HTS) screens.

The OncoSENS team has made significant progress toward making some of these key ALT assays compatible with the HTS format, which should not only speed up the development of ALT-based anti-cancer therapies but also broaden the amount of research performed on ALT. Our team has already begun applying the assays above to test the involvement of several genes in the ALT pathway and the progress on that front will also be showcased. Undoubtedly, successfully shutting down both ALT- and telomerase-based pathways of telomere maintenance in cancers will move the field forward towards realizing the goal of a complete eradication of one of the main age-related fatal diseases burdening society.

Visit www.sens.org/videos to view the rest of our SENS6 videos.

Continue reading “Uncovering the genetic basis of ALT (Alternative Lengthening of Telomeres) — Harold Silva” | >

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