Category Archives: Florida Stem Cells

NAPLES, Fla., Jan. 29, 2021 /PRNewswire/ -- HealthLynked Corp. (OTCQB: HLYK), a global healthcare network focused on care management of its members and a provider of healthcare technologies that connects doctors, patients and medical data, today announced that it will host the first annual Future of Healthcare Summit that will convene the top leaders in the $5 trillion healthcare industry at Arthrex's corporate campus that features a 30,000-SF fitness center and 200,000-SF Innovation Hotelin Naples, Florida from March 15-17th.

The summit is an invitation only event for healthcare providers. The event features world-class CEOs, innovators and industry experts who will come together to present a series of lectures on a wide range of healthcare topics and explore what can be done to both catalyze innovation and improve healthcare.

Dr. Michael Dent, HealthLynked's CEO has developed an agenda that focuses on genomics, functional medicine, anti-aging, stem cells, artificial intelligence, diagnostic advances, telemedicine, intellectual property, tissue regeneration, cancer treatments and medical devices.

The summit venue will be open to the public on Tuesday, March 16th, where a series of Ted Talk style lectures will cover the latest healthcare trends, technology, and treatments. This open forum will allow the public the opportunity to learn about the latest advances in healthcare and how they are being applied today and what to expect in future.

HealthLynked has confirmed a world-class slate of speakers including:

Attendees of the summit include doctors, hospital executives, academics, researchers, venture capitalists, pharmaceutical firms, policymakers, philanthropists, and future leaders. The seating for the summit will follow COVID-19 spacing guidelines and Arthrex campus facilities are equipped with Synexisair purification systems that kill airborne COVID-19 to add an additional layer of safety for the attendees.

For a look at the full agenda, as well as speaker bios, please visit the 2021 Healthcare Summitwebsite. For additional sponsorship opportunities please email [emailprotected].

Dr. Michael Dent, Chief Executive Officer of HealthLynked stated, "The next 15 years will bring a wave of medical breakthroughs in new therapies, medicines, medical devices and data analytics. We have achieved new milestones in gene editing, cancer immunotherapy and artificial intelligence. All of these advances will allow us to more effectively treat disease and find cures that have eluded us. Our goal is to provide an informative series of lectures to show the future of healthcare and create an environment for innovate thought leaders to turn ideas into actionable solutions."

About HealthLynked Corp.

HealthLynked Corp. provides a solution for both patient members and providers to improve healthcare through the efficient exchange of medical information. The HealthLynked Network is a cloud-based platform that allows members to connect with their healthcare providers and take more control of their healthcare. Members enter their medical information, including medications, allergies, past surgeries and personal health records, in one convenient online and secure location, free of charge. Participating healthcare providers can connect with their current and future patients through the system. Benefits to in-network providers include the ability to utilize the HealthLynked patent pending patient access hub "PAH" for patient analytics. Other benefits for preferred providers include HLYK marketing tools to connect with their active and inactive patients to improve patient retention, access more accurate and current patient information, provide more efficient online scheduling and to fill last minute cancelations using the Company's "real time appointment scheduling" all within its mobile application. Preferred providers pay a monthly fee to access these HealthLynked services. For additional information about HealthLynked Corp., please visit http://www.healthlynked.com and connect with HealthLynked on Twitter, Facebook, and LinkedIn.

Forward Looking Statements

Forward-Looking Statements in this press release, which are not historical facts, are forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Our actual results, including as a result of any acquisitions, performance or achievements may differ materially from those expressed or implied by these forward-looking statements. In some cases, you can identify forward-looking statements by the use of words such as "may," "could," "expect," "intend," "plan," "seek," "anticipate," "believe," "estimate," "predict," "potential," "continue," "likely," "will," "would" and variations of these terms and similar expressions, or the negative of these terms or similar expressions. Such forward-looking statements are necessarily based upon estimates and assumptions that, while considered reasonable by our management, and us are inherently uncertain. We caution you not to place undue reliance on any forward-looking statements, which are made as of the date of this press release. We undertake no obligation to update publicly any of these forward-looking statements to reflect actual results, new information or future events, changes in assumptions or changes in other factors affecting forward looking statements, except to the extent required by applicable laws. If we update one or more forward-looking statements, no inference should be drawn that we will make additional updates with respect to those or other forward-looking statements. Certain risks and uncertainties applicable to our operations and us are described in the "Risk Factors" section of our most recent Annual Report on Form 10-K and in other filings we have made with the U.S. Securities and Exchange Commission. These reports are publicly available at http://www.sec.gov.

Contacts:

George O'Leary Chief Financial Officer [emailprotected] (800) 928-7144, ext. 103

Investor Relations Contacts:

Jim HockHanover International Inc.[emailprotected]760-564-7400

SOURCE HealthLynked Corp.

Continue reading here:
HealthLynked's The Future of Healthcare Summit Brings Healthcare Experts and Technology Innovators from Around the World to Naples, Florida -...

(Photo: Bill Ingalls/NASA via Getty Images)CAPE CANAVERAL, FL - JUNE 03: In this handout provided by the National Aeronautics and Space Administration (NASA), the SpaceX Falcon 9 rocket, with the Dragon spacecraft onboard, launches from pad 39A at NASA's Kennedy Space Center on June 3, 2017, in Cape Canaveral, Florida. Dragon is carrying almost 6,000 pounds of science research, crew supplies, and hardware to the International Space Station in support of the Expedition 52 and 53 crew members.

The National Aeronautics and Space Administration (NASA) has confirmed that on January 11, Elon Musk's SpaceX Cargo Dragon would return to Earth from the International Space Station (ISS). The said spacecraft is bringing orbital science analysis observations and other items.

Cargo Dragon embarked on a SpaceX Falcon 9 onDecember 7and landed at the ISS with at least 6,400 pounds of hardware, research samples, and crew supplies roughly 24 hours later.

In apress release, NASA said the spacecraft would make parachute-assisted water landing in the Atlantic Ocean off Florida's coast about 9:00 pm EST. NASA will broadcast the flight and landing live on theirwebsite.

(Photo: Paolo Nespoli - ESA/NASA via Getty Images)IN SPACE - MAY 23: In this handout image provided by the European Space Agency (ESA) and NASA, the International Space Station and the docked space shuttle Endeavour orbit Earth during Endeavour's final sortie on May 23, 2011, in Space.

Some of the scientific investigations Dragon will return to Earth include:

Microgravity induces modifications in the human heart's function and shape, and it is still unclear if these changes will become permanent if an individual stayed in space for more than a year. Using 3D-engineered cardiac tissues, a form of tissue chip, Cardinal Heartstudieshow variations in gravity influence cardiovascular cells at the cellular and tissue stage. The findings could include a new view of Earth's cardiac diseases, help detect new therapies, and facilitate the creation of cardiovascular risk prediction screening measures before spaceflight.

This Japan Aerospace Exploration Agency (JAXA) study shows human stem cell 3D organ buds' development to examine gene expression improvements. To attain 3D growth, cell cultures on Earth require supporting materials or powers. Still, without such instruments, cell cultures may extend into three dimensions in microgravity. The findings of this study could reveal the benefits of utilizing microgravity for state-of-the-art advances in regenerative medicine and could lead to the advancement of the technology required to manufacture artificial organs.

Return to Earth would be the sextant used in theSextant Navigationresearch. Sextants have a tiny telescope-like optical sight to take exact angles across pairs of stars from land or sea. It allows movement without mechanical aids. For decades, travelers have navigated through sextants, and NASA's Gemini missions performed the first spacecraft sextant sightings. This investigation evaluated basic methods for using a sextant for disaster management on satellites such as NASA's Orion, which would bring humans on deep-space flights.

The role of lungs, nerves, and lymphatic systems in the eye and improvements in mice's retina before and after spaceflight was observed in this experiment. The goal is to understand why visual perception is affected by these improvements. On long-duration space missions, at least 40 percent of astronauts suffer visual disorder known as Spaceflight-Associated Neuro-ocular Syndrome (SANS), which could negatively impact mission performance.

Using dynamically heated and cooled amine beds, thistechnologytested a process to extract carbon dioxide (CO2) from the air aboard the International Space Station. Controlling the station's CO2 levels decreases crew members' risk of developing CO2 buildup effects, including nausea, headache, trouble breathing, strained eyes, and itchy hands.

In microgravity, bacteria and other microorganisms have grown as biofilm populations. Thisexperimentdescribes the bacterial genes used during biofilms development and investigates whether stainless steel can be corroded by these biofilms, and assess a silver-based disinfectant's efficacy. This research could offer insight into better methods of managing and eliminating resistant biofilms, leading to potential space flights of long duration.

ALSO READ: SpaceX to Reuse Dragon Spacecraft Fleet After Rocket Booster from NASA Crew-1 'Leaned'

Check out more news and information on SpaceX on Science Times.

More:
SpaceX Cargo Dragon Returning To Earth; First U.S. Commercial Cargo Craft To Return From ISS - Science Times

David Montefiori, a Duke University virologist who is beginning to test the effectiveness of both vaccines against the British strain with help from Weissman, was also encouraged. Nonetheless, he said the Pfizer-BioNTech study was somewhat limited because it only focused on one mutation.

The British strain, he explained, has eight mutations on the spike protein the part of the coronavirus that the pathogen uses to invade a cell that distinguish it from the dominant virus in the pandemic. The same is true of the South African variant, although some mutations differ between the two.

The mutation [Pfizer-BioNTech] studied ... is the one scientists were most concerned about because of where it is located on the Spike protein, Montefiori said in an e-mail. However, it is important to get a more definitive answer with the complete variant containing all 8 mutations.

Montefiori and Weissman are studying how effective both vaccines are against the complete British variant, Montefiori said. Researchers at the National Institute for Communicable Diseases in South Africa are doing the same with the strain that emerged in their country, he added. Montefiori hoped results would be released within a couple of weeks.

The Pfizer-BioNTech findings appeared on a pre-print server and have yet to be subjected to peer review. They indicate the key mutation in both strains does not create resistance to the immune response stimulated by the Pfizer vaccine, according to a statement by the partnership.

The companies and the University of Texas Medical Branch, which participated in the study, acknowledged more research is needed to determine if the vaccine protects recipients against the two new strains.

Researchers used blood samples taken from 20 people who were vaccinated in Pfizer-BioNTechs late-stage clinical study, and mixed them with the virus containing the key mutation.

The new coronavirus variants have rattled people around the world.

The website of the Centers for Disease Control and Prevention identifies three coronavirus variations from the dominant strain: one first detected in September and now highly prevalent in London and southeast England; another first detected in October in South Africa; and a third recently isolated in Nigeria.

There is no evidence that the three variants cause more severe illness, according to the CDC, but they have led to tighter restrictions.

Prime Minister Boris Johnson on Monday announced a new national lockdown for England until at least mid-February to combat the new variant. He said people must stay home, as they were ordered to do so in the first wave of the pandemic in March, because the new strain was spreading in a frustrating and alarming way.

The British variant has been detected in parts of the United States, including California, Colorado, Connecticut, Florida, Georgia and New York. Governor Charlie Baker on Tuesday urged residents to redouble their efforts to control the spread of the coronavirus based on the assumption that the British strain has arrived in Massachusetts, although public health officials have not confirmed that.

The South African strain has not been detected in the United States. But Dr. Scott Gottlieb, the former head of the Food and Drug Administration in the Trump administration, said in an interview on CNBC on Tuesday that it appears to be prevalent in South America and he was worried that it will soon spread in the United States. He also said current medical treatments might not work as well against it, making vaccinations more urgent than ever.

The World Health Organization said Tuesday that the strain in the United Kingdom has been detected in a small number of cases in 40 other countries and areas and that the South African variant has been found in six other countries and areas.

The Pfizer-BioNTech and Moderna vaccines were about 95 percent effective at preventing the dominant strain of COVID-19 in large late-stage clinical trials, according to data released by the FDA. Each vaccine requires two shots a few weeks apart.

Weissman, an immunologist with a medical degree and PhD from Boston University whose lab licensed messenger RNA technology used by both vaccines, had already been optimistic that they would prove effective against new variants.

His reason: The coronavirus strain that has locked down much of the world for the past 10 months, he said, is actually a mutation of the original virus first identified in Wuhan, China, last December. The Moderna and Pfizer vaccines were custom-made to prevent the Wuhan strain, he added, but demonstrated even better results against the second coronavirus strain, according to a recently published study he co-authored with Montefiori and other researchers in the journal Cell Host & Microbe.

Im pretty confident they will be effective against the latest variants, Weissman, 61, told the Globe earlier this week. The spike [protein] is a very big protein, and it has many regions that antibodies can neutralize, so the mutations might affect a few small areas, but theyre not going to change the entire protein to make it resistant.

The Pfizer and Moderna vaccines rely on synthetic messenger RNA -- technology that Weissman has worked on for about 25 years -- to instruct cells to build the spike protein after people are vaccinated. When cells make the distinctive protein, it stimulates an immune response that protects people from the virus.

The emergence of new coronavirus strains comes as no surprise to scientists. When a virus replicates itself inside a cell that it has infected, the copies often have small differences because of errors, and those errors can lead to mutant strains. People get influenza shots every year because new variants emerge after such errors.

The coronavirus replication enzymes are less prone to errors than those of viruses like influenza virus, but still quite prone to errors, Pfizer said in a statement this week.

Ray Jordan, a Moderna spokesman, said his company is also testing its vaccine against several variants, but he had no details.

Weissman has studied messenger RNA since the 1990s with Katalin Kariko, a colleague at Penn who joined BioNTech, Pfizers German partner, in 2013 as senior vice president. After years of trial and error, they figured out a way to create a form of messenger RNA that could sneak its way into cells without being destroyed by the bodys natural defenses.

Derrick Rossi, a stem cell biologist who helped found Moderna in 2010, recently told the Globe that he believes the groundbreaking work of Kariko and Weissman deserves the Nobel Prize in chemistry.

Weissman, whose laboratory has developed a potential COVID-19 vaccine for the government of Thailand, said he would worry about new strains if they proved more deadly. But that hasnt happened where they have spread.

COVID-19 has caused more than 366,000 deaths in the United States, and the mortality rate is averaging under 2 percent.

If the mortality rate suddenly increased to 10 percent [as a result of new strains], thats a big problem, Weissman said.

Jonathan Saltzman can be reached at jonathan.saltzman@globe.com.

Continued here:
Buoyed by study, scientists increasingly hopeful first two COVID-19 vaccines effective against new strains - The Boston Globe

TAMPA, Fla. While health officials and lawmakers continue trying to steer young people away from vaping, the wide variety of enticing flavors added to these products make that a tough task. Although most of the worry over vaping comes from the risk of addiction, lung damage, and threat of switching to conventional cigarettes, a new study finds the flavoring chemicals these products use may be just as harmful as anything else. Researchers from the University of South Florida Health say vaporized flavoring molecules are toxic to the heart and damage the organs ability to beat correctly.

While other studies find that vaping is generally less harmful than smoking traditional tobacco products, the nicotine and other chemicals in e-cigarettes still damages the heart and lungs. Until now however, researchers say the impact of flavoring additives inhaled into the bloodstream remained unclear.

The flavored electronic nicotine delivery systems widely popular among teens and young adults are not harm-free, says principal investigator Dr. Sami Noujaim in a university release. Altogether, our findings in the cells and mice indicate that vaping does interfere with the normal functioning of the heart and can potentially lead to cardiac rhythm disturbances.

Dr. Noujaims study is one of the first to investigate the cardiotoxic effects of flavoring chemicals added to the e-liquids in electronic nicotine delivery systems (ENDS). ENDS include a variety of different vaping products like vape pens, mods, and pods.

Researchers define vaping as inhaling aerosols (tiny droplets) which e-cigarettes create by heating liquid nicotine and solvents like propylene glycol and vegetable glycerin. A vaping devices battery-powered heater converts this liquid into a smoke-like mix, or vapor.

The study tested how three popular e-liquid flavors fruit, cinnamon, and vanilla custard affect cardiac muscle cells (HL-1) of mice. After being exposed to e-vapor in a lab dish, the results reveal all three flavors are toxic to HL-1 cells.

The USF team also examined what happens to cardiac cells grown from human stem cells that are exposed to three types of e-vapors. The first substance containing only solvents interfered with the cells electrical activity and beating rate. The second substance, containing both nicotine and solvents, proved to be even more toxic to the heart cells.

The third substance however, containing nicotine, solvents, and vanilla custard flavoring, caused the most damage to the heart and its ability to spontaneously beat correctly. Researchers also determined that vanilla custard flavoring is the most toxic of the varieties tested.

This experiment told us that the flavoring chemicals added to vaping devices can increase harm beyond what the nicotine alone can do, Dr. Noujaim says.

The study also tested flavored vapings impact on live mice. Researchers implanted each subject with a tiny electrocardiogram device before exposing them to 60 puffs of vanilla-flavored e-vapor five days a week for 10 weeks.

Study authors looked at how this exposure impacted heart rate variability (HRV), which is the change in time intervals between successive heartbeats. The results show that HRV decreased in vaping mice compared to those only exposed to puffs of clean air.

The USF team finds vaping interferes with normal HRV by disrupting the autonomic nervous system and its control over heart rate. Mice exposed to flavored vaping are also more prone to a dangerous heart rhythm problem called ventricular tachycardia.

Researchers say they still have to confirm these results in humans. Dr. Noujaim urges policymakers to continue looking at the growing evidence that vaping is not a particularly safer alternative to smoking.

Our research matters because regulation of the vaping industry is a work in progress, Dr. Noujaim explains. The FDA needs input from the scientific community about all the possible risks of vaping in order to effectively regulate electronic nicotine delivery systems and protect the publics health. At USF Health, in particular, we will continue to examine how vaping may adversely affect cardiac health.

The study appears in the American Journal of Physiology- Heart and Circulatory Physiology.

Read more from the original source:
Flavors added to vaping devices damage the heart, vanilla custard the most toxic of all - Study Finds

New York, Dec 12 (IANS) Researchers have revealed the appealing array of fruit and candy flavours that entice millions of young people to take up vaping are cardiotoxic and disrupt the heart's normal electrical activity.

Mounting studies indicate that the nicotine and other chemicals delivered by vaping, while generally less toxic than conventional cigarettes, can damage the lungs and heart.

"But so far there has been no clear understanding about what happens when the vaporized flavouring molecules in flavoured vaping products, after being inhaled, enter the bloodstream and reach the heart," said study author Sami Noujaim from the University of South Florida in the US.

In the study, published in the American Journal of Physiology-Heart and Circulatory Physiology, the research team reported on a series of experiments assessing the toxicity of vape flavourings in cardiac cells and in young mice.

The flavoured electronic nicotine delivery systems widely popular among teens and young adults are not harm-free.

"Altogether, our findings in the cells and mice indicate that vaping does interfere with the normal functioning of the heart and can potentially lead to cardiac rhythm disturbances," Noujaim said.

In mouse cardiac muscle cells (HL-1 cells), the researchers tested the toxicity of three different popular flavours of e-liquid: fruit flavour, cinnamon, and vanilla custard.

All three were toxic to HL-1 cells exposed to e-vapour bubbled into the laboratory dish where the cells were cultured.

Cardiac cells derived from human pluripotent stem cells were exposed to three distinct e-vapours.

The first e-vapour containing the only solvent interfered with the electrical activity and beating rate of cardiac cells in the dish. A second e-vapour with nicotine added to the solvent increased the toxic effects on these cells.

The third e-vapour comprised of nicotine, solvent, and vanilla custard flavouring (the flavour previously identified as most toxic) augmented damage to the spontaneously beating cells even more.

"This experiment told us that the flavouring chemicals added to vaping devices can increase harm beyond what the nicotine alone can do," Noujaim said.

The findings showed that mice exposed to vaping were more prone to an abnormal and dangerous heart rhythm disturbance known as ventricular tachycardia compared to control mice.

"Our research matters because regulation of the vaping industry is a work in progress," Noujaim noted.

--IANS

bu/bg

Read more:
Flavours added to vaping devices can damage the heart: Study - Sify News

More than 300 of your friends and neighbors have already been vaccinated against the novel coronavirus.

They are volunteers in vaccine trials taking place in a DeLand lab, one of only two sites in the country testing vaccines from multiple drug companies.

The work ongoing at Accel Clinical Research has put DeLand on the map in the fight against COVID-19.

Both companies, Moderna and Pfizer, picked 90 sites. We ended up being chosen by both, Accel Medical Director Dr. Bruce Rankin told The Beacon.

Two groups of volunteers are now taking part in the vaccine trials.

Weve done vaccine trials for over 20 years. I was surprised to get two companies, Rankin said.

A third biotech firm, Novavax, is also eyeing Accel for possible trials of its COVID-19 vaccine, and Rankin said other companies have contacted him about trying their vaccines at the DeLand research site.

Were going to be busy for several months, Rankin said.

In conversations with The Beacon, Rankin described his role in the research.

The Beacon: Dr. Rankin, as we near the end of summer 2020, what is the status of the Accel clinical trials of a COVID-19 vaccine?

Dr. Bruce Rankin: We already have over 300 participants vaccinated to date. We started in the last two days of July. We are choosing over 2,000 participants all over Central Florida.

We are looking for high-risk participants, and they will include people over 65. Were looking for people with health conditions such as COPD or asthma, and the essential workers, like the first responders and health care workers. We also have those related to the essential workers. Were having mothers. I have a mom whose husband is an ER doctor, and she thinks she may get it.

Were looking for minorities, ethnic groups, especially Blacks and Hispanics. The trials are geared for having a certain number of Blacks and Hispanics.

We need about 3,000 volunteers from all over Central Florida for the vaccine trials.

There are over 14 vaccine trials now going on in this country.

For more information, contact Accel Clinical Research:

http://www.covidorlando.com

386-785-2400

Beacon: How does the vaccine research work?

Rankin: Its a blinded randomization study, like flipping a coin. Half get the vaccine, and half get a placebo. We do not know. We do not want any bias in the studies.

There is a computer program that randomizes people. Everything is kept separate. None of the study staff knows who is getting what. That keeps the bias out of the studies. There is a very strict protocol that we have to follow on who is getting the vaccine.

Those who come in get a first shot. The second shot comes about three weeks after.

Beacon: What sort of commitment are the volunteers making?

Rankin: People are signing up and committing to be followed for 24 months. Were going to be following them to see if they come down with the virus. If they have COVID-like symptoms, they will be tested for the virus.

They have an app on their smartphones, and they have to inform us if they have any reaction to the first dose or the second dose, and thats uploaded to us.

Beacon: Do the study volunteers receive any compensation?

Rankin: Its around $1,000 compensation for time and travel. People interested in participating in the vaccine trials may go to http://www.covidorlando.com for more information. They may also call Accel at 386-785-2400.

Each participant must read and sign an informed consent explaining the entire study process prior to beginning the study.

Beacon: Can you say if there will be any side effects?

Rankin: There may be mild to moderate symptoms, like muscle soreness and low-grade fever.

There is no way you can catch the coronavirus virus from the new vaccine. We dont use attenuated viruses.

Beacon: What is in the vaccine, and how is it made?

Rankin: Its called mRNA little m RNA. The m stands for messenger,

RNA, ribonucleic acid, produces the proteins that are identical to the proteins in the coronavirus. That is called an antigen. Were injecting mRNA. Its in the protein chain that is produced in the lab from basic amino acid, the basic building block of protein.

It goes into the cells, and the body sees those spikelike projections, and it produces antibodies against the virus. The virus needs those spikes, because that is how it attaches itself to cells in the body. The antibodies are in the bloodstream.

The early studies are showing it takes 14 days to produce the antibodies.

Were doing the booster shot at three weeks, and antibody levels are higher than for those who have had the infection.

Beacon: Some people are concerned about reports they have heard or read that say the vaccines are developed from aborted human fetuses, and this poses a moral dilemma. Are fetal tissue or stem cells used to make these vaccines?

Rankin: No. There is nothing in this that came from aborted fetuses. It is an amino acid that is produced in the lab. There is no fetal tissue.

Beacon: Do we know if the vaccines give lifetime immunity against the coronavirus?

Rankin: We dont know how long the antibodies last. How long are you protected? We dont know. We may have to get booster shots in the future.

Beacon: Meanwhile, are masks really effective in combating the spread of the disease?

Rankin: Even if theyre 30 percent effective, it will help stop the spread. Masks help the asymptomatic patients from spreading the particles. Masks have been effective in slowing the transmission and the spread of the disease.

Beacon: If a coronavirus vaccine is determined to be effective and receives the endorsement of the U.S. Food and Drug Administration, do you foresee mass-vaccination events similar to those in the 1950s when polio was rampant?

Rankin: I think there will be strategically set-up vaccination centers. I see vaccination sites being set up, with people coming in for vaccinations.

If it is something effective, we want to vaccinate the public.

See the article here:
Jabbed for a good cause: Hundreds already getting COVID-19 shots as part of clinical trial - The West Volusia Beacon

ORLANDO, Fla.--(BUSINESS WIRE)--Hesperos Inc., pioneers of the Human-on-a-Chip in vitro system, today announced the publication of a new peer-reviewed publication that describes how the companys technology can be used to investigate immune responses following treatment with biological therapeutics for multi-organ systemic diseases, including cancer, infectious diseases and inflammatory disorders. The study was part of a collaboration between Hesperos, Hoffman-La Roche Pharmaceuticals and the University of Central Florida. The manuscript, titled Differential Monocyte Actuation in a Three-Organ Functional Innate Immune System-on-a-Chip, was published today in the prestigious journal Advanced Science. Click here to view a multimedia version of the press release, including media-ready images, downloadable resources, and more.

The immune system plays an important role in coordinating with other organ systems to combat infection, eliminate damaged cells and repair tissue. However, modeling immune response following drug treatment in preclinical studies is challenging due to poor predictability, especially for the innate portion of the system. As the scientific community begins to turn more towards using multi-organ, human-on-a-chip systems as a cost-effective way to increase efficiency and lower toxicity, many of these models lack a systemic immune component.

Hesperos, in collaboration with Hoffmann-La Roche Pharmaceuticals, describe an in vitro, pumpless, three-organ system containing functional human cardiomyocytes, skeletal muscle and hepatocytes in a serum-free medium, along with recirculating human monocyte THP-1 immune cells. Monocytes are a vital immune system cells involved in wound healing, pathogen clearance and activation of the innate immune response, but are also responsible for the cytokine storm found in conditions such as sepsis.

One application where the immune-system-on-a-chip can be immediately useful is for uncovering how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) directly affects multi-organ systems by activating the cytokine storm from inflammatory macrophages and to support the rapid development of therapeutics. As the global pandemic of COVID-19 continues to grow, this system has the potential to quickly evaluate antiviral and repurposed drugs to help combat this devastating disease, said Michael L. Shuler, Ph.D., Chief Executive Officer of Hesperos.

In the study, the researchers evaluated two different innate immune responses: 1) targeted immune response following tissue-specific damage, which simulates indirect activation of THP-1 cells and, 2) pro-inflammatory immune response following direct activation of immune cells, mimicking acute inflammation and the cytokine storm. Though not reported in this study, Hesperos has also shown that peripheral blood mononuclear cells (PBMCs) and T-cells are sustainable in these multi-organs systems, which would allow some aspects of adaptive immunity to also be modeled.

In the targeted immune response experiments, the cardiotoxic compound amiodarone was used to selectively damage cardiac cells to evaluate how THP-1 immune cells affect the three-organ system. The presence of both amiodarone and THP-1 immune cells led to a more pronounced reduction in cardiac force, conduction velocity and beat frequency compared to amiodarone alone. THP-1 cells were also found to infiltrate the damaged cardiomyocytes and induce significantly increased cytokine IL-6 expression, indicating an M2 macrophage phenotype. No immune-activated damage was reported in the skeletal muscle or liver cells.

The most striking features of our immune-system-on-a-chip is that it emulates different immune reactions for direct tissue-damage and acute inflammation, as well as distinguishes between M1 vs. M2 macrophage phenotypes, said James Hickman, Ph.D., Chief Scientist at Hesperos and Professor at the University of Central Florida.

The study was initially funded by Roche Pharmaceuticals and completed under an NIH grant from National Center for Advancing Translational Sciences (NCATS) Small Business Innovation Research program, which supports studies to advance tissue chip technology toward commercialization.

Tissue chips are a promising technology for accelerating the preclinical timeline and getting treatments to patients more efficiently, said Danilo A. Tagle, Ph.D., associate director for special initiatives at NCATS. Finding improved ways to study immune responses has tremendous implications for drug discovery and the development of more effective personalized medicines in diseases that affect multiple organ systems.

In the pro-inflammatory response experiments, the three-organ system was exposed to lipopolysaccharide (LPS) and interferon gamma (IFN-) to stimulate acute inflammation/cytokine storm and provoke monocyte differentiation and activation. In the absence of THP-1 immune cells, LPS/IFN- treatment had no significant effect on function of the three-organ system. However, with the addition of THP-1 immune cells, LPS/IFN- treatment caused cellular damage to all three-organ components, including THP-1 cell infiltration in liver tissue, and led to significant alterations in cardiac force and beat frequency, as well as skeletal muscle force. Additionally, there was an upregulation of pro-inflammatory cytokines, including TNF-, IL-6 and IL-10, indicating an M1 macrophage phenotype, which is analogous to the cytokine storm found during certain reactions to biologic therapeutics and emulates what occurs during sepsis.

To read the full manuscript, please visit https://doi.org/10.1002/advs.202000323.

About Hesperos

Hesperos, Inc. is a leader in efforts to characterize an individuals biology with Human-on-a-Chip microfluidic systems. Founders Michael L. Shuler and James J. Hickman have been at the forefront of every major scientific discovery in this realm, from individual organ-on-a-chip constructs to fully functional, interconnected multi-organ systems. With a mission to revolutionize toxicology testing as well as efficacy evaluation for drug discovery, the company has created pumpless platforms with serum-free cellular mediums that allow multi-organ system communication and integrated computational PKPD modeling of live physiological responses utilizing functional readouts from neurons, cardiac, muscle, barrier tissues and neuromuscular junctions as well as responses from liver, pancreas and barrier tissues. Created from human stem cells, the fully human systems are the first in vitro solutions that accurately utilize these platforms to predict in vivo functions without the use of animal models, as featured in Science. More information is available at https://hesperosinc.com

Hesperos and Human-on-a-Chip are trademarks of Hesperos Inc. All other brands may be trademarks of their respective holders.

Read this article:
Hesperos demonstrates innovative Human-on-a-Chip approach to modeling innate immune system response following tissue damage and acute inflammation -...

-- Peer-reviewed publication in Alzheimer's & Dementia: Translational Research & Clinical Interventions validates potential of drug discovery platform and ability to study early stages of disease pathology --

Hesperos Inc., pioneers of the Human-on-a-Chip in vitro system, today announced a new peer-reviewed publication that describes how the companys functional Human-on-a-Chip system can be used as a drug discovery platform to identify therapeutic interventions targeting the preclinical stages of Alzheimers disease (AD) and mild cognitive impairment (MCI). The manuscript, titled "A human induced pluripotent stem cell-derived cortical neuron human-on-a-chip system to study A42 and tau-induced pathophysiological effects on long-term potentiation," was published this week in Alzheimer's & Dementia: Translational Research & Clinical Interventions. The work was conducted in collaboration with the University of Central Florida and with David G. Morgan, Ph.D., Professor of Translational Neuroscience at Michigan State University, and expert in AD pathology.

To date, more than 100 potential therapeutics in development for AD have been abandoned or failed during clinical trials. These therapeutics relied on research conducted in preclinical animal studies, which often are unable to accurately capture the full spectrum of the human disease phenotype, including differences in drug metabolism and excretion between humans and animals. Therefore, there is a need for human models, especially those that accurately recapitulate the functional impairments during the preclinical phases of AD and MCI.

"Hesperos offers a breakthrough technology that provides a human cell-based assay based on cognitive function metrics to evaluate drugs designed to restore cognition at early stages of the Alzheimers continuum," said Dr. Morgan. "This system can serve as a novel drug discovery platform to identify compounds that rescue or alleviate the initial neuronal deficits caused by A1-42 and/or tau oligomers, which is a main focus of clinical trials."

In 2018, Hesperos received a Phase I Small Business Innovation Research (SBIR) grant from the National Institute on Aging (NIA) division within the US National Institutes of Health (NIH) to help create a new multi-organ human-on-a-chip model for testing AD drugs. Research conducted under this grant included a study to assess therapeutic interventions based on functional changes in neurons, not neuronal death.

In the recent Alzheimer's & Dementia publication, Hesperos describes its in vitro human induced pluripotent stem cell (iPSC)-derived cortical neuron human-on-a-chip system for the evaluation of neuron morphology and function after exposure to toxic A and tau oligomers as well as brain extracts from AD transgenic mouse models.

"Researchers are now focusing on biomarker development and therapeutic intervention before symptoms arise in AD and MCI," said James Hickman, Ph.D., Chief Scientist at Hesperos and Professor at the University of Central Florida. "By studying functional disruption without extensive cell loss, we now have a screening methodology for drugs that could potentially evaluate therapeutic efficacy even before the neurodegeneration in MCI and AD occurs."

The researchers found that compared to controls, treatment with toxic A and tau oligomers or brain extracts on the iPSC cortical neurons significantly impaired information processing as demonstrated by reduction in high-frequency stimulation-induced long-term potentiation (LTP), a process that is thought to underlie memory formation and learning. Additionally, oligomer and brain extract exposure led to dysfunction in iPSC cortical neuron electrophysiological activity, including decreases in ion current and action potential firing.

While exposure to the toxic oligomers and brain extracts caused morphological defects in the iPSC cortical neurons, there was no significant loss in cell viability.

"Clinical success for AD therapies has been challenging since preclinical animal studies often do not translate to humans," said Michael L. Shuler, Ph.D., Chief Executive Officer of Hesperos. "With our recent study, we are now one step closer in developing an AD multi-organ model to better evaluate drug metabolism in the liver, penetration through the blood-brain barrier and the effects on neuronal cells."

Story continues

About Alzheimers Disease/Preclinical Stage AD

AD is a progressive disease that is characterized by memory loss and deterioration of cognitive function. Preclinical AD is the first stage of the disease, and it begins long before any symptoms become apparent. It is thought that symptoms do not manifest until there is a significant death of neuronal cells, which is caused by the aggregation of toxic amyloid beta (A) and tau oligomers, typically during the earliest stages of the disease. Unfortunately, treatment after the diagnosis of MCI may be too late to reverse or modify disease progression.

To read the full manuscript, please visit https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/trc2.12029.

About Hesperos

Hesperos, Inc. is a leading provider of Human-on-a-Chip microfluidic systems to characterize an individuals biology. Founders Michael L. Shuler and James J. Hickman have been at the forefront of every major scientific discovery in this realm, from individual organ-on-a-chip constructs to fully functional, interconnected multi-organ systems. With a mission to revolutionize toxicology testing as well as efficacy evaluation for drug discovery, the company has created pumpless platforms with serum-free cellular mediums that allow multi-organ system communication and integrated computational PKPD modeling of live physiological responses utilizing functional readouts from neurons, cardiac, muscle, barrier tissues and neuromuscular junctions as well as responses from liver, pancreas and barrier tissues. Created from human stem cells, the fully human systems are the first in vitro solutions to accurately predict in vivo functions without the use of animal models. More information is available at http://www.hesperosinc.com.

Hesperos and Human-on-a-Chip are trademarks of Hesperos Inc. All other brands may be trademarks of their respective holders.

View source version on businesswire.com: https://www.businesswire.com/news/home/20200529005128/en/

Contacts

Michelle LinnBioscribe774-696-3803michelle@bioscribe.com

Original post:
Hesperos Human-on-a-Chip System Used to Model Preclinical Stages of Alzheimers Disease and Mild Cognitive Impairment - Yahoo Finance

The single biggest threat to mans continued dominance on the planet is thevirus. Joshua Lederberg, Nobel Prize in Physiology or Medicine, 1958

One of the most terrifying aspects of the COVID-19 pandemic is that we dont know what makes one person die, another suffer for weeks, another have just a cough and fatigue, and yet another have no symptoms at all. Even the experts are flummoxed.

Ive been puzzled from the beginning by the sharp dichotomy of who gets sick. At first it was mostly older people with chronic disease, and then a young person with low risk would show up. It can be devastating and rapid in one individual but mild in another, said Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Disease on a media webinar.

What lies behind susceptibility to COVID-19? Gender? Genetics? Geography? Behavior? Immunity? All of these factors may be at play, and they overlap.

Comedian Bill Maher blames poor immunity on eating too much sugar, and a thriving industry pitches immune-boosters, but much of the strength or weakness of an individuals immune response arises from specific combinations of inherited gene variants. Thats my take as a geneticist, and Dr. Faucis. Perhaps genetics and the immune response play a role in why one person has a mild response, yet another rapidly deteriorates into viral pneumonia and respiratory failure, he said.

During the first weeks of the pandemic, the observation that many victims were either older, had certain chronic medical conditions, or both, fed a sense of denial so widespread that young people flocked to Spring Break beaches as older folks boarded cruise ships in Florida as recently as early March. And then the exceptions began to appear among the young people.

While clinicians on the front lines everywhere are saving as many lives as possible, researchers are racing to identify factors that the most vulnerable, and the most mildly affected, share, especially the asymptomatic carriers. And as the numbers continue to climb and more familiar possible risk factors are minimized or dismissed age, location, lifestyle habits genetics is emerging as an explanation for why otherwise young, strong, healthy people can die from COVID-19.

Following are possible genetic explanations for why some people become sicker than others. These are hypotheses, the language of science: ideas eventually fleshed out with observations and data. Proof is part of mathematics; in science, conclusions can change with new data. The public is getting a crash course in the scientific method.

The most obvious genetic risk factor in susceptibility to COVID-19 is being male. The details of disease demographics change daily, but males are about twice as likely to die if theyre infected as are women: 4.7% versus 2.8%.

At first people blamed the sex disparity on stereotypes, like the riskier habits of many a male compared to females. But the sex difference comes down to chromosomes.

In humans, a gene, SRY, on the Y chromosome determines sex. Males have one X and a puny Y; females have two Xs. Fortunately, nature takes care of this fundamental inequality of the sexes, which I detailed hereand in every biology textbook Ive ever written.

To compensate for the X deficit of the male, one X in every cell of a female is silenced beneath a coating of methyl groups, an epigenetic change. But which X is silenced differs, more or less at random. In a liver cell, the turned off X might be the one that the woman inherited from her father; in a skin cell, the silenced X might be the one inherited from her mother.

The immune system seems to benefit from the females patchwork expression of her X-linked genes, with a dual response. Gene variants on one X may recognize viruses, while gene variants on the other X may have a different role, such as killing virally-infected cells.

Women also make more antibodiesagainst several viral pathogens. But some of us pay the price for our robust immune response with the autoimmune disorders that we are more likely to get.

People with type O blood may be at lower risk, and with type A blood at higher risk, of getting sick from SARS-CoV-2, according to results of a recent population-based study. But the idea of type O blood protecting against viral infections goes back years.

We have three dozen blood types. Theyre inherited through genes that encode proteins that dot red blood cell (RBC) surfaces, most serving as docks for sugars that are attached one piece at a time. The RBCs of people with type O blood do not have an extra bit of a sugar that determines the other ABO types: A, B, or AB.

The unadorned RBCs of people with type O blood, like me, are less likely to latch onto norovirus (which explains why I rarely throw up), hepatitis B virus, and HIV.

An investigation of ABO blood types from the SARS epidemic of 2002 to 2003 provides a possible clue to the differences. People with blood types B and O make antibodies that block the binding of the SARS viruss spikes to ACE2 receptors on human cells growing in culture. Since the novel coronavirus enters our cells through the same receptors, are people with type O blood less likely to become infected?

Thats what researchers from several institutions in China have found in the new study. They compared the blood types of 2,173 patients with COVID-19 from three hospitals in Wuhan and Shenzhen to the distribution of blood types in the general population in each area.

People with type A blood were at higher risk than people with type 0 blood for both infection and severity of the illness.

In the general population 31% of the people are type A, 24% are type B, 9% are type AB, and 34% are type O. But among infected individuals, type A is up to 38%, type B up to 26%, AB at 10%, and type O way down to 25%.

The researchers conclude that the findings demonstrate that the ABO blood type is a biomarker for differential susceptibility of COVID-19. I think thats a bit strong for a trend, considering the exceptions. But the researchers suggest that their findings, if validated for more people, can be used to prioritize limited PPE resources and implement more vigilant surveillance and aggressive treatment for people with blood type A.

Immunity and genetics are intimately intertwined. Links between mutations both harmful and helpful and immunity to infectious diseases are well known.

Mutations in single genes lie behind several types of severe combined immune deficiencies (SCIDs), like bubble boy disease. Sets of human leukocyte antigen gene variants (HLA types) have long been associated with increased risk of autoimmune conditions such as celiac disease, type 1 diabetes, and rheumatoid arthritis, and were for many years the basis of tissue typing for transplants.

In HIV/AIDS, two specific mutations in theCCR5 gene remove a chunk of a co-receptor protein to which the virus must bind to enter a human cell. The mutation has inspired treatment strategies, including drugs, stem cell transplants, and using CRISPRto recreate the CCR5 deletion mutation by editing out part of the gene.

Might variants of the gene that encodes ACE2, the protein receptor for the novel coronavirus, protect people in the way that a CCR5 mutation blocks entry of HIV? The search is on.

Another clue to possible genetic protection against the novel coronavirus may come from the SARS experience from years ago and parasitic worm diseases in Africa. (This hypothesis I came up with on my own so Im prepared to be shouted down.)

In a human body, the SARS virus disrupts the balance of helper T cells, boosting the number of cells that fight parasitic worms (the Th2 response) while depleting the cells that protect against bacteria and viruses (the Th1 response). The resulting Th2 immune bias, in SARS as well as in COVID-19, unleashes the inflammatory cytokine storm that can progress to respiratory failure, shock, and organ failure.

In subSarahan Africa alone, a billion people have intestinal infections of parasitic worms, the most common of which is schistosomiasis. Its also called snail fever because the worms are released into fresh water from snails and burrow into peoples feet when they wade in the water.

The worms mate inside our blood vessels, releasing eggs that leave in urine and feces into the water supply. Remaining eggs can inflame the intestines and bladder. The infection begins with a rash or itch, and causes fever, cough, and muscle aches in a month or two. A drug treatment is highly effective.

Genetics determines susceptibility, or resistance to, schistosomiasis. And thats what got me thinking about COVID-19.

People who resist the flatworm infection have variants of eight genes that ignite a powerful Th2 immune response that pours out a brew of specific interferons and interleukins. Could the Th2 immune bias of the novel coronavirus SARS-CoV-2 not be as devastating to people who already have the bias, to resist schistosomiasis? If so, then places in Africa where many people are immune to schistosomiasis might have fewer cases of COVID-19.

So far parts of Africa have reported low incidence of the new disease. On April 7, the World Health Organization reported approximately 10,000 cases in all of Africa. Thats similar to the number of deaths in New York City, although Africa could be on track for the exponential growth seen elsewhere. But if the lower number in Africa persists, then maybe those eight genes are protecting people. Adding to the evidence is that the 8-gene set varies more between West Africans and Europeans than do other sets of genes.

Like the ABO blood type study, if the 8-gene signature that protects against schistosomiasis protects against COVID-19, then the signature should be overrepresented among those exposed to the virus who do not get very sick, and underrepresented among those who do. However, its possible that Africa is just behindthe rest of the world in reporting COVID-19 cases. So, a thought experiment for now.

Before researchers zero in on a highly predictive genetic signature of COVID-19 risk, we can think about how the information would best be used:

I hope that discovery of a genetic basis for COVID-19 vulnerability or resistance will not inspire discrimination unfortunately, genetic information has had a legacy of misuse.

Ricki Lewis is the GLPs senior contributing writer focusing on gene therapy and gene editing. She has a PhD in genetics and is a genetic counselor, science writer and author of The Forever Fix: Gene Therapy and the Boy Who Saved It, the only popular book about gene therapy. BIO. Follow her at her website or Twitter @rickilewis

Here is the original post:
Can genetics explain the degrees of misery inflicted by the coronavirus? - Genetic Literacy Project

April 6, 2020

Athena Aktipis could be called a Renaissance woman. After all, shes a psychologist, evolutionary biologist, cancer biologist and studies conflict and cooperation. She crosses boundaries and colors outside the lines in her quest to find answers to questions about human nature and the nature of life on earth.

At Arizona State University, she is a co-leader of theArizona Cancer Evolution Center; at theBiodesign Instituteat ASU, she is a member of three different research centers; she is an assistant professor in the Department of Psychology, director of the Interdisciplinary Cooperation Initiative, a Lincoln Professor at theLincoln Center for Applied Ethics;she is the creator and host of the"Zombified"podcast; she directs ASUsCooperation and Conflict Lab;and she is co-director of the internationalHuman Generosity Project. Driven by multispecies research, Aktipis illustrates how evolution has paved the way for cancers ubiquity, and why cancer will exist as long as multicellular life does. Download Full Image

If thats not enough, shes a mother of three ages 8, 13, and 14.

So just when didAktipisfind the time, energy and motivation to write what is currently one of Amazons top sellers in new releases about cancer, "The Cheating Cell: How Evolution Helps Us Understand and Treat Cancer"?

She persevered because she saw an opportunity to help us rethink our relationship with this vexing disease. Seven years in the making, the book published on March 24 is already getting five-star reviews. One reader commented, Aktipis' writing is refreshing like sitting down for a candid conversation with a knowledgeable friend. Some books about cancer can be too clinical, while others merely scratch the surface; Athena has struck a perfect balance.

Driven by multispecies research, Aktipis illustrates how evolution has paved the way for cancers ubiquity, and why cancer will exist as long as multicellular life does. Even so, she argues, this doesnt mean we should give up on treating cancer in fact, evolutionary approaches offer new and promising options for the diseases prevention and treatments that aim at long-term management rather than simple eradication.

By accepting that cancer is a part of our biological past, present, and future and that we cannot win a war against evolution treatments can become smarter, more strategic and more humane.

Question: What inspired you to write "The Cheating Cell"?

Answer:I wanted to write a book about cancer that was more than just an academic summary of cancer; I wanted to show how cancer is fundamentally tied into who we are as multicellular life forms, and to explain how our ability to treat cancer effectively is based on our understanding of the evolutionary and ecological dynamics underlying it. Really, I wanted to write an epic story about what cancer is, how it emerged during the origins of multicellular life, and how we can use evolutionary and ecological approaches to better prevent and treat cancer. It was also very important to me to write a book that would be accessible to a broad audience without sacrificing scientific rigor.

Q: What is the book about?

A: "The Cheating Cell" is a book about a new way of looking at cancer. It is about the fundamental evolutionary and ecological underpinnings of the disease. And it is also a book about the ways that cancer is entwined with our very existence as multicellular organisms. We are essentially made of cellular cooperation. Each of us is a cooperative cellular society of about 30 trillion cells descended from the fertilized cell that gave rise to us. In a healthy body, these cells cooperate to make us function effectively as multicellular organisms. But sometimes this cellular cooperation can break down, and when it does, cancer can arise. In "The Cheating Cell" I explain the many ways that cellular cheating can arise and how this cellular cheating can evolve in the ecosystem of the body. I also take a look at how our bodies have evolved, because of selection among organisms for better cancer suppression system, to deal with the threat of cellular cheating. I end the book by showing how new evolutionarily-informed approaches to cancer hold the promise for changing how we treat cancer and helping us to live longer and more fulfilling lives even with a diagnosis of the disease.

Athena Aktipis.

Q: How can cells in our body cooperate and cheat when they presumably dont have consciousness or intentions?

A:When I talk about cells cooperating or cheating, I dont mean to imply that there is any intention behind their behavior. In the case of the normal cells in our body working together to make us function, the cells in our body perform all sorts of amazing feats of coordination and cooperation, including sharing resources throughout the body and dividing labor every one of our different cell types does a different job to keep us functional and healthy.

Our cells also cooperate by restraining their rates of division, which allows us to help maintain our tissues without growing out of control. Cancer represents a breakdown of all of these aspects of cellular cooperation (and more). None of this cellular cheating involves consciousness or intention on the part of cancer cells. It is simply evolution happening within the body, favoring those cheating cells because they can replicate more quickly and monopolize resources, giving them a survival advantage.

Of course this evolutionary process inside the body can ultimately undermine the viability of the organisms of which the cancer cells are a part. But, because cancer cells do not have the ability to consciously look to the future, they essentially evolve themselves into an evolutionary dead end. Cells dont consciously or intentionally cheat, instead they evolve to cheat because the cells that cheat can have higher evolutionary fitness within the organism, which allows them to increase in frequency. Its Evolution 101, happening inside the body among cells that vary in their traits. Unfortunately, cells that cheat can get an evolutionary leg-up on the normal cells around them, leading to the emergence of cancer.

Q: In your book you say that susceptibility to cancer is simply part of being a multicellular organism. Does this mean that cancer is inevitable?

A:Cancer is part of our evolutionary legacy. It is part of the evolutionary legacy of every multicellular organism on this planet. But this does not mean cancer is an inevitability. In fact, our long evolutionary history with cancer means that we, as multicellular organisms, have actually evolved many defenses against cancer: This is because selection operates among organisms in a population, favoring those organisms that have more effective cancer suppression systems. For example, we humans have two copies of the cancer suppressor geneTP53that helps protect against cancer by initiating DNA repair and if necessary cellular suicide in cells that are behaving abnormally. Cancer defenses like the geneTP53can be thought of as cellular cheater detection systems, monitoring cells for signs of abnormal proliferation, unusual metabolic patterns, aberrant proteins or any other signs of suspicious behavior that suggest cellular cheating. Some large organisms like elephants have extra copies of cancer suppressor genes elephants have 40 copies ofTP53, and many other large and long-lived organisms have other "extra" cancer suppression genes.

The work we have been doing looking at cancer across the tree of life suggests that large and long-lived organisms have more sensitive cellular cheater detection systems, which help protect them from cancer. This is simply a reflection of a fundamental reality of cooperation theory: The larger the group and the longer it is around, the more vulnerable it will be to cheaters taking over. If you want it to last, there need to be effective systems for monitoring and regulating cooperation. Large multicellular organisms are essentially a giant cooperative group facing a fundamental social dilemma, where cheaters, in this case, cancer cells, can benefit from exploiting the group the organism. And they have evolved special systems for keeping this cellular cheating under control long enough so that they can effectively survive and reproduce.

Q: You point out that cancer happens across the tree of life, including in plants like cacti. Can you tell us more about crested cacti?

A:A wonderful project that grew out the book and the work Ive been doing looking at cancer across life is the Endless forms most beautiful cactus garden. It shows that we humans are not alone in our struggle with cancer. Plants, like these beautiful crested cacti, can harbor cancer-like growths as well. These cancer-like forms happen as a result of mutation or damage to the meristem the stem-cell like cells on the growing tip of the plant that lead to many unusual fan-like patterns, called fasciations. And these plants can live with these cancer-like growths; they do not necessarily threaten the lives of the plants, though they can make them more vulnerable.

Crested cacti require extra care because they are more delicate, but they are also highly prized by botanists because of their unique and beautiful patterns. We created the garden as a place to appreciate how we share the burden of cancer with all multicellular life forms. It is also a place to come to remember loved ones who were impacted by cancer, and a place to appreciate the beauty of these unique growth patterns formed by the mutated cells. This garden is also an inspiration to keep innovating in our approaches to cancer, looking for ways to keep it under control so that we can live with it, as our ancestors have since the beginning of multicellular life on this planet.

Q: What are the most important opportunities for using evolutionarily informed approaches to treat cancer?

A: My colleagues and I are now working to bring clinical trials of evolutionarily informed therapies to Arizona. One of those therapies is called adaptive therapy, an approach pioneered byRobert Gatenby at Moffitt Cancer Center in Florida.Adaptive therapy is aimed at keeping cancer under control rather than trying to eradicate it. Adaptive therapy avoids the often inevitable evolution of therapeutic resistance that often undermines the effectiveness of therapy because cells evolve resistance in traditional therapy. This just like what happens if you spray a field with pesticides: You select for resistant pests. The goal of adaptive therapy is to extend patient life, focusing on keeping the tumor under control rather than eradicating it.

This is an approach that some people arent emotionally comfortable with because they just want to eliminate the cancer with high dose therapy. But often it is not possible to eradicate the cancer because resistance evolves and treatment stops working. So there is a tremendous opportunity here to change our mindset about cancer, and an evolutionary approach is central to that on two different levels. First, we need to recognize that cancer is an evolutionary system and that resistance is likely to evolve.

Our treatments should, from the very beginning, include a plan for how to manage resistance and ideally keep the treatment effective for as long as possible. Adaptive therapy is one such approach. And second, we must come to terms with the reality that cancer is part of our evolutionary legacy, and that we as multicellular organisms have evolved with cancer, but as a result we have also evolved various ways of keeping cancer under control.

Approaches like adaptive therapy have been successful at keeping advanced metastatic prostate cancer under control for years in the trials that have been done at Moffitt. These are very exciting developments, and I think there is great promise in shifting our focus to controlling cancer and away from eradicating it.

Q: Will we ever find a cure for cancer?

A:The fact is, cancer is here to stay, it will always be a part of life on earth, and our best bet is to accept that it is a part of our evolutionary legacy. As we move forward, we can develop treatments and preventative measures that acknowledge cancers evolutionary nature and the many important ways cancer has shaped life on this planet.

I think that in the future we will all think about what a cure means differently; that the idea of cure via control will come to be the norm, rather than cure via eradication, which is the current way that people typically think about it. All of us, cancer patients or not, harbor cells with cancer mutations, but most of us are able to keep those mutated cells under control with our toolbox of cancer suppression systems. So cancer control is the normal state for multicellular life forms ourselves included.

By switching our attention from eradicating cancer to simply keeping it under control, we can change the way we think about a cure for cancer, and in the process make finding a cure much more likely.

Modified, with permission, from Princeton University Press by Dianne Price

Read this article:
Beating cancer by taking the unbeaten path | ASU Now: Access, Excellence, Impact - ASU Now