Posts tagged with "medical research"

Dentistry illustration by Kaelen Felix for 360 Magazine

Cold Sore Flareup Triggers

Virus Highjacks Important Immune Response, UVA Discovery Reveals

Researchers at the University of Virginia School of Medicine have shed light on what causes herpes simplex virus to flare up, explaining how stress, illness and even sunburn can trigger unwanted outbreaks.

The discovery could lead to new ways to prevent cold sores and recurrent herpes-related eye disease from reoccurring, the researchers report.

“Herpes simplex recurrence has long been associated with stress, fever and sunburn,” said researcher Anna R. Cliffe, PhD, of UVA’s Department of Microbiology, Immunology and Cancer Biology. “This study sheds light on how all these triggers can lead to herpes simplex-associated disease.”

About Herpes Simplex Recurrence

Once you’re infected with herpes simplex virus (HSV) – and more half of Americans are – the virus never really goes away. Instead, it lurks inside neurons, waiting for the right moment to strike again, a process known as reactivation.

Cold sores, also known as fever blisters, are one of the most common symptoms of HSV reactivation. Recurrent reactivation in the eye leads to herpes keratitis, which, if left untreated, can result in blindness. HSV infection has also been linked to the progression of Alzheimer’s disease.

Recurrences of HSV are typically associated with stress, illness or sunburn, but doctors have been uncertain exactly what causes the virus to reactivate. Cliffe and her collaborators found that when neurons harboring the virus were exposed to stimuli that induce “neuronal hyperexcitation,” the virus senses this particular change and seizes its opportunity to reactivate.

Working in a model developed by the Cliffe lab using mouse neurons infected with HSV, the researchers determined that the virus highjacks an important immune response within the body. In response to prolonged periods of inflammation or stress, the immune system releases a particular cytokine, Interleukin 1 beta. This cytokine is also present in epithelial cells in the skin and eye and is released when these cells are damaged by ultraviolet light.

Interleukin 1 beta then increases the excitability in the affected neurons, setting the stage for HSV to flare up, the UVA researchers discovered.

“It is really remarkable that the virus has hijacked this pathway that is part of our body’s immune response,” Cliffe said. “it highlights how some viruses have evolved to take advantage of what should be part of our infection-fighting machinery.”

The scientists say that more research will need to be done to fully understand the potential factors which play into herpes simplex disease. It may vary depending on the virus strain or the type of neuron infected, even. And it is still unknown if the virus alters how neurons respond to cytokines such as Interleukin 1 beta. But the new insights help doctors better understand what is happening in neurons and the immune system, and that could lead to ways to prevent unwanted outbreaks, the researchers hope.

“A better understanding of what causes HSV to reactivate in response to a stimulus is needed to develop novel therapeutics,” Cliffe said. “Ultimately, what we hope to do is target the latent virus itself and make it unresponsive to stimuli such as Interleukin 1 beta.”

Findings Published

The researchers have published their findings in the scientific journal eLife. The research team consisted of Sean R. Cuddy, Austin R. Schinlever, Sara Dochnal, Philip V. Seegren, Jon Suzich, Parijat Kundu, Taylor K. Downs, Mina Farah, Bimal N. Desai, Chris Boutell and Cliffe.

The work was supported by the National Institutes of Health’s National Institute of Neurological Disorder and Stroke, grant R01NS105630; the National Institute of Allergy and Infectious Diseases, grant T32AI007046; the National Eye Institute, grant F30EY030397; the National Institute of General Medical Sciences, grants T32GM008136, T32GM007267, GM108989 and GM007055and Medical Research Council grant MC_UU_12014/5.

To keep up with the latest medical research news from UVA, subscribe to the Making of Medicine blog.

AC_LatinoCovid by Allison Christensen for 360 Magazine

Antibody Cocktail May Prevent Symptomatic COVID-19 Infections

An antibody cocktail being tested at UVA Health and other sites was able to block 100% of symptomatic COVID-19 infections among people exposed to the virus, early results from the clinical trial suggest.

In addition, those who developed asymptomatic infections accumulated far less virus in their bodies than usual and saw their infections resolve within a week, according to interim data released by the cocktail’s manufacturer, Regeneron Pharmaceuticals.

“This is the first treatment shown to prevent COVID-19 after a known exposure, and offers protection for unvaccinated individuals caring for a family member with COVID-19,” said UVA Health’s William Petri Jr., MD, PhD, one of the leaders of the trial at UVA. “We expect that Regeneron will file for Emergency Use Authorization from the FDA so that this drug can be used outside of the context of a clinical trial.”

Antibodies for COVID-19

The phase 3 clinical trial aims to determine if the antibodies will prevent COVID-19 infection in people who have been exposed but not yet developed the disease. This is known as “passive immunization.”

Regeneron’s new analysis, which has not yet been published in a scientific journal, looked at outcomes in approximately 400 trial participants. Of 186 people who received the antibodies, none developed symptomatic COVID-19. Of the 223 who received a placebo, eight developed symptomatic COVID-19, the company reports.

Asymptomatic infections occurred in 15 of the antibody recipients and in 23 of the placebo recipients. Overall rates of infection, including both symptomatic and asymptomatic infections, were approximately 50% lower in the antibody group.

Among those who developed infections, placebo recipients had, on average, a peak viral load (the amount of virus in the body) that was more than 100 times greater than antibody recipients. The antibody group also recovered more quickly–all the infections resolved within seven days, while 40 percent of infections in the placebo group lasted three to four weeks, Regeneron said.

The cocktail also appears to shorten the duration of viral shedding, the time when the virus is being manufactured in the body. The viral shedding period was nine weeks among antibody recipients and 44 weeks among the placebo recipients. While people with COVID-19 are not infectious for this entire time, reducing the duration of viral shedding may shorten the period when they can spread the disease.

There were more adverse events reported among placebo recipients than among antibody recipients – 18 percent and 12 percent, respectively. Regeneron attributed this to the larger number of COVID-19 infections in the placebo group.

There was one death and one COVID-19-related hospitalization in the placebo group and none in the antibody group. Injection-site reactions were reported among 2 percent of both groups.

“We are profoundly grateful to the nurses and staff of the UVA COVID-19 clinic, led by Dr. Debbie-Anne Shirley,” Petri said. “Their day-to-day support made our participation in this trial possible.”

About the Clinical Trial

Phase 3 clinical trials, such as the one under way at UVA, examine the safety and effectiveness of new drugs and treatments in large numbers of people. Positive results in the phase 3 trial could spur the federal Food and Drug Administration to make the antibody cocktail available for post-exposure COVID-19 prevention.

The antibody cocktail is not a vaccine and is not expected to provide permanent immunity to COVID-19.

The team conducting the study at UVA is led by Petri and Shirley and includes Gregory Madden, MD; Chelsea Marie, PhD; Jennifer Sasson, MD; Jae Shin, MD; Cirle Warren, MD; Clinical Research Coordinator Igor Shumilin; assistant Rebecca Carpenter; and COVID-19 Clinic nurses Michelle Sutton, Elizabeth Brooks, Danielle Donigan, Cynthia Edwards, Jennifer Pinnata, Samantha Simmons and Rebecca Wade.

To keep up with the latest medical research news from UVA, subscribe to the Making of Medicine blog.

Woman at Computer by Mina Tocalini for 360 Magazine

UVA’s DNA Discovery

Scientists have identified a group of drugs that may help stop a leading cause of vision loss after making an unexpected discovery that overturns a fundamental belief about DNA.

The drugs, known as Nucleoside Reverse Transcriptase Inhibitors, or NRTIs, are commonly used to treat HIV. The new discovery suggests that they may be useful against dry macular degeneration as well, even though a virus does not cause that sight-stealing condition.

A review of four different health insurance databases suggests that people taking these drugs have a significantly reduced risk of developing dry macular degeneration, a condition that affects millions of Americans.

“We are extremely excited that the reduced risk was reproduced in all the databases, each with millions of patients,” said Jayakrishna Ambati, MD, a top macular degeneration researcher at the University of Virginia School of Medicine. “This finding provides real hope in developing the first treatment for this blinding disease.”

Targeting Macular Degeneration

The new discovery comes from Ambati; Fred H. Gage, PhD, of the Salk Institute for Biological Studies; and collaborators around the world. The work rewrites our understanding of DNA, revealing for the first time that it can be manufactured in the cytoplasm of our cells, outside the cell nucleus that is home to our genetic material.

The buildup of a certain type of DNA in the cytoplasm, Alu, contributes to macular degeneration, the researchers found. This buildup appears to kill off an important layer of cells that nourishes the retina’s visual cells.

Based on this discovery, the researchers decided to look at drugs that block the production of this DNA, to see if they might help prevent vision loss. They analyzed multiple U.S. health insurance databases – encompassing more than 100 million patients over two decades – and found that people taking NRTIs were almost 40% less likely to develop dry macular degeneration.

The researchers are urging further study to determine if these drugs or safer derivatives known as Kamuvudines, both of which block a key inflammatory pathway, could help prevent vision loss from dry macular degeneration.

“A clinical trial of these inflammasome-inhibiting drugs is now warranted,” said Ambati, the founding director of UVA’s Center for Advanced Vision Science. “It’s also fascinating how uncovering the intricate biology of genetics and combining it with big data archeology can propel insights into new medicines.”

Ambati, of UVA’s Department of Ophthalmology, previously determined that NRTIs may help prevent diabetes as well.

Findings Published

The researchers have published their findings in the scientific journal PNAS. The research team consisted of Shinichi Fukuda, Akhil Varshney, Benjamin J. Fowler, Shao-bin Wang, Siddharth Narendran, Kameshwari Ambati, Tetsuhiro Yasuma, Joseph Magagnoli, Hannah Leung, Shuichiro Hirahara, Yosuke Nagasaka, Reo Yasuma, Ivana Apicella, Felipe Pereira, Ryan D. Makin, Eamonn Magner, Xinan Liu, Jian Sun, Mo Wang, Kirstie Baker, Kenneth M. Marion, Xiwen Huang, Elmira Baghdasaryan, Meenakshi Ambati, Vidya L. Ambati, Akshat Pandey, Lekha Pandya, Tammy Cummings, Daipayan Banerjee, Peirong Huang, Praveen Yerramothu, Genrich V. Tolstonog, Ulrike Held, Jennifer A. Erwin, Apua C.M. Paquola, Joseph R. Herdy, Yuichiro Ogura, Hiroko Terasaki, Tetsuro Oshika, Shaban Darwish, Ramendra K. Singh, Saghar Mozaffari, Deepak Bhattarai, Kyung Bo Kim, James W. Hardin, Charles L. Bennett, David R. Hinton, Timothy E. Hanson, Christian Röver, Keykavous Parang, Nagaraj Kerur, Jinze Liu, Brian C. Werner, S. Scott Sutton, Srinivas R. Sadda, Gerald G. Schumann, Bradley D. Gelfand, Fred H. Gage and Jayakrishna Ambati.

Jayakrishna Ambati is a co-founder of Inflammasome Therapeutics, iVeena Holdings, iVeena Delivery Systems and DiceRx; a full list of the authors’ disclosures is included in the paper.

The research was supported by UVA’s Strategic Investment Fund, the National Institutes of Health Director’s Pioneer Award, the National Institutes of Health’s National Eye Institute and many other generous contributors. A full list is included in the paper.

To keep up with the latest medical research news from UVA, subscribe to the Making of Medicine blog.

COVID-19 Trial Tests if Common Drug Can Keep Patients Out of Hospital

At-risk people diagnosed with COVID-19 across the United States and Canada can participate in a clinical trial testing whether a common drug can keep them from getting sicker and keep them out of the hospital.­­

The trial, conducted by Washington University School of Medicine in St. Louis, is based on a discovery by the University of Virginia School of Medicine’s Alban Gaultier, PhD, and a former graduate student, Dorian A Rosen, PhD.

Gaultier and Rosen found last year that the antidepressant fluvoxamine may stop the deadly inflammation known as sepsis, in which the immune response spirals out of control. The drug’s apparent benefit for dampening dangerous inflammation prompted the Washington University researchers to begin investigating its potential benefit for COVID-19, which can also cause dangerous overreactions of the immune system.

“If this clinical trial is proven successful, fluvoxamine could become a standard treatment for patients newly diagnosed with COVID-19, especially patients at risk,” Gaultier said. “Even the best vaccines do not protect 100% of the population, and discovery of safe and affordable treatments to prevent COVID-19-associated complications is critical.”

Fluvoxamine and COVID-19

Earlier this year, the Washington University researchers launched their first clinical trial of the drug in patients with COVID-19. That trial compared fluvoxamine with a harmless placebo in 152 adult outpatients. None of the 80 participants who received fluvoxamine became seriously ill after 15 days, while six patients who received placebo did. Of those six, four were hospitalized, for periods ranging from four to 21 days. One was on a ventilator for 10 days.

Based on those initial results, Washington University is now launching a much larger trial open to residents across the United States and Canada. The trial is seeking approximately 880 at-risk participants, age 18 and older, who have tested positive for COVID-19 and are experiencing mild symptoms.

Participants will be provided with either fluvoxamine or a placebo for approximately 15 days. No face-to-face contact is required; everything necessary will be sent to the participants’ doorsteps.

Contactless Check-Ins

The researchers will track the patients by videochat, email or telephone to determine if fluvoxamine provides a benefit and helps keep participants out of the hospital. During brief daily check-ins, trial participants will report their oxygen levels, blood pressure and temperature, along with whether they are feeling shortness of breath or have had any other problems.

The study team will continue to follow the participants for approximately 90 days after they have finished taking fluvoxamine or the placebo.

The trial is open to people who have at least one risk factor for severe COVID-19, such as being 40 or older, being part of a high-risk racial/ethnic group (such as African-American, Hispanic, Native American or biracial), or having one or more medical conditions such as obesity, diabetes, high blood pressure, heart disease, a lung disease or an immune disorder such as rheumatoid arthritis.

For more information about the trial, visit this website.

Mina Tocalini, 360 Magazine, COVID-19

Rice University’s Charcoal Research

Researchers at Rice University find that charcoal, and other materials described in the American Chemical Society journal ACS Applied Nano Materials, could aid treatment COVID-19 patients.

In the project co-led by Rice chemist James Tour, researchers found oxidized charcoal nanoparticles are not only effective antioxidants, but can also be made from an activated carbon source that is inexpensive, good manufacturing practice (GMP) certified, and already being used in humans to treat acute poisoning.

“That these nanozymes are made from a GMP source opens the door for drug manufacturers,” said Tour, who led the project with A&M neurologist Thomas Kent and UTHealth biochemist Ah-Lim Tsai. “While coal was effective, an issue is that it can have a variety of toxic metallic elements and impurities that are not consistent across samples. And the clusters made from carbon nanotubes are very expensive.”

The researchers noted it may be worthwhile to study the application of their nanozymes to treat the cytokine storms – an excessive immune system response to infection – suspected of contributing to tissue and organ damage in COVID-19 patients.

“While speculative that these particles will be helpful in COVID-19, if administration is timed correctly, they could reduce the damaging radicals that accompany the cytokine storm and could be further chemically modified to reduce other injury-causing features of this disease,” Kent said.

Gang Wu, an assistant professor of hematology at McGovern, and Rice graduate student Emily McHugh are co-lead authors of the study. Co-authors are Vladimir Berka, a senior research scientist at McGovern; Rice graduate students Weiyin Chen, Zhe Wang and Jacob Beckham; Rice undergraduate Trenton Roy; and Paul Derry, an assistant professor at Texas A&M’s Institute of Biosciences and Technology.

Tour is the T.T. and W.F. Chao Chair in Chemistry as well as a professor of computer science and of materials science and nanoengineering at Rice. Kent is the Robert A. Welch Chair Professor in the Institute of Biosciences and Technology at Texas A&M-Houston Campus and an adjunct chemistry professor at Rice and at Houston Methodist Hospital. Tsai is a professor of hematology at UTHealth. Click here to read all of the findings of the Rice University researchers’ work.

Alcoholism in the Family

Alcoholism in the family affects how your brain switches between active and resting states.

A family history of alcoholism affects a process that the brain uses when transitioning from a mentally demanding state to a resting state, researchers have found.

You don’t have to be a drinker for your brain to be affected by alcoholism. A new study shows that just having a parent with an alcohol use disorder affects how your brain transitions between active and resting states – regardless of your own drinking habits.

The study, performed by researchers at Purdue University and the Indiana University School of Medicine, discovered that the brain reconfigures itself between completing a mentally demanding task and resting.

But for the brain of someone with a family history of an alcohol use disorder, this reconfiguration doesn’t happen.

While the missing transition doesn’t seem to affect how well a person performs the mentally demanding task itself, it might be related to larger scale brain functions that give rise to behaviors associated with addiction. In particular, study subjects without this brain process demonstrated greater impatience in waiting for rewards, a behavior associated with addiction.

Brain-Reconfiguration
Multiple regions of the brain are involved in a “reconfiguration” that happens between completing a difficult task and resting. But for people with a family history of alcoholism, this reconfiguration is diminished.

Findings are published in the journal NeuroImage. The work was led by Enrico Amico, a former Purdue postdoctoral researcher who is now a researcher at EPFL in Lausanne, Switzerland.

How the brain reconfigures between active and resting states is like how a computer closes down a program after you’re finished with it. “The moment you close a program, a computer has to remove it from memory, reorganize the cache and maybe clear out some temporary files. This helps the computer to prepare for the next task,” said Joaquín Goñi, a Purdue assistant professor in the School of Industrial Engineering and the Weldon School of Biomedical Engineering.

“In a similar way, we’ve found that this reconfiguration process in the human brain is associated with finishing a task and getting ready for what’s next.” Goñi’s research group, the CONNplexity Lab, takes a computational approach to neuroscience and cognitive science.

Past research has shown that a family history of alcoholism affects a person’s brain anatomy and physiology, but most studies have looked at this effect only in separate active and quiet resting states rather than the transition between them.

“A lot of what brains do is switch between different tasks and states. We suspected that this task switching might be somewhat lower in people with a family history of alcoholism,” said David Kareken, a professor of neurology at the Indiana University School of Medicine and director of the Indiana Alcohol Research Center.

The study defined a “family history of alcoholism” as someone with a parent who had enough symptoms to constitute an alcohol use disorder. About half of the 54 study participants had this history.

Researchers at Indiana University measured the brain activity of subjects with an MRI scanner as they completed a mentally demanding task on a computer. The task required them to unpredictably hold back from pressing a left or right key. After completing the task, the subjects rested while watching a fixed point on the screen.

A separate task outside of the MRI scanner gauged how participants responded to rewards, asking questions such as if they would like $20 now or $200 in one year.

Amico and Goñi processed the data and developed a computational framework for extracting different patterns of brain connectivity between completing the mentally demanding task and entering the resting state, such as when brain areas rose and fell together in activity, or one brain area rose while another fell at the same time.

The data revealed that these brain connectivity patterns reconfigured within the first three minutes after finishing the task. By the fourth minute of rest, the effect had completely disappeared.

And it’s not a quiet process: Reconfiguration involves multiple parts
of the brain at once.

“These brain regions talk to each other and are very strongly implicated in the task even though by this point, the task is already completed. It almost seems like an echo in time of what had been going on,” Kareken said.

Subjects lacking the transition also had the risk factors that researchers have seen to be consistent with developing alcoholism. These include being male, a greater number of symptoms of depression,
and reward-impatience.

A family history of alcoholism, however, stood out as the most statistically significant difference in this brain reconfiguration.

The finding affects research going forward.

“In the past, we’ve assumed that a person who doesn’t drink excessively is a ‘healthy’ control for a study. But this work shows that a person with just a family history of alcoholism may also have some subtle differences in how their brains operate,” Goñi said.

This research was funded by the National Institute on Alcohol Abuse and Alcoholism (grant P60AA07611) and the Purdue Discovery Park Data Science Award “Fingerprints of the Human Brain: A Data Science Perspective.” The work was also partially supported by the National Institutes of Health (grants R01EB022574, R01MH108467, and R00AA023296).

About Discovery Park
Discovery Park is a place where Purdue researchers move beyond traditional boundaries, collaborating across disciplines and with policymakers and business leaders to create solutions for a better world. Grand challenges of global health, global conflict and security, and those that lie at the nexus of sustainable energy, world food supply, water and the environment are the focus of researchers in Discovery Park. The translation of discovery to impact is integrated into the fabric of Discovery Park through entrepreneurship programs and partnerships.

Harvard & Texas A&M

I write to inform you of my dismay over recent actions by Harvard faculty Dr. Walter Willett and Dr. Frank Hu and their associates, Dr. David Katz and the True Health Initiative (THI). Their actions, as
described in a recent JAMA article here
are unethical, distort the results of important scientific research, and, in our opinion, are false and harmful to Texas A&M University and its faculty. These are serious matters that undermine the values espoused by your institution and must be corrected immediately. 

I trust you were as surprised as I was after reading the JAMA article and ask that you take a look at the outrageous actions by THI. JAMA found that THI and several of its council members, including Harvard faculty Dr. Willett and Dr. Hu, mischaracterized scientific research
and falsely accused Texas A&M scientists of selling out to industry interests. According to JAMA, THI not only broke journal embargo policy but apparently used automated bots to flood the email inbox of the Editor in Chief of the Annals of Internal Medicine.

Several of your faculty are involved as council members or advisers of THI and collaborated with THI in their effort to discredit scientific evidence that runs contrary to their ideology. I can assure you that Texas A&M’s research is driven by science. Period.

In addition to my concern about JAMA findings, I am attaching an illustration
Dr. Willett presented at a cardiology conference to attack a distinguished Texas A&M professor and the university itself as being influenced by industry. This unsubstantiated claim has been independently rejected and shown to be false in the JAMA article.

At this time, we have no hard basis to show that these actions against Texas A&M and its faculty are endorsed or condoned by your institution, and we hope we can work together to resolve this problem. Such
resolution should include a serious assessment by Harvard of its affiliation with THI and a comprehensive ethical review into any Harvard faculty involved with THI. Several scientists have severed ties with THI because of the issues discussed in this letter. Texas A&M applauds the stand taken by these scientists and encourages Harvard to show the same courage.


Texas A&M asks that Harvard join us for a purely scientific approach to nutrition for the sake of public health and public trust and reject the politics and unethical actions of THI that have sought to discredit science and interfere in the scientific process.

rice university, 360 MAGAZINE, health, study, leukemia

Cocktail proves toxic to leukemia cells

Rice University, MD Anderson research points toward better personalized therapy

A combination of drugs that affect mitochondria — the power plants inside cells — may become the best weapons yet to fight acute myeloid leukemia, according to Rice University researchers.

A study led by Rice bioscientist Natasha Kirienko and postdoctoral researcher Svetlana Panina found that mitocans, anti-cancer drugs that target mitochondria, are particularly adept at killing leukemia cells, especially when combined with a glycolytic inhibitor, while leaving healthy blood cells in the same sample largely unaffected.

Their open access paper, a collaboration with the University of Texas MD Anderson Cancer Center, appears in the Nature journal Cell Death & Disease. The research could lead to new ways to personalize treatment for patients with leukemia.
“We started with the idea of finding an underlying connection between types of cancer and their sensitivity to specific kinds of chemotherapeutics, mitochondria-targeting drugs,” Kirienko said. “Our bioinformatic analysis, which included 60 cell lines from nine different cancer types, showed that leukemia cells are particularly sensitive to mitochondrial damage.”

The researchers exposed the cell lines to multiple known mitocan molecules. They found low doses of a mitocan/glycolytic inhibitor cocktail killed all of the leukemia cell lines they tested at concentrations lower than what was necessary to kill healthy cells. Conversely, they reported that solid tumor cells, like ovarian cancers, proved highly resistant to mitocans. Glioblastoma cells were sensitive to mitocans, but unfortunately more resistant than healthy blood cells.

In their best experimental results, 86% of targeted leukemia cells were killed, compared to only 30% of healthy blood cells. “A number of drugs currently used in the clinic have some cancer preference, but here we’re talking about a five-fold difference in survival,” Kirienko said.
The researchers also showed a significant correlation between how efficiently mitochondria can turn energy from incoming oxygen into useful adenosine triphosphate (ATP) and how resistant they are to treatment.

“The more efficient they are, the more resistant they will be to mitochondria-targeting drugs,” Kirienko said. “If this holds true, doctors can perform a relatively simple test of this specific parameter of mitochondrial health from a patient’s sample and predict whether the treatment would be effective.”
Panina said computational models led them to think the glycolysis pathway could be enlisted to help mitocans. “Glycolysis also provides ATP, so targeting that will decrease energy as well as block the precursor for energy production in mitochondria, which mitocans will exacerbate further,” she said. “It led us to believe this combination would have a synergistic effect.

“Cancer cells are usually more metabolically active than normal cells, so we predicted that they be might be more sensitive to this combined strike, and they are,” Panina said.

Kirienko said a presentation of the research she and Panina gave at MD Anderson’s recent Metabolism in Cancer Symposium drew a large response. “People were very interested, and they immediately started asking, ‘Did you test my favorite drug or combination?’ and ‘Are you going to test it in a wider panel of cancers?’”

That work is well underway, Panina said. “We’re currently doing high-throughput screening of these potential synergistic drug combinations against leukemia cells,” she said. “We’ve gone through 36 combinations so far, building landscapes for each one.”
“And we found some that are more effective than what’s reported in this paper,” Kirienko added. “But we’ve also found some that are antagonistic — two drugs that negate each other’s effects — so it’s also important to know what therapeutic cocktails should not go together.”

Co-authors of the paper are postdoctoral fellow Natalia Baran; Marina Konopleva, a physician-scientist and professor in the Department of Leukemia at MD Anderson; and Rice graduate student Fabio Brasil da Costa. Kirienko is an assistant professor of biosciences.
The Cancer Prevention Research Institute of Texas, the Welch Foundation and the National Institutes of Health supported the research.

Read the paper at http://www.nature.com/articles/s41419-019-1851-3.pdf.

This news release can be found online at http://news.rice.edu/2019/10/31/cocktail-proves-toxic-to-leukemia-cells/

Follow Rice News and Media Relations via Twitter @RiceUNews.

Related materials:


Kirienko Lab: http://kirienkolab.rice.edu/index.html
Marina Konopleva: http://faculty.mdanderson.org/profiles/marina_konopleva.html
Rice Department of BioSciences: http://biosciences.rice.edu
Wiess School of Natural Sciences: http://naturalsciences.rice.edu