Tag: medicine

Help with Heavy Menstrual Bleeding

In women with uterine fibroids, the drug elagolix suppresses ovarian hormone production and prevents heavy menstrual bleeding

About 50 % of women with uterine fibroids—non-cancerous muscle tumors that grow in the uterus—experience heavy menstrual bleeding and other symptoms.  Surgery is commonly recommended when these symptoms are severe enough to prompt a woman to seek treatment.  The most common surgery used to treat fibroids is removal of the uterus (hysterectomy), though in some cases, removal of the fibroids and repair of the uterus (myomectomy) are performed.  Surgery is usually extensive in both cases.  Long-acting hormone injections can reduce symptoms such as heavy bleeding in women with fibroids, but side effects can be significant and it can take months for the effects of the medications to wear off.

In a study published in the New England Journal of Medicine on January 23, 2020, researchers reported on the effectiveness of a new, rapidly reversible oral pill that was used to reduce heavy menstrual bleeding in women with uterine fibroids. The study, which included a large group of researchers from across the country, was led by Dr. William Schlaff, Chair of the Department of Obstetrics and Gynecology at the Sidney Kimmel Medical College at Thomas Jefferson University.

A total of 790 women, ages 18-51, with heavy bleeding due to fibroids, were enrolled into one of three study arms. One group received the oral pill, elagolix, which reduces the production of the hormones estrogen and progesterone normally produced by a woman’s ovaries.  When these hormones are suppressed, fibroids usually get smaller and bleeding is reduced.  A second group received elagolix plus a low dose of estrogen and progestin (“add-back” therapy) with the hope that the additional hormones would produce the same benefit but reduce the side effects of elagolix used alone (like hot flushes and bone loss).  A third group received identical placebo pills that did not contain elagolix or the “add back” hormones.  All of the women enrolled in the two identical trials reported by these researchers were confirmed to have uterine fibroids by ultrasound and heavy menstrual bleeding (more than 80mLs of blood loss per cycle) for at least two cycles. 

The results showed that 80.4% of the women treated with elagolix alone had a reduction of menstrual bleeding of 50% or more compared to 9.6% of the women in the placebo group.  Of those women treated with elagolix plus “add back” therapy, 72% had a reduction of 50% or more.  Women treated with elagolix alone had significantly more loss of bone mineral as compared with the women treated with placebo, a known and clinically significant side effect of this class of medications.  However, there was no difference between the loss of bone mineral in the group treated with elagolix and “add-back” as compared to those in the placebo group. 

For many women with fibroids, severe symptoms like bleeding have a major impact on the quality of life.  Surgery and long-acting injectable medications are acceptable treatments for many, but certainly not all women in this situation. 

“The potential value of an oral, easily reversible medication that can be combined with low-dose hormonal “add back” to reduce heavy menstrual bleeding while avoiding problematic symptoms and side effects could be a major step forward,” says Dr. Schlaff.

AbbVie Inc. funded these studies and participated in the study design, research, analysis, data collection, interpretation of data, reviewing and approval of the publication. Consult article reference for complete list of disclosures.

Article reference: William Schlaff et al., “Elagolix Therapy for Heavy Menstrual Bleeding in Women with Uterine Fibroids,” New England Journal of Medicine, DOI: 10.1056/NEJMoa1904351, 2019.

Rethinking interactions with mental health patients

Credit: Pixabay

New research overturns the belief that people with severe mental illness are incapable of effective communication with their psychiatrist, and are able to work together with them to achieve better outcomes for themselves.

“Interviews are a critical part of assessing people suffering from thought disorder (TD), and deciding what the best therapy is for them,” says Professor Cherrie Galletly from the Adelaide Medical School, University of Adelaide.

“Clinical interactions with people suffering with severe mental illness can be challenging, especially if the patient has disordered communication.”

Published in the journal Australian Psychiatry the study analysed 24 routine clinical interviews between psychiatrists and inpatients, with a mean age of just under 30 years, who were suffering from TD.

“The study, the first of its kind, examined the expertise with which psychiatrists conducted clinical interviews of people suffering from TD, and the shared goals that were accomplished,” says Professor Galletly.

“When interviewing people with TD psychiatrists need to adopt a mindset that the information the patient provides in that particular moment is, for them, meaningful, truthful, relevant and clear.

“They have to piece together snippets of information in order to create and interpret meaning and build respectful relationships by inviting patients to share their perspectives no matter how disordered or delusional their responses appear.”

Thought disorder is common in psychotic disorders. The thoughts and conversation of people suffering from TD appear illogical and lacking in sequence and may be delusional or bizarre in content.

In 2010, 0.3% of Australians aged 18-64 years, had a psychotic illness with men aged 25-34 experiencing the highest rates (0.5%) of illness.

“Patients are positioned as active participants by psychiatrists who adopt a non-confrontational, non-judgemental approach, conveying support and safety, and ask open ended questions which allows the patient to engage, feel listened to, and work with the psychiatrist to achieve a shared understanding,” says Professor Galletly.

“Findings from this study of sample interviews between psychiatrists and their patients highlight the need to rethink the notion that patients experiencing TD are incapable of communicating productively with the people trying to help them.

“Psychiatrists use transactional, relational and interactional techniques when they are talking to patients with thought disorder, which go beyond techniques normally employed in clinical interviews.

“Experienced psychiatrists undertake meaningful interviews with these patients, who in turn respond in ways that belie the notion that effective communication is not possible.

“The findings from this research can be used to develop training resources for clinicians who work with people with psychotic disorders.”

Animals can lie to themselves too

Like Humans, Crayfish Talk a Tough Game

Self-deception like this seems very human. Now, thanks to a recent study led by an Arizona State University biologist, for the first time we know that it happens in the animal kingdom, too.

Crayfish are some of the most aggressive creatures on earth. They fight with big claws capable of doing real damage. But sometimes there’s not much muscle under the bravado.

“What males are doing is making as little crappy muscle as possible, which is energetically saving,” said Michael Angilletta, a biology professor in the School of Life Sciences.

It’s like buying designer knockoffs. You save a lot of money, and most people can’t tell the difference. In the case of crayfish, you make a big claw without much muscle, and you put crappy muscle on it to boot. Everyone sees you wave your big claw and they presume that you’re a powerful crayfish.

“Since they signal to each other before fighting, this is a way they can convince someone to back down without fighting,” Angilletta said. “Importantly, this only works if there’s enough crayfish out there that have big claws that are actually strong. If you accidentally fight one of those and call a bluff, you’re going to lose a claw.”

In the crayfish world, losing a claw is a disaster: It takes up to two years for a claw to regenerate. In the meantime, no one is mating with anyone who has a puny claw. 

Angilletta and his co-authors have been studying self-deception in crayfish for about 10 years. In 2006 they accidentally discovered that many crayfish with big claws were quite weak. There was about a tenfold variation.

“You would go, ‘Oh, this (pinch) is going to hurt,’ but it doesn’t hurt at all,” Angilletta said. “The question is are they not trying, or are they really not strong? And it’s repeatable from day after day with the same individuals.”

They combined mathematical modeling with an experiment to show that crayfish meet the criteria for self-deception. This approach opens up the possibility of studying self-deception in nonhuman animals, without being able to talk to them. They used 97 adult males, staging fights between 20 select crayfish and 77 opponents.

“How do we know what a crayfish would do if it knows whether it’s weak or it’s strong?” Angilletta asked. “If it knows that (it has a weak claw), it should actually be less aggressive.”

It might escalate up to the point of a fight, and then run away. The probability that a crayfish engaged in a fight depended on two factors: the relative size of its claws and the expected difference in force. How do they know how strong (or not) they are? Crayfish use claws to deter predators, defend territory and capture prey. They have a pretty good idea of how strong their own claws are. They’re also skilled at assessing their size versus an opponent’s. They can even recognize previous opponents.

So natural selection has given them an ability to detect size and identity. Given that they have those abilities, it naturally follows that they have an ability to gauge strength when knowing it will improve decisions.

“In our population of crayfish, deceptive signalers largely ignored their own strength when escalating or evading aggression,” Angilletta said. “If this benefit of heightened aggression outweighs any long-term cost, natural selection should favor individuals who escalate aggression through self-deception.”

In other words, they buy into their own bluff. Angilletta teaches a biology course on human behavior called “Why people steal, cheat, and lie,” which explores the ecological and evolutionary causes of selfishness and cooperation in human societies.

“What’s new about this study is that if you’re ever in a situation where I’m lying to you, there’s also a possibility I’m selling my lie exceptionally well because I’ve convinced myself that it’s true,” he said. “That’s because of self-deception. It’s very common in psychology but it’s not really that much in biology because we’re usually thinking about nonhuman animals and we don’t know what they’re thinking. We have a hard time understanding what they know and don’t know.”

The paper was published last summer in Behavioral Ecology.

Video Credits:  Ken Fagan, ASU

Photo Credit: Charlie Leight, ASU

About ASU

Arizona State University has developed a new model for the American Research University, creating an institution that is committed to access, excellence and impact. ASU measures itself by those it includes, not by those it excludes. As the prototype for a New American University, ASU pursues research that contributes to the public good, and ASU assumes major responsibility for the economic, social and cultural vitality of the communities that surround it.

Medicinal Cannabis Research

Researchers will look at how CBD might help remedy schizophrenia, rheumatoid arthritis, insomnia, alcohol dependence and anorexia anxiety

The Center for Medicinal Cannabis Research (CMCR) at University of California San Diego School of Medicine, the nation’s oldest research center for scientific inquiry into the safety and efficacy of cannabis, has announced $3 million in research grants to explore new applications of cannabis for a number of novel medical applications.

The cannabis plant produces a number of compounds called cannabinoids, the most widely known of which are tetrahydrocannabinol (THC), its principle psychoactive agent, and cannabidiol (CBD), which has been linked to reduced pain, anxiety and inflammation in previous studies. The five new studies all focus on CBD.

“Within the medical community, there is a lot of interest in the role of medical cannabis and CBD,” said Igor Grant, MD, Distinguished Professor in the Department of Psychiatry and CMCR director. “There is a hope that it could be yet another useful agent in some of these conditions, which are difficult to treat or disabling.”

The five grants are funded by California Proposition 64, which was passed on the November 8, 2016 ballot and legalized recreational marijuana in the state. The measure allocated tax revenue for research on potential new drugs, treatment and health and safety programs related to marijuana and medical cannabis.

This year marks CMCR’s first such funding. All five grants are for proof-of-principle studies that would seek to establish the basis for future research.

Effects of Cannabidiol versus Placebo as an Adjunct to Treatment in Early Psychosis

The $825,000 grant was awarded to Kristin Cadenhead, MD, professor of psychiatry at UC San Diego School of Medicine, and colleagues, who will explore whether medical cannabis could serve as an alternative treatment for patients facing early psychosis, a time when traditional treatments, such as antipsychotic medications, are moderately effective but produce debilitating side effects.

Therapeutic Response of Cannabidiol in Rheumatoid Arthritis

The $825,000 grant was awarded to Veena Ranganath, MD, a rheumatologist at UCLA Medical Center. Ranganath’s research focuses on CBD’s use an anti-inflammatory agent, an application she hopes to exploit in treating rheumatoid arthritis, a chronic autoimmune condition that affects an estimated 1.5 million persons in the United States.

Cannabidol for Sedative/Hypnotic-sparing Management of Insomnia in Adults

The $825,000 grant was awarded to Mariana Cherner, PhD, professor of psychiatry at UC San Diego School of Medicine, and colleagues, who will investigate whether CBD might be a viable alternative for sleeping pills among patients with chronic sleep disorders.

“Sleeping pills are moderately safe but they can also be habit-forming and they do have side effects, particularly in older people,” said Grant. “So many people are prescribed sleeping pills so there’s good reason to look for something that might be safer and not have that side effect profile.”

Cannabidiol as a Strategy to Treat Alcohol Dependence

The $300,000 grant was awarded to Giordano de Guglielmo, PhD, assistant adjunct professor in the UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences, and colleagues. This study is the only one of the five using an animal model. It will look at the role CBD might play in reducing alcohol cravings and withdrawal syndromes among alcohol-addicted rats, with findings perhaps applicable to future human research.

The Role of Cannabidiol in Regulating Meal Time Anxiety in Anorexia Nervosa

The $300,000 grant was awarded to Emily Gray, MD, associate clinical professor of psychology at UC San Diego School of Medicine, and colleagues, who will explore whether CBD can help reduce a core symptom of anorexia — anxiety about food — and whether or not that reduction helps patients also reduce their food aversions overall.

A second round of CMCR grants is scheduled for 2020.

Sweating People

Photo by Food Photographer | Jennifer Pallian

When people become stressed, their bodies can respond by sweating. Now, researchers at the University of Missouri are monitoring how much adolescents severely affected by autism sweat in order to better understand when behavioral issues, such as aggression, are likely to occur.

Bradley Ferguson analyzed the stress levels of eight adolescents who are severely affected by autism spectrum disorder at The Center for Discovery, a residential facility in New York that provides advanced care and research for individuals with complex conditions. Using wrist and ankle monitors, Ferguson found that there was a rise in the body’s electrodermal activity – which results from increased levels of sweat – 60% of the time before an individual showed behavioral issues.

“A spike in electrodermal activity is telling us that the individual’s body is reacting physiologically to something that is stressful, which could be their internal state, something in the environment, or a combination of the two,” said Ferguson, assistant research professor in the departments of health psychology, radiology and the Thompson Center for Autism and Neurodevelopmental Disorders. “If parents or caregivers are notified ahead of time that their child’s stress levels are rising, they might have a chance to intervene and de-escalate the situation before problem behaviors occur.”

Ferguson explained that possible intervention methods could include removing the child from the environment or activity that is causing the stress, as well as providing access to an item that the child enjoys interacting with in an effort to calm them.

“Individuals who are severely affected by autism spectrum disorder are often unable to verbally communicate their discomfort when they become stressed,” Ferguson said. “However, their body still responds to stressors just like anyone else. Therefore, being alerted of increases in electrodermal activity can allow parents and caregivers to intervene prior to engagement in problem behavior with the goal of ensuring the health and safety of those involved.”

Ferguson collaborated on the study with David Beversdorf, a professor of radiology, neurology and psychology in the MU College of Arts and Science as well as principal investigator of the Cognitive Neuroscience Laboratory in the MU School of Medicine. Ferguson also collaborated with Theresa Hamlin, Johanna Lantz, and Tania Villavicencio at The Center for Discovery, and John Coles at Calspan-University of Buffalo Research Center and The State University of New York at Buffalo.

“Important work is being done to try to identify predictors for when a person with autism is at greatest risk of having a behavioral episode,” Beversdorf said. “This research highlights the individual variability in this response that must be considered, and may also have implications for individualized treatment approaches moving forward.”

“Examining the association between electrodermal activity and problem behavior in severe autism spectrum disorder: A feasibility study,” was published in Frontiers in Psychiatry.

The study was funded by the New York State Center of Excellence, New York State Department of Health and Office for People with Developmental Disabilities, as well as private monies donated to The Center for Discovery. The content is solely the responsibilities of the authors and does not necessarily represent the official views of the funding agencies.

The Department of Health Psychology is in the MU School of Health Professions, and the Department of Radiology is in the MU School of Medicine.

Harvard University to Launch Center for Autism Research

Autism and related disorders—a constellation of neurodevelopmental conditions affecting one in 59 children in the United States alone—have become one of modern medicine’s most confounding mysteries. The condition is believed to arise from the complex interplay between genes and environment, yet its basic biology remains largely a black box.

Now, a new research effort at Harvard University led by Harvard Medical School is poised to identify the biologic roots and molecular changes that give rise to autism and related disorders with the goal of informing the development of better diagnostic tools and new therapies. Harvard University has received a $20 million gift from philanthropists Lisa Yang and Hock Tan, an alumnus of Harvard Business School, to establish The Hock E. Tan and K. Lisa Yang Center for Autism Research at Harvard Medical School. The latest gift brings the total autism-related research funding provided by Yang and Tan to nearly $70 million.

The center will serve as a hub that brings together the diverse expertise of scientists and clinicians working throughout Harvard University, Harvard Medical School and its affiliated hospitals.

“There is an urgent need to understand the fundamental biology of autism,” said Michael Greenberg, chair of the Department of Neurobiology at Harvard Medical School and the center’s inaugural faculty leader. “I strongly believe that the multidisciplinary expertise convened by this center will propel us into a new era of autism research, enhancing our understanding of the condition and yielding critical new insights into its causes. This generous gift will be transformative for the field.”

Working under the premise that autism’s complexity demands the cross-pollination of diverse expertise across different modes of scientific inquiry, the center will encompass the efforts of basic, translational and clinical scientists from the entire Harvard ecosystem. The center will have its administrative home within the Harvard Brain Science Initiative, which brings together researchers from Harvard Medical School and its affiliated hospitals as well as from the Harvard Faculty of Arts and Sciences, the Harvard T.H. Chan School of Public Health and the Harvard John A. Paulson School of Engineering and Applied Sciences. “Neuroscience has reached a unique inflection point. Advances such as single-cell analysis and optogenetics, coupled with an unprecedented ability to visualize molecular shifts down to the minutest level, will enable today’s researchers to tackle a disorder as dauntingly complex as autism,” said Harvard Medical School Dean George Q. Daley.

“Medical history has taught us that truly transformative therapies flow only from a clear understanding of the fundamental biology that underlies a condition,” Daley added. “This gift will allow our researchers to generate critical insights about autism and related disorders.”

Investigators at the new Harvard University center will collaborate with peer researchers at MIT and complement efforts already underway at The Hock E. Tan and K. Lisa Yang Center for Autism Research at the McGovern Institute for Brain Research at MIT, with the unique strengths of each institution converging toward a shared goal: understanding the roots of autism, explaining the condition’s behavior and evolution and translating those insights into novel approaches to treat its symptoms.

“In a short time, the Tan-Yang Center at the McGovern Institute has supported groundbreaking research we believe will change our understanding of autism,” said Robert Desimone, the director of the sibling center at MIT. “We look forward to joining forces with the new center at Harvard, to greatly accelerate the pace of autism-related research.”

“We are excited and hopeful that these sibling centers at Harvard and MIT—two powerhouses of biomedical research—will continue to collaborate in a synergistic way and bring about critical new insights to our understanding of autism,” Yang said. Yang is a former investment banker who has devoted much of her time to mental health advocacy. Tan is president and CEO of Broadcom, a global infrastructure technology company. 

Autism-spectrum disorders—neurodevelopmental conditions that typically emerge in the first few years of life—are marked by a cluster of symptoms, impaired social interactions and compromised communication skills. Yet exactly what portion of these cases is rooted in genetic mutations and how they are influenced by environmental factors is an area of lingering uncertainty. Another key area of uncertainty is how much of autism’s fundamental features arise in the brain and what influence organs and systems outside of the brain might have.

Two of the new center’s initial areas of inquiry will address these critical gaps in knowledge.

One group of researchers will focus on understanding precisely what goes awry during critical windows in the first two years of life—a period marked by rapid brain development, great neuroplasticity and intense wiring of the brain’s circuits. This is also the typical window of autism diagnosis. The scientists will try to understand what molecular, cellular or neural-circuitry changes underlie autism-fueling processes during this stage. Identifying such critical changes can help illuminate how experiences modulate brain development in individuals with autism.

Another group of researchers will examine the role of factors arising from organs and organ systems outside the brain that may drive autism risk. For example, the peripheral nervous system—made up of nerve cells throughout the body that act as nodes to collect and transmit signals to the brain—has emerged as a central player in the development of autism.

Heightened sensitivity to even light touch is a common feature in autism and one of the disorder’s many perplexing symptoms. Recent research from neurobiologists and geneticists at Harvard Medical School has not only identified the molecular changes that give rise to heightened touch sensitivity in autism-spectrum disorders but also points to a possible treatment for the condition.

Autism rates increasing fastest among black and Hispanic children

Autism rates among racial minorities in the United States have increased by double digits in recent years, with black rates now exceeding those of whites in most states and Hispanic rates growing faster than any other group, according to new University of Colorado Boulder research.

The study, published this month in the Journal of Autism and Developmental Disorders, also found that prevalence of autism among white youth is ticking up again, after flattening in the mid-2000s.

While some of the increase is due to more awareness and greater detection of the disorder among minority populations, other environmental factors are likely at play, the authors conclude.

“We found that rates among blacks and Hispanics are not only catching up to those of whites — which have historically been higher — but surpassing them,” said lead author Cynthia Nevison, an atmospheric research scientist with the Institute of Arctic and Alpine Research. “These results suggest that additional factors beyond just catch-up may be involved.”

For the study, Nevison teamed up with co-author Walter Zahorodny, an autism researcher and associate professor of pediatrics at Rutgers New Jersey Medical School, to analyze the most recent data available from the Individuals with Disabilities Education Act (IDEA) and the Autism and Developmental Disabilities Monitoring (ADDM) Network.

IDEA tracks prevalence, including information on race, among 3-to-5-year-olds across all 50 states annually. ADDM tracks prevalence among 8-year-olds in 11 states every two years.

The new study found that between birth year 2007 and 2013, autism rates among Hispanics age 3-5 rose 73%, while rates among blacks that age rose 44% and rates among whites rose 25%.

In 30 states, prevalence among blacks was higher than among whites by 2012.

In states with “high prevalence,” 1 in 79 whites, 1 in 68 blacks and 1 in 83 Hispanics born in 2013 have been diagnosed with autism by age 3-5.

Other states like Colorado fell in a “low-prevalence” category, but the authors cautioned that differences between states likely reflect differences in how well cases are reported by age 3-5. They also said the real prevalence is substantially higher, as many children are not diagnosed until later in life.

“There is no doubt that autism prevalence has increased significantly over the past 10 to 20 years, and based on what we have seen from this larger, more recent dataset it will continue to increase among all race and ethnicity groups in the coming years,” said Zahorodny.

In 2018, the Centers for Disease Control reported that about 1 in 59 children of all races have been diagnosed with autism and that rates had risen 15 percent overall from the previous two year period, largely due to better outreach and diagnosis among historically underdiagnosed minority populations. The new study challenges that explanation.

“Our data contradict the assertion that these increases are mainly due to better awareness among minority children,” said Zahorodny. “If the minority rates are exceeding the white rates that implies some difference in risk factor, either greater exposure to something in the environment or another trigger.”

Established risk factors associated with autism include advanced parental age, challenges to the immune system during pregnancy, genetic mutations, premature birth and being a twin or multiple.

The authors said that, based on current research, they cannot pinpoint what other environmental exposures might be factoring into the increases in autism. But they would like to see more research done in the field.

New Data on Several Oncology Compounds at ASCO 2015

WOODCLIFF LAKE, N.J., May 14, 2015 — Eisai Inc. announced today the presentation of seven abstracts at the 51st Annual Meeting of the American Society of Clinical Oncology (ASCO) highlighting the breadth of the company’s oncology portfolio. The meeting will be held May 29-June 2 in Chicago.
“We are excited by our data at this year’s ASCO Annual Meeting, which exemplify the strength and diversity of Eisai’s oncology portfolio and our ongoing dedication to providing potential treatment options to underserved patient populations,” said Kenichi Nomoto, Ph.D., President, Oncology Product Creation Unit at Eisai Inc. “In support of our human health care (hhc) mission, we remain committed to the development of compounds that have the potential to positively affect the lives of patients with cancer and thereby their loved ones.”
Of note, the results of a Phase 3 study of eribulin mesylate for investigational use in advanced soft tissue sarcoma (STS) will be included in the ASCO press conference on Saturday, May 30. The data will also be presented in an oral session on June 1.
In addition, the results of a Phase 2 study of lenvatinib for investigational use in metastatic renal cell carcinoma will be presented in an oral session on June 1.
Additional presentations will include ongoing analyses of the Phase 3 trial evaluating lenvatinib, a receptor tyrosine kinase (RTK) inhibitor, in radioactive iodine-refractory differentiated thyroid cancer; palonosetron in the prevention of chemotherapy-induced nausea and vomiting (CINV) in pediatric patients; and NEPA, an oral fixed combination of netupitant and palonosetron, in the prevention of CINV in patients receiving carboplatin chemotherapy.
The following abstracts are accepted for presentation at this year’s ASCO meeting:
Abstract Name
Session
Eribulin Mesylate Abstracts
Randomized, open-label, multicenter, phase 3 study of eribulin versus dacarbazine in patients (pts) with leiomyosarcoma (LMS) and adipocytic sarcoma (ADI)
Abstract #LBA10502
Oral presentation
Monday, June 1
Oral: 3:48 p.m. – 4:00 p.m. CT
Schöffski P.
Lenvatinib Abstracts
Randomized phase II three-arm trial of lenvatinib (LEN), everolimus (EVE), and LEN+EVE in patients (pts) with metastatic renal cell carcinoma (mRCC)
Abstract #4506
Oral presentation
Monday, June 1
Oral: 11:45 a.m. – 11:57 a.m. CT
Motzer R.
Effect of age and lenvatinib treatment on overall survival for patients with 131I-refractory differentiated thyroid cancer in SELECT
Abstract #6048
Poster presentation
Saturday, May 30
Poster: 1:15 p.m. – 4:45 p.m. CT
Brose M.
Pharmacodynamic biomarkers of outcomes in the phase 3 study of lenvatinib in 131I-refractory differentiated thyroid cancer (SELECT)
Abstract #6014
Poster presentation
Saturday, May 30
Poster: 1:15 p.m. – 4:45 p.m. CT
Panel Discussion: 4:45 p.m. – 6:00 p.m. CT
Tahara M.
Efficacy and safety of lenvatinib for the treatment of patients with 131I-refractory differentiated thyroid cancer with and without prior VEGF-targeted therapy
Abstract #6013
Poster presentation
Saturday, May 30
Poster: 1:15 p.m. – 4:45 p.m. CT
Panel Discussion: 4:45 p.m. – 6:00 p.m. CT
Newbold K.
NEPA Abstracts
Should all antiemetic guidelines recommend adding a NK1 receptor antagonist (NK1RA) in patients (pts) receiving carboplatin (carbo): Efficacy evaluation of NEPA, a fixed combination of the NK1RA, netupitant, and palonosetron
Abstract #9597
Poster presentation
Saturday, May 30
Poster: 1:15 p.m. – 4:45 p.m. CT
Jordan K.
Palonosetron Abstracts
Palonosetron vs ondansetron: Prevention of chemotherapy-induced nausea and vomiting in pediatric patients in a multicycle study
Abstract #10077
Poster presentation
Sunday, May 31
Poster: 8:00 a.m. – 11:30 a.m. CT
Kabickova E.
The information discussed in this release presents investigational uses for FDA-approved products. It is not intended to convey conclusions about efficacy and safety. There is no guarantee that any of these investigational uses of FDA-approved products will successfully complete clinical development or gain FDA approval.
About Lenvatinib (Available as LENVIMA™)Lenvatinib is indicated for the treatment of patients with locally recurrent or metastatic, progressive, radioactive iodine-refractory differentiated thyroid cancer (DTC).
Lenvatinib, discovered and developed by Eisai, is a receptor tyrosine kinase (RTK) inhibitor that inhibits the kinase activities of vascular endothelial growth factor (VEGF) receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (FLT4). Lenvatinib also inhibits other RTKs that have been implicated in pathogenic angiogenesis, tumor growth, and cancer progression in addition to their normal cellular functions, including fibroblast growth factor (FGF) receptors FGFR1, 2, 3, and 4; the platelet derived growth factor receptor alpha (PDGFRα), KIT, and RET. Lenvatinib was approved under Priority Review designation for locally recurrent or metastatic, progressive, radioactive iodine-refractory differentiated thyroid cancer by the FDA in February 2015. Eisai was granted Orphan Drug Designation (ODD) for lenvatinib in various types of thyroid cancer in the United States, Japan, and Europe.
Important Safety Information
Warnings and Precautions
Hypertension was reported in 73% of lenvatinib-treated patients (of which 44% were ≥ Grade 3) and 16% of patients in the placebo group. Control blood pressure prior to treatment and monitor blood pressure after 1 week, then every 2 weeks for the first 2 months, and then at least monthly during treatment.  Withhold lenvatinib for Grade 3 hypertension; resume at a reduced dose when hypertension is controlled at ≤ Grade 2. Discontinue lenvatinib for life-threatening hypertension.
Cardiac dysfunction was reported in 7% of lenvatinib-treated patients (2% Grade 3 or greater). Monitor patients for clinical symptoms or signs of cardiac decompensation. Withhold lenvatinib for development of Grade 3 cardiac dysfunction until improved to Grade 0 or 1 or baseline. Resume at a reduced dose or discontinue lenvatinib depending on the severity and persistence of cardiac dysfunction. Discontinue lenvatinib for Grade 4 cardiac dysfunction.
Arterial thromboembolic events were reported in 5% of lenvatinib-treated patients; events of Grade 3 or greater were 3%. Discontinue lenvatinib following an arterial thrombotic event. Lenvatinib has not been studied in patients who have had an arterial thromboembolic event within the previous 6 months.
4% of lenvatinib-treated patients experienced an increase in ALT and 5% experienced an increase in AST that was Grade 3 or greater. Monitor liver function before initiation and during treatment with lenvatinib. Withhold lenvatinib for the development of ≥ Grade 3 liver impairment until resolved to Grade 0 to 1 or baseline. Resume at a reduced dose or discontinue lenvatinib depending on the severity and persistence of hepatotoxicity. Discontinue lenvatinib for hepatic failure.
Proteinuria was reported in 34% of lenvatinib-treated patients (of which 11% were Grade 3). Monitor for proteinuria before initiation of, and periodically during treatment. Obtain a 24 hour urine protein if urine dipstick proteinuria ≥2+ is detected. Withhold lenvatinib for ≥ 2 grams of proteinuria/24 hours and resume at a reduced dose when proteinuria is <2 gm/24 hours. Discontinue lenvatinib for nephrotic syndrome.
Events of renal impairment were reported in 14% of lenvatinib-treated patients. Renal failure or impairment ≥ Grade 3 was 3% in lenvatinib-treated patients. Withhold lenvatinib for development of Grade 3 or 4 renal failure/impairment until resolved to Grade 0 to 1 or baseline. Resume at a reduced dose or discontinue lenvatinib depending on the severity and persistence of renal impairment. 
Events of gastrointestinal perforation or fistula were reported in 2% of lenvatinib-treated patients.  Discontinue lenvatinib in patients who develop gastrointestinal perforation or life-threatening fistula.
QT/QTc interval prolongation was reported in 9% of lenvatinib-treated patients (2% Grade 3 or greater).  Monitor ECG in patients with congenital long QT syndrome, CHF, bradyarrhythmias, or patients taking drugs known to prolong the QT interval. Monitor and correct electrolyte abnormalities in all patients.  Withhold lenvatinib for the development of ≥ Grade 3 QT interval prolongation. Resume lenvatinib at a reduced dose when QT prolongation resolves to Grade 0 or 1 or baseline.
Hypocalcemia ≥ Grade 3 was reported in 9% of lenvatinib-treated patients. Monitor blood calcium levels at least monthly and replace calcium as necessary during lenvatinib treatment. Interrupt and adjust lenvatinib dosing as necessary depending on severity, presence of ECG changes, and persistence of hypocalcemia.
Reversible posterior leukoencephalopathy syndrome (RPLS) was reported in 3 patients across clinical studies in which 1108 patients received lenvatinib. Confirm the diagnosis of RPLS with MRI. Withhold lenvatinib for RPLS until fully resolved. Resume at a reduced dose or discontinue lenvatinib depending on the severity and persistence of neurologic symptoms.
Hemorrhagic events occurred in 35% of lenvatinib-treated patients and in 18% of the placebo group.  The incidence of Grade 3-5 hemorrhage was similar between arms at 2% and 3%, respectively. The most frequently reported hemorrhagic event was epistaxis (11% Grade 1 and 1% Grade 2). Discontinuation due to hemorrhagic events occurred in 1% of lenvatinib-treated patients. There was one case of fatal intracranial hemorrhage among 16 patients who received lenvatinib and had CNS metastases at baseline. Withhold lenvatinib for the development of Grade 3 hemorrhage until resolved to Grade 0 to 1.  Resume at a reduced dose or discontinue lenvatinib depending on the severity and persistence of hemorrhage. Discontinue lenvatinib in patients who experience Grade 4 hemorrhage.
Lenvatinib impairs exogenous thyroid suppression. Elevation of TSH level above 0.5 mU/L was observed post baseline in 57% of lenvatinib-treated patients. Monitor TSH levels monthly and adjust thyroid replacement medication as needed.
Lenvatinib can cause fetal harm when administered to a pregnant woman. Advise pregnant women of the potential risk to a fetus. Advise females of reproductive potential to use effective contraception during treatment with lenvatinib and for at least 2 weeks following completion of therapy.
Advise women not to breastfeed during treatment with lenvatinib.
Adverse Reactions
The most common adverse reactions observed in lenvatinib-treated patients vs. placebo-treated patients respectively were hypertension (73% vs 16%), fatigue (67% vs 35%), diarrhea (67% vs 17%), arthralgia/myalgia (62% vs 28%), decreased appetite (54% vs 18%), weight decreased (51% vs 15%), nausea (47% vs 25%), stomatitis (41% vs 8%), headache (38% vs 11%), vomiting (36% vs 15%), proteinuria (34% vs 3%), palmar-plantar erythrodysesthesia syndrome (32% vs 1%), abdominal pain (31% vs 11%), and dysphonia (31% vs 5%).
For more information about lenvatinib, click here for the full Prescribing Information.
About Eribulin Mesylate Injection (available as Halaven®)
Eribulin is indicated for patients with metastatic breast cancer who have received at least two chemotherapeutic regimens for the treatment of metastatic breast cancer. Prior therapy should have included an anthracycline and a taxane in either the adjuvant or metastatic setting. Eribulin is a synthetic analog of halichondrin B, a natural product that was isolated from the marine sponge Halichondria okadai. First in the halichondrin class, eribulin is a microtubule dynamics inhibitor with a distinct binding profile. Based on in vitro studies, eribulin exerts its effect via a tubulin-based antimitotic mechanism ultimately leading to apoptotic cell death after prolonged and irreversible mitotic blockage.
Important Safety Information
Neutropenia
  • Monitor complete blood counts prior to each dose, and increase the frequency of monitoring in patients who develop Grade 3 or 4 cytopenias. Delay administration and reduce subsequent doses in patients who experience febrile neutropenia or Grade 4 neutropenia lasting longer than 7 days
  • Severe neutropenia (ANC <500/mm3) lasting more than 1 week occurred in 12% (62/503) of patients. Patients with elevated liver enzymes >3 × ULN and bilirubin >1.5 × ULN experienced a higher incidence of Grade 4 neutropenia and febrile neutropenia than patients with normal levels
  • Grade 3 and Grade 4 neutropenia occurred in 28% and 29%, respectively, of patients who received eribulin. Febrile neutropenia occurred in 5% of patients and two patients (0.4%) died from complications
Peripheral Neuropathy
  • Patients should be monitored closely for signs of peripheral motor and sensory neuropathy
  • Grade 3 peripheral neuropathy occurred in 8% of patients, and Grade 4 in 0.4% of patients who received eribulin. Delay administration of eribulin until resolution to Grade 2 or less
  • Neuropathy lasting more than 1 year occurred in 5% of patients. Twenty-two percent of patients developed a new or worsening neuropathy that had not recovered within a median follow-up duration of 269 days (range 25-662 days)
  • Peripheral neuropathy (5%) was the most common adverse reaction resulting in discontinuation
Pregnancy Category D
  • Eribulin is expected to cause fetal harm when administered to a pregnant woman and patients should be advised of these risks
QT Prolongation
  • In an uncontrolled ECG study in 26 patients, QT prolongation was observed on Day 8, independent of eribulin concentration, with no prolongation on Day 1. ECG monitoring is recommended for patients with congestive heart failure; bradyarrhythmias; concomitant use of drugs that prolong QT interval, including Class Ia and III antiarrhythmics; and electrolyte abnormalities
  • Correct hypokalemia or hypomagnesemia prior to initiating eribulin and monitor electrolytes periodically during therapy. Avoid in patients with congenital long QT syndrome
Hepatic and Renal Impairment
  • For patients with mild (Child-Pugh A) or moderate (Child-Pugh B) hepatic and/or moderate or severe (CrCl 15-49 mL/min) renal impairment, a reduction in starting dose is recommended
Most Common Adverse Reactions
  • Most common adverse reactions (≥25%) reported in patients receiving eribulin were neutropenia (82%), anemia (58%), asthenia/fatigue (54%), alopecia (45%), peripheral neuropathy (35%), nausea (35%), and constipation (25%)
  • The most common serious adverse reactions reported in patients receiving eribulin were febrile neutropenia (4%) and neutropenia (2%)
For more information about eribulin, click here for the full Prescribing Information.
About Netupitant/Palonosetron (Available as AKYNZEO®) Netupitant/palonosetron (NEPA) is indicated for the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of cancer chemotherapy, including, but not limited to, highly emetogenic chemotherapy. NEPA is an oral fixed combination of a 5-HT3 receptor antagonist, palonosetron, and an NK1 receptor antagonist, netupitant: palonosetron prevents nausea and vomiting during the acute phase and netupitant prevents nausea and vomiting during both the acute and delayed phase after cancer chemotherapy.
On March 26, 2015, the Committee for Medicinal Products for Human Use (CHMP) adopted a positive opinion recommending that NEPA be granted marketing authorization in the European Union for the prevention of acute and delayed nausea and vomiting associated with highly emetogenic cisplatin‑based cancer chemotherapy and moderately emetogenic cancer chemotherapy.
Important Safety Information
Warnings and Precautions
  • Hypersensitivity reactions, including anaphylaxis, have been reported with or without known hypersensitivity to other 5-HT3 receptor antagonists
  • Serotonin syndrome has been reported with 5-HT3 receptor antagonists alone but particularly with concomitant use of serotonergic drugs.  Serotonin syndrome can be life threatening.  Symptoms associated with serotonin syndrome may include the following combination of signs and symptoms: mental status changes, autonomic instability, neuromuscular symptoms, seizures, and gastrointestinal symptoms. Patients should be monitored for the emergence of serotonin syndrome, and if symptoms occur, discontinue NEPA and initiate supportive treatment.  Patients should be informed of the increased risk of serotonin syndrome, especially if NEPA is used concomitantly with other serotonergic drugs
Adverse Reactions
  • Most common adverse reactions: headache, asthenia, dyspepsia, fatigue, constipation and erythema
Drug Interactions
  • Use with caution in patients receiving concomitant medications primarily metabolized by CYP3A4. The plasma concentrations of CYP3A4 substrates can increase when co-administered with NEPA. The inhibitory effect on CYP3A4 can last for multiple days
    • Dexamethasone doses should be reduced when given with NEPA. A two-fold increase in the systemic exposure of dexamethasone was observed 4 days after single dose of netupitant
    • Consider the potential effects of increased plasma concentrations of midazolam or other benzodiazepines metabolized via CYP3A4 (alprazolam, triazolam) when administering with NEPA. When administered with netupitant, the systemic exposure to midazolam was significantly increased
  • Avoid concomitant use of NEPA in patients on chronic use of a strong CYP3A4 inducer such as rifampin as this may decrease the efficacy of NEPA
Use in Specific Populations
  • Avoid use of NEPA in patients with severe hepatic impairment, severe renal impairment, or end-stage renal disease
NEPA is available by prescription only.
For more information about NEPA, click here for the full Prescribing Information.
About Palonosetron HCl (available as ALOXI®)
Indication in Pediatrics Palonosetron injection 20mcg/kg (max 1.5mg) is indicated in patients ≥ 1 month up to 17 years of age, for the prevention of acute nausea and vomiting associated with initial and repeat courses of emetogenic cancer chemotherapy, including highly emetogenic chemotherapy.
Indication in Adults Palonosetron injection 0.25 mg is indicated in adults for the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of moderately emetogenic chemotherapy, and the prevention of acute nausea and vomiting associated with initial and repeat courses of highly emetogenic chemotherapy.
Important Safety Information
Contraindications
  • Palonosetron is contraindicated in patients known to have hypersensitivity to the drug or any of its components
Warnings and Precautions
  • Hypersensitivity reactions, including anaphylaxis, have been reported with or without known hypersensitivity to other 5-HT3 receptor antagonists
  • Serotonin syndrome has been reported with 5-HT3 receptor antagonists alone, but particularly with the use of serotonergic drugs. Serotonin syndrome can be life threatening. Symptoms may include the following combination of signs and symptoms: mental status changes, autonomic instability, neuromuscular symptoms, seizures, and gastrointestinal symptoms. Patients should be monitored for the emergence of serotonin syndrome, and if symptoms occur, discontinue palonosetron and initiate supportive treatment.  Patients should be informed of the increased risk of serotonin syndrome, especially if palonosetron is used concomitantly with other serotonergic drugs.  
Adverse Reactions
  • In pediatric patients, while they require a higher dose of palonosetron, the safety profile is consistent with the established profile in adults; however, adverse reactions were reported in <0.1% of pediatric patients
  • In adults, the most commonly reported adverse drug reactions include headache (9%) and constipation (5%)
Palonosetron is available by prescription only.
For more information about palonosetron, click here for the full Prescribing Information.
About Helsinn and EisaiHelsinn signed a licensing agreement with Eisai Inc. granting Eisai commercial rights for NEPA in the United States. Under the terms of the agreement, Helsinn is responsible for conducting all development activities, obtaining regulatory approvals and holding the New Drug Application (NDA). NEPA is co-promoted in the United States by Eisai Inc. and Helsinn Therapeutics U.S. Inc., the U.S. subsidiary of Helsinn.
About the Helsinn GroupHelsinn is a family run, privately owned pharmaceutical group focused on building quality cancer care with a large portfolio of products. Founded in 1976 with headquarters in Lugano, Switzerland, Helsinn also has operating subsidiaries in Ireland, the U.S. and a representative office in China. Helsinn’s business model is focused on the licensing of pharmaceuticals, medical devices and nutritional supplement products in the therapeutic area of cancer care.
Helsinn Group in-licenses early-to-late stage new chemical entities, completing their development by performing preclinical and clinical studies and associated manufacturing activities. Helsinn then prepares necessary regulatory filings in order to achieve marketing approvals worldwide. Helsinn’s products are out-licensed to its global network of marketing and commercial partners that have been selected for their local market knowledge. Helsinn supports these partners by providing a full range of product and scientific management services, including commercial, regulatory, and medical marketing advice. In March 2013, Helsinn established a new commercial organization within its subsidiary, Helsinn Therapeutics (U.S.), Inc., in order to conduct direct sales and marketing activities within the U.S. market. Helsinn’s products are manufactured according to the highest quality, safety, and environmental standards at Helsinn’s GMP facilities in Switzerland and Ireland from where they are then supplied worldwide to customers. Further information on Helsinn Group is available at www.helsinn.com.
About Eisai Inc.At Eisai Inc., human health care is our goal. We give our first thoughts to patients and their families, and helping to increase the benefits health care provides. As the U.S. pharmaceutical subsidiary of Tokyo-based Eisai Co., Ltd., we have a passionate commitment to patient care that is the driving force behind our efforts to help address unmet medical needs. We are a fully integrated pharmaceutical business with discovery, clinical, manufacturing and marketing capabilities. Our key areas of commercial focus include oncology and specialty care (Alzheimer’s disease, epilepsy and metabolic disorders). To learn more about Eisai Inc., please visit us at www.eisai.com/US
Eisai Inc. has affiliates that are part of a global product creation organization that includes R&D facilities in Massachusetts, New Jersey, North Carolina and Pennsylvania, as well as a global demand chain organization that includes manufacturing facilities in Maryland and North Carolina. Eisai’s global areas of R&D focus include neuroscience; oncology; metabolic disorders; vascular, inflammatory and immunological reaction; and antibody-based programs.
About the SFJ Pharmaceuticals GroupThe SFJ Pharmaceuticals Group, which includes SFJ Pharma Ltd., is a global drug development company, which provides a unique co-development partnering model for some of the world’s top pharmaceutical and biotechnology companies. SFJ uses its financial strength and core team of pharmaceutical development experts to provide highly customized partnering models in which SFJ provides the funding and clinical development supervision, necessary to obtain regulatory approval for some of the most promising drug development programs of pharmaceutical and biotechnology companies.
Contacts:
Media Inquiries
Laurie Landau
Eisai Inc.
(201) 746-2510
Investor Inquiries
Alex Scott
Eisai Inc.
(201) 746-2177

SOURCE Eisai Inc.

RELATED LINKS
http://www.eisai.com

Rise in cost of MS drugs over past two decades

Study shows cost of multiple sclerosis drugs increased five to seven times greater than prescription drug inflation; researchers voice concern about patient access to life-changing treatments

 

PORTLAND, Ore., April 24, 2015 / — A new study shows an “alarming rise” over the last 20 years in the costs of drugs used to slow the progression of multiple sclerosis or reduce the frequency of attacks, according to a study led by researchers at Oregon Health & Science University (OHSU) and Oregon State University (OSU).
A substantial increase in the number of MS drugs in the marketplace over the past 20 years, paradoxically, did not lead to lower or stabilized costs for patients who use those drugs. Researchers found the costs of all drugs used to treat MS – including first-generation therapies – skyrocketed. Their work is published online today in the May 26, 2015, issue of Neurology®, the medical journal of the American Academy of Neurology.
The costs of MS drugs accelerated at rates five to seven times higher than prescription drug inflation and substantially higher than rates for drugs in a similar class between 1993 and 2013, the researchers report. Drug costs for several MS agents rose on average 20 to 30 percent per year over this time period.
In response to mounting concerns about the affordability of drugs used to treat MS, researchers examined 20 years of drug pricing data for nine MS drug treatments beginning with the initially approved injectable medications, up through the approval of the newest oral drugs.
“The inexplicable increase in the cost of MS drugs, particularly older, first- generation drugs, is at odds with how we think the marketplace should work. A growth in the number of MS drugs should lower costs for patients. What we see here is the opposite happened: costs have risen sharply, and at a pace that’s far greater than drugs in a similar biologic class,” said Daniel M. Hartung, Pharm.D., M.P.H., lead author of the study and associate professor in the OSU/OHSU College of Pharmacy.
Researchers found that long-standing drugs, such as Betaseron™, Avonex™ and Copaxone™, originally costing $8,000 to $11,000, now cost approximately $60,000 per year  – an average increase of 21 to 36 percent annually. Their cost acceleration corresponded with the approval of newer agents, including Gilenya™, Aubagio™, and Tecfidera™, which have increased 8 to 17 percent annually since their approval. During that same period, general and prescription drug inflation only increased 3 to 5 percent per year.
The study shows that U.S. prices for MS drugs were also out of step with costs in other developed countries. In comparing current U.S. costs for all MS drugs with estimates from the United Kingdom, Canada and Australia, researchers found that the costs of MS drugs in the U.S. market are two to three times higher. MS drug costs in those industrialized countries were often more than 70 percent lower than U.S. costs.
Researchers also examined the costs paid by the U.S. Department of Veterans Affairs (VA) because of its ability to negotiate discounts directly with manufacturers. Their analysis shows that on average costs for the VA were 36 percent less than those paid by Medicaid, including a nearly 80 percent discount for Betaseron™. This cost disparity suggests the sharp rise in U.S. prices is not the result of increases in manufacturing costs.
“This study confirms what many of us treating patients with MS had suspected: The pricing trajectories of MS drugs are unsustainable for our health care system and need to be addressed,” said Dennis N. Bourdette, M.D., F.A.N.A., F.A.A.N., co-author of the study and chair of the Department of Neurology in the OHSU School of Medicine and executive director of the Multiple Sclerosis Center at OHSU.
The lack of transparency within pharmaceutical pricing and purchasing, and the absence of a national health care system within the U.S. to negotiate prices directly with the pharmaceutical industry may have contributed to the soaring costs of these drugs, according to the researchers.
( function() { if (window.CHITIKA === undefined) { window.CHITIKA = { ‘units’ : [] }; }; var unit = {“calltype”:”async[2]”,”publisher”:”fguzzardi”,”width”:550,”height”:120,”sid”:”Chitika Default”}; var placement_id = window.CHITIKA.units.length; window.CHITIKA.units.push(unit); document.write(‘

‘); }()); “As a doctor, I’m deeply concerned about making sure these life-changing drugs are within reach for patients. The driving force behind this study was our experience that the high cost of MS drugs interferes with our ability to take good care of our patients,” said Ruth H. Whitham, M.D., F.A.A.N., co-author of the study, professor of neurology in the OHSU School of Medicine, and co-founder of the Multiple Sclerosis Center at OHSU.

“We decided to shine a light on this growing problem so that those of us who care for patients with chronic illness can work together and advocate for changes to drug pricing mechanisms.”
“The Cost of Multiple Sclerosis Drugs in the U.S. and the Pharmaceutical Industry: Too big to fail?” was authored by Daniel M. Hartung, Pharm.D., M.P.H.; Dennis N. Bourdette, M.D., F.A.N.A., F.A.A.N.; Sharia Ahmed, M.P.H.; Ruth H. Whitham, M.D., F.A.A.N.
About OHSU
Oregon Health & Science University is a nationally prominent research university and Oregon’s only public academic health center. It serves patients throughout the region with a Level 1 trauma center and nationally recognized Doernbecher Children’s Hospital. OHSU operates dental, medical, nursing and pharmacy schools that rank high both in research funding and in meeting the university’s social mission. OHSU’s Knight Cancer Institute helped pioneer personalized medicine through a discovery that identified how to shut down cells that enable cancer to grow without harming healthy ones. OHSU Brain Institute scientists are nationally recognized for discoveries that have led to a better understanding of Alzheimer’s disease and new treatments for Parkinson’s disease, multiple sclerosis and stroke. OHSU’s Casey Eye Institute is a global leader in ophthalmic imaging, and in clinical trials related to eye disease.
About the OSU/OHSU College of Pharmacy
The College of Pharmacy prepares students to be pharmacy practitioners and pharmaceutical sciences researchers able to advance societal health through leadership in pharmacy education, research, community engagement, and improved patient care.
Media Toolkit
Download photos of the study’s authors on OHSU News.
Related Content
The study can be found on the website of the journal Neurology®.
SOURCE Oregon Health & Science University
RELATED LINKS