Category: 8. Health

In 1965, a group of Michigan State University researchers accidentally discovered a new cancer-fighting drug: cisplatin. Since then, cisplatin has become the industry standard for cancer-fighting chemotherapy treatments.

As announced today, MSU will receive a 2025 Golden Goose Award for the scientific success and global impact of cisplatin. The Golden Goose Award is meant to highlight the practical value of curiosity-driven research. The idea is that fundamental research can lead to unexpected, but profound, societal benefits.

The Golden Goose award committee is housed within the American Association for the Advancement of Science and includes organizations like the Association of American Universities as well as previous winners.

The award will be presented to MSU on Tuesday, Sept. 16, at the Library of Congress in Washington, D.C. During the award ceremony, members of both parties of the U.S. Congress will speak about the importance of the award and the federal funding of scientific research.

“We are thrilled to have this important discovery by Barney Rosenberg honored, but what is truly significant are the countless lives saved by Cisplatin,” said Doug Gage, vice president for MSU Research and Innovation. “This is a stellar example of how fundamental research can have unexpected, profound impact in a completely different domain. The combination of curiosity driven research and applied research toward a specific outcome has been at the heart of the nation’s international leadership in science and technology. Strong federal support of both basic and applied research is essential for our continued dominance.”

In addition to cisplatin, another research group — one that was led by the late Joseph Gall at Carnegie Science — will be honored with a Golden Goose Award. Gall is often referred to as the father of modern cell biology for his contributions to our understanding of chromosomes and the cellular nucleus.

How cisplatin was discovered

Cisplatin was first created in 1844 by Italian chemist Michele Peyrone and was largely forgotten until 1965 when MSU Professor of Biochemistry Barnett “Barney” Rosenberg and his lab team discovered its use as a breakthrough cancer treatment.

Rosenberg, in the College of Natural Science, and his lab technician Loretta VanCamp and a team of postdocs including Thomas Krigas were studying how electricity affects bacterial growth, not cancer drug development. He noticed that bacteria did not grow well around the platinum electrode he was using. Rosenberg then isolated some platinum containing compounds from the media and tested them in cell culture. He noticed that cell division was slowed — and only then did he consider its application to cancer.

After a couple years of follow-up experiments, they discovered the true cause: platinum compounds released from the electrodes, not the electric field itself. As a result, the chemical compound prevents the DNA in cancer cells from replicating, confusing them and causing them to die. This accidental discovery led to the development of cisplatin, a platinum-based chemotherapy drug approved in 1978.

The discovery, patenting and FDA approval of cisplatin was a 13-year process made possible by federal funding from the National Institutes of Health and the National Science Foundation, an unusually brief period of time in the research world prior to the development of the COVID-19 vaccine.

“The discovery of cisplatin is a powerful example of how basic scientific curiosity can save lives,” said Eric Hegg, dean of the College of Natural Science. “What began as an unexpected result in a Michigan State University lab led to one of the most effective cancer treatments in the world. It is a testament to the power of exploratory-driven research and the transformative impact it can have on humanity.”

While cisplatin is used to treat many types of cancer, it is most widely prescribed for testicular, ovarian, bladder, lung and stomach cancers. Most notably, cisplatin increased the cure rate for testicular cancer from around 10% to over 90%. Cisplatin’s impact has been especially profound in treating testicular cancer, which:

• affects about 9,760 new patients who are diagnosed each year, and is responsible for the death of 500 men annually;  

• is the most common cancer in males aged 15–34 at a time when cancer cases and deaths among men are predicted to increase 93% by 2050, according  to a new study; 

• if in the 1960s had metastasized, resulted in a 90% death rate within one year of diagnosis. Today, the survival rate for testicular cancer is about 95%.  

Cisplatin has saved countless lives, including that of legendary figure skater Scott Hamilton, who has been diagnosed with cancer three times.

In 1997, Hamilton, who won gold at the 1984 Winter Olympics, was diagnosed with stage 3 testicular cancer, which had spread to his stomach.

“When they told me, I was like, ‘I want it to be something else,’” said Hamilton in an interview in 2018. “But they said, ‘No, this is a good one to get, if you had to choose one,’ which is kind of crazy. But I’m grateful there was a proven treatment. I know many cancers don’t really have one.”

Cisplatin’s impact today

Cisplatin is responsible for saving millions of lives and remains one of the most effective chemotherapy treatments. In fact, cisplatin was added to the World Health Organization’s Essential Medicines List in 2015 for the treatment of early-stage cervical cancer, concurrently with radiotherapy.

Cisplatin also has paved the way for new cancer-fighting drugs and continues to fund scientific breakthroughs at MSU. Royalties earned from sales of cisplatin and its derivative, carboplatin, fuel the work of and investments by the MSU Research Foundation, an independent, nonprofit corporation through offices such as MSU Technologies. There, it supports investments in research and economic development initiatives through the commercialization of cutting-edge technologies invented by MSU faculty, staff and students.

PROVIDENCE, R.I. [Brown University] — Doctors and researchers are puzzled by a recent rise in what might seem like an antiquated problem: iodine deficiency.

Iodine, a trace element that helps regulate metabolism and produce vital hormones, is essential for many aspects of human development, especially in children. Specialists like Dr. Monica Serrano-Gonzalez, a pediatric endocrinologist and associate professor of pediatrics, clinician educator, at Brown University’s Warren Alpert Medical School, are hoping that studies like one she recently led can shed light on how to combat a growing challenge that transcends many population groups.

In a Q&A, Serrano-Gonzalez shared how experiences with patients inspired her and other Brown-affiliated colleagues to study iodine deficiency, and how they’re educating the public on how to get enough.

Q: Why are physicians seeing an increase in patients with iodine deficiency?

There are very few food sources for iodine. The main ones are dairy products, seafood and eggs, as well as meat and poultry. In some countries, grain products like bread are made with iodized salt, but this is usually not the practice in the United States. Other foods like fruits and vegetables have very low levels as they depend on the soil iodine content. 

In the 1920s, American manufacturers began adding iodine to table salt widely available in stores. Part of the problem is that now there are a lot of trendy salts — Himalayan, sea, kosher and others — so many people have moved away from eating iodized salts. Organic dairy also has less iodine, as do processed foods and bread. Patients who have restricted diets, such as practicing vegans or people with dairy intolerance, food allergies or autism spectrum disorder, are also at higher risk for deficiency. Children and pregnant or breastfeeding women are more susceptible, as their iodine requirements are higher.

There is no public health mandate for iodization in the U.S., so many of the salts you buy in the grocery store don’t have iodine, and the salts that do have varying concentrations. The public health messaging has been so strong against salt due to its connection with blood pressure issues, and people appear to be hyper-aware of that. In the clinic, we have noticed that patients often think that iodized salt, specifically, is bad for health, as opposed to all types of salt. 

Q: Why do we need iodine?

Our bodies need iodine to make thyroid hormone, which helps regulate metabolism and is key to brain development. Without adequate iodine, the gland has to figure out ways of compensating, which is why someone can have a goiter — enlarged thyroid — and be otherwise okay. But if you reach a point of chronic deficiency where you can no longer compensate, the thyroid hormone levels go down, so the pituitary gland makes more of another hormone that stimulates the thyroid. The thyroid gland grows as it tries to keep up, but simply can’t. 

In children, low thyroid function can significantly affect linear growth and cognitive development, causing irreversible intellectual disability, and it affects metabolism overall at any age. There are thyroid hormone receptors all throughout the body, and if thyroid hormone levels are severely low for a long time, that could lead to the worst case scenario of a coma.

Before iodine fortification in the 1920s, there were “goiter belts” around the Great Lakes, the Appalachian and Northwestern regions. There are reports that analyzed military data from the first world war that found 30% of young people from iodine-deficient areas couldn’t be recruited into the military because they had large goiters, as it was so common back then. Salt fortification made a big difference.

Q: Why did you start studying this issue?

I saw a 13-year-old patient a few years ago who had a goiter that rapidly enlarged over the course of a few weeks. We often see patients with goiters in the clinic, but the vast majority of the time it’s from an autoimmune condition called Hashimoto’s disease, where the immune system is misfiring and attacking the thyroid gland. However, the patient’s blood tests for the disease were all negative, so we were puzzled. This boy had autism spectrum disorder and had a highly restricted diet, so we started thinking it could be iodine deficiency. He wasn’t eating eggs, dairy or seafood, and his family cooked with non-iodized salt. A urine test confirmed he was deficient, so we added an iodine supplement to his diet and the goiter decreased in size over the next few weeks. Eventually, his family managed to expand his diet so that he wouldn’t need the supplement anymore.

This incident sparked interest among me and my colleagues, so we began paying attention to iodine deficiency. We eventually published a case series reporting our experience with six patients, who we tracked from diagnosis to follow-up care. All of the patients shared a restricted diet, due to reasons like developmental delays, autism, vegan diets and dairy intolerance. We are seeing iodine deficiency spanning all ages, from toddlers to adolescents, and in patients belonging to different socioeconomic groups.

Q: How can physicians address the risk of iodine deficiency?

One of the things we are learning about is the stigma associated with iodine deficiency. Diet is always a tricky subject to discuss with patients, but I also think that there is a stigma in this case due to the association of iodine deficiency with poverty in underdeveloped countries. 

In our pediatric endocrine practice, we are educating our patients about the risks of an iodine-free diet. We’re also educating pediatricians as well as medical residents and fellows who work with us in the clinic, and we will give a hospital-wide grand rounds presentation at Hasbro Children’s on the topic of deficiencies of micronutrients such as iodine. 

To avoid deficiency of iodine and other micronutrients, we encourage patients to diversify their diets. If you have a mix of foods in your diet including seafood, eggs, chicken and dairy, you are likely okay in terms of iodine intake. But especially for patients who have a low dietary diversity because of food allergies, autism, developmental delay, dietary preferences or other reasons, we recommend that they use iodized salt when cooking — in moderation and in the context of a healthy diet.

This Q&A was originally published on the Warren Alpert Medical School website.

Regardless of patients’ kidney function, abelacimab (Anthos Therapeutics) had consistently reduced the risk of bleeding compared with rivaroxaban (Xarelto; Bayer HealthCare; Johnson & Johnson), wrote investigators of the AZALEA-TIMI 71 clinical trial (NCT04755283). The findings, which were published in JAMA Cardiology, suggested that abelacimab might offer a notably favorable safety profile, especially among those with chronic kidney disease (CKD), but larger studies are needed.^1,2

About the Trial

Trial Name: Safety and Tolerability of Abelacimab (MAA868) vs. Rivaroxaban in Patients With Atrial Fibrillation (AZALEA-TIMI 71)

ClinicalTrials.gov ID: NCT04755283

Sponsor: Anthos Therapeutics, Inc.

Completion Date (Estimated): December 29, 2028

CKD is a common disease present in patients with atrial fibrillation (AF) and is often associated with higher rates of bleeding with anticoagulation, explained the authors. Although direct oral anticoagulants (DOACs) are safer than vitamin K antagonists (VKAs) regarding bleeding across a range of kidney function, bleeding risk with DOACs in those with impaired kidney function remains a considerable risk.¹

The authors explain that factor XI (FXI) inhibitors are an experimental class of anticoagulants that cause less bleeding than DOACs. Abelacimab, a novel FXI inhibitor, is a monoclonal antibody without renal elimination, whereas about one-third of rivaroxaban is directly renally excreted. In the multicenter, randomized, active-controlled phase 2b AZALEA-TIMI 71 trial, the investigators evaluated the safety and tolerability of 2 blinded doses of abelacimab compared with open-label rivaroxaban in patients with AF who had a range of kidney function.^1,2

The trial enrolled 1284 patients aged 55 years and older (median age: 74 years) with AF and a CHA₂DS₂VASc score of 4 or higher, or 3 or higher for those with planned concomitant antiplatelet use or creatinine clearance (CrCl) of 50 mL/min or less, who were randomly assigned to receive either 150 mg or 90 mg of abelacimab administered subcutaneously monthly or to rivaroxaban daily. Patients with a CrCl less than 15 mL/min or receiving dialysis were not eligible for enrollment.^1,2

The primary end point for this analysis was International Society on Thrombosis and Haemostasis (ISTH) major or clinically relevant or nonmajor (CRNM) bleeding. Other outcomes for this analysis included ISTH major bleeding alone and a broader bleeding composite of ISTH major, CRNM bleeding, or minor bleeding. Further, exploratory efficacy outcomes—including stroke or systemic embolism and a net clinical outcome composite of ischemic stroke, systemic embolism, major or CRNM bleeding, or death—were also evaluated. Outcomes were prospectively captured during trial follow-up and adjudicated by an independent clinical events committee who were blinded to treatment assignment.^1,2

The findings demonstrated that, in the rivaroxaban group, patients with a CrCl of 50 mL/min or less experienced higher rates of major or CRNM bleeding compared with those with a CrCl greater than 50 mL/min despite dose reduction (incidence rates: 13.6 vs 7.0/100 person-years). Additionally, abelacimab reduced major or CRNM bleeding compared with rivaroxaban regardless of CrCl (CrCl ≤50 mL/min: hazard ratio [HR], 0.26 [95% CI, 0.12–0.54]; >50 mL/min: HR, 0.40 [95% CI, 0.26–0.62]; P value for interaction = .33), with absolute risk reductions of about 10.1 and 4.2 per 100 person-years in those with CrCl of 50 mL/min or less and greater than 50 mL/min, respectively (P value for interaction = .09).¹

This risk reduction was consistent for major bleeding alone and for a broader composite inclusive of major, CRNM, and minor bleeding, wrote the study authors. Notably, results were similar when comparing the individual abelacimab doses to rivaroxaban.¹

“[Limitations include] AZALEA-TIMI 71[’s design] to assess the bleeding profile of abelacimab relative to rivaroxaban; larger studies are necessary to examine the efficacy of abelacimab for stroke prevention. Each of the 4 approved DOACs for AF have variable renal elimination and may differ in their bleeding profiles; thus, our results may not be generalizable to other DOACs,” wrote the study authors. “In this secondary analysis of the AZALEA-TIMI 71 randomized clinical trial, abelacimab consistently reduced the risk of bleeding compared with rivaroxaban across a range of kidney function and irrespective of rivaroxaban dose reduction among patients with AF; however, further data are necessary to evaluate the efficacy of abelacimab for stroke prevention in AF.”¹

REFERENCES

1. Patel SM, Giugliano RP, Morrow DA, et al. Safety of Factor XI Inhibition With Abelacimab in Atrial Fibrillation by Kidney Function: A Prespecified Analysis of the AZALEA-TIMI 71 Randomized Clinical Trial. JAMA Cardiol. Published online September 01, 2025. doi:10.1001/jamacardio.2025.3393

2. Safety and Tolerability of Abelacimab (MAA868) vs. Rivaroxaban in Patients With Atrial Fibrillation (AZALEA-TIMI 71). ClinicalTrials.gov identifier: NCT04755283. Updated September 2, 2025. Accessed September 3, 2025. https://clinicaltrials.gov/study/NCT04755283

A Nature study published today and led by researchers at the University of South Florida’s USF Health Byrd Alzheimer’s Institute pinpoints how a genetic variant disrupts microglia – the brain’s “cleanup crew” – increasing the risk of Alzheimer’s disease.

To better understand microglia, imagine the brain as a bustling city, full of nerve cells or neurons, sending important messages back and forth, said Gopal Thinakaran, CEO and endowed chair of the USF Health Byrd Alzheimer’s Institute and the paper’s senior co-author.

Microglia, tiny cells making up about 10 percent of the brain, act like sanitation and emergency responders and even urban planners, removing harmful proteins, repairing damage and helping the brain adapt to change, Thinakaran said. But when impaired, microglia slow down, swell with fatty deposits and lose their ability to protect neurons.

Microglia are immune cells in the brain and they are scavengers. They play an important role in clearing up debris in the brain. And they also have a very important role in Alzheimer’s disease.”

Gopal Thinakaran, CEO and endowed chair of the USF Health Byrd Alzheimer’s Institute

The study, PICALM Alzheimer’s risk allele causes aberrant lipid droplets in microglia, done in collaboration with the University of Chicago and Endeavor Health Research Institute, focused on PICALM, the third-most significant risk gene for late-onset Alzheimer’s.

“We found that a variant of PICALM affected the immune cells of the brain, reducing their ability to clear debris and causing a buildup of cholesterol and lipids,” said Ari Sudwarts, co-first author and postdoctoral research scholar at USF’s Morsani College of Medicine. “Understanding the functions disrupted by a specific risk gene gives new targets for developing pharmaceuticals for patients who have this genetic variant.”

About 30% of the population carries a protective PICALM variant. But the “major allele” reduces levels of the PICALM protein in microglia, impairing waste-processing organelles called lysosomes. This failure causes harmful lipid droplets to accumulate, further weakening microglia.

“This creates compact structures that cause havoc in a cell and impedes the microglia from doing its job,” Thinakaran said. “It’s extremely rare to have a story develop like this, and it took five years to unfold.”

The findings advance understanding of how genetic risk factors disrupt brain function and move scientists closer to targeted treatments.

“Many risks are being identified in microglia,” Thinakaran said. “And we are giving kind of a roadmap for one risk, and how the process results in lipid dysregulation and how the further accumulation of lipid droplets really starts to make the microglia ineffective. The knowledge we have gained adds one more piece to the Alzheimer’s puzzle we are putting together.”