Colorectal cancer rates in adults under age 50 have been increasing in the U.S. and globally. The risk of developing such cancers has been rising with each generation since the 1950s, but scientists have not been able to explain why. Understanding the underlying causes will help design prevention strategies for future generations.
<a href="https://surgery.wustl.edu/people/yin-cao/">Yin Cao, ScD</a>, an associate professor of surgery and of medicine in the <a href="https://publichealthsciences.wustl.edu/">Public Health Sciences Division</a> at Washington University School of Medicine in St. Louis, is leading an international team seeking to understand what is driving the increase in early-onset colorectal cancers globally. Her team will do so with an award of up to $25 million over five years from <a href="https://cancergrandchallenges.org/">Cancer Grand Challenges</a>, a global research funding initiative co-founded by Cancer Research UK and the National Cancer Institute (NCI), part of the National Institutes of Health (NIH). According to the organization, the mission of Cancer Grand Challenges is to unite the world’s brightest minds against cancer’s toughest challenges.
The team is funded by Cancer Research UK, the National Cancer Institute, the Bowelbabe Fund for Cancer Research UK, and Institut National Du Cancer in France, through Cancer Grand Challenges.
“The alarming rise of colorectal cancer in young people around the world demands immediate action,” said Cao, also a research member of <a href="https://siteman.wustl.edu/">Siteman Cancer Center</a>, based at Barnes-Jewish Hospital and Washington University School of Medicine. “We used to think colorectal cancer was a disease of the older population, but in the past two decades, the median age of diagnosis for this cancer in the U.S. dropped from 72 to 66 years. Our team aims to unravel and ultimately reverse the intricate network of causal factors throughout the life course that contribute to early-onset colorectal cancer.”
The award will provide funding for Cao’s research team — named Pathways, Risk Factors and Molecules to Prevent Early-onset Colorectal Tumors (PROSPECT) — to develop disruptive and transdisciplinary approaches to address this challenge. Among 176 international teams that applied, Cao’s team is one of five to receive funding this year through Cancer Grand Challenges. The other funded teams are focused on cancer inequities, solid tumors in children, and T cell receptors.
Cao co-leads the team with Andrew Chan, MD, at Massachusetts General Hospital (MGH). The research team also involves nine interdisciplinary co-investigators across the globe, including <a href="https://chemistry.wustl.edu/people/gary-patti">Gary Patti, PhD</a>, the Michael and Tana Powell Professor of Chemistry at Washington University. Patti, a pioneer of mass spectrometry-based technologies, will lead state-of-the-art molecular and metabolic analyses to identify possible new risk factors.
Cao’s lab has led the field of early-onset colorectal cancer research by uncovering risk factors throughout the life course that may contribute to the cancer’s rising incidence, such as obesity; diabetes; metabolic comorbid conditions such as high blood pressure and high cholesterol; prolonged sitting; poor diet; sugar-sweetened beverages; alcohol drinking patterns; and birth via cesarean delivery. Cao’s team also leads work in early detection and understanding molecular pathways of this cancer.
Building upon this past research, Cao will lead the first consortium dedicated to early-onset colorectal cancer risk factor discovery. The PROSPECT Global Consortium will have support from more than 15 international cohorts and electronic health record-based biobanks from high-, middle- and low-income countries. Her team will examine known risk factors and seek to find new ones. The query will encompass environmental exposures throughout the life course, including lifestyle, genetic, environmental and social factors. The team then will characterize possible causal factors and the cumulative impact of exposures over the life course on colorectal cancer initiation and progression, using animal models.
Cao also will also collaborate with clinicians at Siteman Cancer Center’s <a href="https://siteman.wustl.edu/treatment/cancer-types/colorectal/young-onset-colorectal-cancer-program/">Young Onset Colorectal Cancer Program</a> to collect biospecimens along the continuum of early-onset colorectal cancer development. The researchers will analyze these specimens to characterize the cumulative effects of risk factors for early-onset colorectal cancer on the biochemical and molecular states of tissues.
“An understanding of what causes early-onset cancers is important for the development of interventions based on an individual’s risk so that we can prevent disease and death,” Cao said. “Our goal is to maximally integrate human and mechanistic evidence to develop precision prevention strategies.”
In addition to identifying risk factors and evaluating causal factors, the team also will translate these findings to develop and test prevention strategies, including precision prevention trials and community risk-assessment trials.
“By pushing the boundaries of our individual fields, we hope to move quickly to identify opportunities for preventive interventions that can benefit younger populations,” Cao said. “It’s a joint adventure shared by scientists, providers, patients and the public under a unified goal: shaping a hopeful and healthier future for our younger generations.”

Preventing early-onset colorectal cancers aim of $25 million award

For over a century, cancer cell metabolism has been viewed as something of a paradox. New work from researchers at Washington University in St. Louis shows that it might not be such an anomaly after all. The study is published Aug. 15 in <a href="https://www.cell.com/molecular-cell/fulltext/S1097-2765(22)00703-1">Molecular Cell</a>.
<img src="https://storage.googleapis.com/labrulez-bucket-strapi-h3hsga3/Washington_University_in_St_Louis_Shutterstock_Sugar_metabolism_is_surprisingly_conventional_in_cancer_Mitochondria_the_cell_s_powerhouses_play_an_active_role_in_most_cancers_726527b95c.jpg" alt="Washington University in St. Louis /Shutterstock: Washington University in St. Louis/Shutterstock: Mitochondria — the cell’s powerhouses — play an active role in most cancers. Research from Washington University in St. Louis shows that cancer cells only waste glucose (sugar) because transport into mitochondria is too slow. The study has implications for targeting sugar metabolism in cancer treatment."/>
Glucose, a common sugar in food, is one of the most important nutrients in the body. Cancer cells tend to consume it at an astounding pace. At first glance, that seems to make good sense because cancer cells have a lot of synthesis to do. After all, as tumors grow rapidly, each cell has to replicate its entire contents.
But here’s the catch. Cancer cells don’t use the glucose very efficiently. Instead of sucking all of the energy they can out of glucose, they release most of it as a waste material.
“To extract the maximum amount of energy from glucose, cells must transport its transformation products into mitochondria,” said Gary Patti, the Michael and Tana Powell Professor of Chemistry in Arts &amp; Sciences and of genetics and of medicine at the School of Medicine. Patti, a member of Siteman Cancer Center at Barnes-Jewish Hospital and the School of Medicine, is senior author of the new study.
“There are certain biochemical rules that metabolism is supposed to follow. It’s been interesting to think about why tumors might be allowed to break them,” Patti said. “However, the findings we report here demonstrate that cancer cells do follow conventional principles.”
<img src="https://storage.googleapis.com/labrulez-bucket-strapi-h3hsga3/Washington_University_in_St_Louis_Wash_U_leads_new_multi_omics_production_center_for_NIH_research_consortium_Patti_fa8e4a9e2a/Washington-University-in-St.-Louis-WashU-leads-new-multi-omics-production-center-for-NIH-research-consortium-Patti.jpg" alt="Washington University in St. Louis: Patti."/>
<h4>Overflowing</h4>
Mitochondria are tiny compartments inside cells, often referred to as the cell’s power plants or powerhouses. What goes in and out of them is tightly controlled.
As a bit of backstory, a famous biochemist named Otto Warburg first discovered the wasteful nature of tumors in the 1920s. To explain why more energy isn’t harvested from glucose, he postulated that mitochondria are damaged in cancer cells.
“We now know that this is not true. Mitochondria are functional and, in fact, active in most cancers,” Patti said. But that leaves a persistent and vexing question unanswered: Why do cancer cells metabolize so little of the glucose they consume in mitochondria?
“I think what has been confounding is that there has been this notion that cancer cells prefer not to oxidize glucose in their mitochondria,” Patti said. “Perhaps as a legacy of Warburg’s original thinking or maybe because it happens so extensively, the assumption has often been that cancer cells want to use glucose wastefully.”
<img src="https://storage.googleapis.com/labrulez-bucket-strapi-h3hsga3/Washington_University_in_St_Louis_Shutterstock_Sugar_metabolism_is_surprisingly_conventional_in_cancer_c350558047.jpg" alt="Washington University in St. Louis/Shutterstock"/>
“When we restrict the amount of glucose taken up by cancer cells, almost all of it makes its way into mitochondria,” Patti said. “But as glucose consumption is increased, the speed of moving glucose-derived molecules into mitochondria can’t keep up.”
In other words, cancer cells only waste glucose away because transport into mitochondria is too slow.
Imagine a bathtub faucet that is spitting out water faster than the drain can remove it. Eventually, the water overflows onto the floor.
“This is not a radically new metabolic paradigm. Most cells do prefer to oxidize glucose in mitochondria rather than excrete it as waste,” Patti said. “Our data suggest that cancer cells are not an exception. They appear to follow the same biochemical patterns as other cells.”
All sorts of explanations have been offered as to why cancer cells might want to be wasteful with their glucose. However, Patti and his team contend that these rationalizations may be unnecessary. In the end, cancer metabolism may not be as unusual as scientists thought.
Cancer cells really do want to metabolize glucose in their mitochondria, and they do so. Until they can’t.
<h4>Saturated</h4>
The Patti team’s discovery was made possible by a powerful technology called metabolomics.
“During the past decade, advances in the field of metabolomics and mass spectrometry have been extraordinary,” Patti noted. “We have now reached a point where measuring molecules in single cells is even possible.”
In this study, the researchers combined metabolomics with stable isotope tracers. This allowed them to tag different parts of glucose so that they could track it inside of cells, watching the speed at which things entered mitochondria or were excreted from cells. That is how the scientists discovered that the normal pathways for transporting fuel were getting outpaced, or saturated, in cancer cells.
The rate at which tumors consume glucose has been exploited by doctors in the clinic for decades as a way to diagnose cancer and identify its stage. It also has led some to believe that limiting glucose uptake with drugs or by eating a sugar-free diet might “starve” the cancer cells to death.
This study’s findings raise questions about such a strategy.
“We may need to rethink how best to target glucose metabolism in cancer,” Patti said. “If cancer cells take up more glucose than they need, and using it wastefully is not a driver of disease, then glucose metabolism may not be as attractive of a therapeutic target as we had hoped.”
<h6>Funding: Financial support was received for this work from NIH awards R35ES028365 and R24OD024624, as well as the Edward Mallinckrodt Jr. Foundation and the Pew Charitable Trusts.</h6>

Sugar metabolism is surprisingly conventional in cancer

A new study with zebrafish shows that a deadly form of skin cancer — melanoma — alters the metabolism of healthy tissues elsewhere in the body. The research from Washington University in St. Louis suggests that these other tissues could potentially be targeted to help treat cancer.<img src="https://storage.googleapis.com/labrulez-bucket-strapi-h3hsga3/Washington_University_in_St_Louis_Cancer_has_ripple_effect_on_distant_tissues_Patti_bca1fbd7a0.jpg" alt="Washington University in St. Louis: Patti." srcset="https://storage.googleapis.com/labrulez-bucket-strapi-h3hsga3/thumbnail_Washington_University_in_St_Louis_Cancer_has_ripple_effect_on_distant_tissues_Patti_bca1fbd7a0.jpg 228w," sizes="100vw" width="1400" height="959">“Tumors rely on a constant supply of nutrients to grow. Instead of competing with tumors for nutrients, other tissues can reprogram their metabolism to be complementary. In some instances, this may even allow healthy tissues to feed the tumor,” said <a target="_blank" rel="noopener noreferrer" href="https://chemistry.wustl.edu/people/gary-patti">Gary Patti</a>, the Michael and Tana Powell Professor of Chemistry in Arts &amp; Sciences at Washington University and a professor of chemistry and medicine at the School of Medicine.Patti is the corresponding author of the study published May 13 in <a target="_blank" rel="noopener noreferrer" href="https://www.cell.com/cell-metabolism/fulltext/S1550-4131(21)00180-7">Cell Metabolism</a>.Cancer consumes tremendous amounts of glucose, a key source of energy for cells in the body. Glucose, or blood sugar, is derived from food and transported around the body through the bloodstream after eating. Tumors actively soak up glucose as a fuel to support their rapid growth.This trait is so well known that physicians regularly use it as a diagnostic test for cancer, where patients are administered a specific form of glucose that can be monitored with a PET scan. What is less clear is how a tumor’s penchant for glucose affects other tissues.“Glucose levels are tightly regulated,” Patti said. “When glucose levels get too low, it’s dangerous. We wanted to know whether a tumor with a high avidity for glucose might influence glucose levels in the blood.”Even when healthy people go a long period of time without eating, blood glucose levels are kept relatively constant. That is because glucose can be made by the liver when it cannot be obtained directly from food.“As it turns out, the liver counters the impact of the tumor by synthesizing glucose,” Patti said. “It’s very similar to what occurs during a fast.”<blockquote><h5>What is metabolic crosstalk?</h5><img src="https://storage.googleapis.com/labrulez-bucket-strapi-h3hsga3/Washington_University_in_St_Louis_Cancer_has_ripple_effect_on_distant_tissues_afa2b13b9e.jpg" alt="Washington University in St. Louis: Cancer has ripple effect on distant tissues." srcset="https://storage.googleapis.com/labrulez-bucket-strapi-h3hsga3/thumbnail_Washington_University_in_St_Louis_Cancer_has_ripple_effect_on_distant_tissues_afa2b13b9e.jpg 214w," sizes="100vw" width="1125" height="820"><a target="_blank" rel="noopener noreferrer" href="https://lcms.labrulez.com/articles?search=Gary+Patti">Gary Patti</a> is an expert in the field of <a target="_blank" rel="noopener noreferrer" href="https://source.washu.edu/2018/10/metabolomics-for-the-masses/">metabolomics</a>, the comprehensive study of small molecules within a biological system.“In metabolic crosstalk, two tissues within one biological system exchange molecules,” Patti explained.“One tissue takes up a metabolite and transforms it into a different molecule that is released. The released molecule is then taken up by another tissue,” Patti said. “Imagine that happening a bunch of times with metabolites flowing in bidirectional ways between various pairs of tissues.”</blockquote>Working with zebrafish, Patti and co-authors including other researchers at the School of Medicine developed a new approach to study melanoma’s impact on different tissues in the body that uses a technology called metabolomics.The scientists fed the zebrafish special versions of nutrients tagged with isotope labels. These labels allowed the scientists to track where nutrients go and into what molecules they get broken down. They found that a molecule being spit out by the tumor was being taken up by the liver to make glucose.By applying metabolomics to individual zebrafish, the scientists observed that melanoma tissues in the body consume about 15 times more glucose than the other tissues they measured. Despite this burden, the zebrafish were able to maintain circulating glucose levels, apparently by making glucose in the liver through a process that is ordinarily triggered when we go without eating.But it was clear that otherwise healthy tissues were affected in many ways by the presence of melanoma.The scientists examined tissues in the liver, intestine, fin, muscle, brain, blood, and eye of the zebrafish. They observed metabolic dysregulation across most of the tissues — indicating that melanoma broadly impacts whole-body metabolism.“There is clear metabolic crosstalk between melanoma and other tissues,” Patti said. “The metabolic relationship between melanoma and liver is partly characterized by a gene called BCAT1 in the cancer cells. BCAT1 goes from essentially being turned off in healthy skin cells to being highly expressed in zebrafish melanoma. By looking at melanoma from human patients, we were able to confirm that the same pattern holds in people.”Much of the previous research on cancer has focused on the metabolism of the tumor itself.“Our work shows that a lot of interesting metabolic changes are also occurring beyond the tumor,” Patti said. “We have demonstrated that, at least in some cases, these metabolic changes in non-malignant tissues occur to support the tumor. This is exciting because it means that we might be able to target the metabolism of healthy tissues as a potential treatment for cancer.”<blockquote>A special note: The authors of this paper dedicated their work to the late Stephen L. Johnson, who was an inspiring mentor to them. His collaborative generosity was essential to carrying out these studies. Read more about Johnson on the School of Medicine <a target="_blank" rel="noopener noreferrer" href="https://medicine.wustl.edu/news/obituary-stephen-l-johnson-professor-genetics-56">website</a>.</blockquote>Financial support was received for this work from National Institutes of Health awards R35ES028365, U01CA235482, and R24OD024624, as well as the Edward Mallinckrodt, Jr. Foundation and the Pew Charitable Trusts.

Cancer has ripple effect on distant tissues

Batteries have become so integral to everyday life – powering everything from mobile devices to electric vehicles and renewable energy storage systems – that people often don’t even think about them. But our increasing reliance on batteries has made considerations like their sustainability and ability to hold charge in a range of environments and the ability to reliably source materials needed to produce them urgent considerations.<img src="https://storage.googleapis.com/labrulez-bucket-strapi-h3hsga3/Washington_University_in_St_Louis_Peng_Bai_Rajeev_Gopal_and_Ethan_Boutelle_Beyond_lithium_Sodium_based_batteries_may_power_the_future_Peng_Bai_s_research_group_combines_stable_536989e74c.jpg" alt="Washington University in St. Louis / Peng Bai, Rajeev Gopal and Ethan Boutelle: Peng Bai’s research group combines stable sodium metal plated in liquid electrolyte (left) with precisely engineered particles of sodium vanadium phosphate (right) to create safe and efficient sodium batteries." srcset="https://storage.googleapis.com/labrulez-bucket-strapi-h3hsga3/thumbnail_Washington_University_in_St_Louis_Peng_Bai_Rajeev_Gopal_and_Ethan_Boutelle_Beyond_lithium_Sodium_based_batteries_may_power_the_future_Peng_Bai_s_research_group_combines_stable_536989e74c.jpg 234w," sizes="100vw" width="1200" height="800"><a target="_blank" rel="noopener noreferrer" href="https://engineering.washu.edu/faculty/Peng-Bai.html">Peng Bai</a>, associate professor of energy, environmental &amp; chemical engineering in the McKelvey School of Engineering at Washington University in St. Louis, received a two-year, $550,000 Partnerships for Innovation – Technology Translation award from the National Science Foundation to support his work on sodium-based batteries. The award will allow Bai to expand his prior NSF-funded research to scale up and commercialize his sodium battery technology.&nbsp;Bai’s sodium-based batteries deliberately move away from lithium and other rare elements used in traditional batteries. Sodium, a more abundant and easier to process material, promises lower production costs and alleviated supply chain vulnerabilities, fostering a more sustainable and economically efficient energy landscape. Sodium-based batteries may also offer enhanced fast-charging capabilities and improved operation in cold environments, expanding their potential application in large-scale energy storage and portable electronics, including electric vehicles.The project, “<a target="_blank" rel="noopener noreferrer" href="https://www.nsf.gov/awardsearch/showAward?AWD_ID=2431923">Development of high-performance long-life electrodes for sustainable sodium-based batteries</a>,” has three main goals: ensuring consistency in larger production batches, developing greener manufacturing processes using water instead of toxic solvents, and optimizing production processes at a commercial scale. These advancements would pave the way for sodium-based batteries to make their way into everyday technologies within five years, Bai says.

Beyond lithium: Sodium-based batteries may power the future

Amyloid-beta (A-beta) aggregates are tangles of proteins most notably associated with neurodegenerative diseases such as Alzheimer’s. Despite its constant stint in the limelight, however, researchers have been unable to get a good understanding of how A-beta comes together and breaks apart.“The way A-beta behaves in a variety of environments, including the human brain, is elusive,” said Brian Sun, an electrical systems and engineering alumnus of&nbsp;Washington University in St. Louis who is now an MD/PhD student at the School of Medicine.“There’s an understanding of growth and decay that isn’t fully fleshed out,” he added.That’s going to change, thanks to research recently <a target="_blank" rel="noopener noreferrer" href="https://pubs.acs.org/doi/10.1021/acs.nanolett.4c01263">published</a> by Sun with colleagues in <a target="_blank" rel="noopener noreferrer" href="https://engineering.wustl.edu/faculty/Matthew-Lew.html">Matthew Lew’s lab</a> in the Preston M. Green Department of Electrical &amp; Systems Engineering at WashU’s McKelvey School of Engineering.In first-of-its-kind work, Sun and colleagues were able to measure amyloid fibril beta-sheet assemblies, the underlying girders of the protein conglomeration, while they were changing. Previous high-resolution microscopy studies have only gotten static shots.“We wanted to look specifically at dynamics of the underlying structure of A-beta that could be responsible for the changes we’re seeing, not just changes in the overall shape,” said Sun, the paper’s first author.Lew used Lego bricks in an analogy, noting that current imaging technology shows you the full Lego building but not a look at how individual bricks are organized.“The individual proteins are always changing in response to their environment,” said Lew, an associate professor. “It is like having certain Lego bricks causing other bricks to change their shape. The changing architecture of the proteins and the assembled aggregates together leads to the complexity of neurodegenerative disease.”The Lew lab has developed a new type of imaging tech that allows researchers to see the orientation and other minute details in nanostructures of biological systems that were previously invisible. Their technique — single-molecule orientation–localization microscopy (SMOLM) — uses flashes of light from chemical probes to visualize the sheets of peptides underlying Aβ42, one kind of A-beta peptide.Using SMOLM lets them look at individual orientation of the underlying beta-sheets to see the relationship between their organization and how that relates to the amyloid protein’s overall structure.<h4>Multiple ways to remodel</h4>Aβ42 is constantly changing, and step one is to try to find a method to the madness, a model or pattern of action to predict the protein’s behavior.Now that the Lew lab can make these measurements, they made some intuitive observations and found some surprises hidden in the amyloid-beta architecture.As expected, stable Aβ42 structures tend to retain stable underlying beta-sheets; growing structures have underlying beta-sheets that become more defined and rigid as the growth continues. Decaying structures exhibit increasingly disordered and less rigid beta-sheets. But they also found more than one way that Aβ42 can renovate.“There are multiple different ways for Aβ42 structures to remain stable, or grow and decay,” Sun said.The researchers also discovered that Aβ42 can grow and decay in ways that defy expectations. For example, Aβ42 can grow and decay in ways that preserve the underlying structure; sometimes there’s growth where the peptides just pile on, but the underlying beta-sheet orientations don’t change. In other cases, Aβ42 undergoes “stable decay,” where the opposite happens, i.e. peptides leave, but beta-sheet structure remains.&nbsp; Finally, Aβ42’s beta-sheets sometimes reorganize and change orientations without immediate accompanying changes to the overall shape. These nano-structural reorganizations can predispose to future large-scale remodeling.“Because SMOLM can track Aβ42’s underlying organization and not just its shape, we can see different kinds of subtypes of remodeling that aren’t visible to diffraction-limited, non-orientation imaging modalities,” Sun said.If it all sounds a bit vague, keep in mind this is the first pass at even looking at these constantly shifting nanoscale structures. It’s all the more notable that Sun crafted this work while juggling COVID-19 lockdown restrictions and his undergraduate course load at WashU, which he completed in three years. It paves the way for him and others to really get a handle on amyloid architecture.During the graduate phase of his MD/PhD training, Sun plans to design nanoscale imaging systems and sensors that could reveal the hidden mechanisms of difficult-to-treat diseases.Sun credits McKelvey Engineering and the Lew lab for the rigorous training that made this study and academic trajectory possible, as well as the MSTP for supporting his continued research post-graduation. “I’m really glad I went through this journey,” he said.

WashU researchers shine light on amyloid architecture

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