Nicole Marie Hoitsma, PhD [HHMI Fellow], with her sponsor Karolin Luger, PhD, at University of ŷ���ڱ���Ƶ, Boulder, has been named one of 13 new Damon Runyon Fellows by the Damon Runyon Cancer Research Foundation.

The Damon Runyon Cancer Research Foundation has named 13 new Damon Runyon Fellows, exceptional postdoctoral scientists conducting basic and translational cancer research in the laboratories of leading senior investigators. This prestigious Fellowship encourages the nation's most promising young scientists to pursue careers in cancer research by providing them with independent funding to investigate cancer causes, mechanisms, therapies, and prevention. In July 2023, the Board of Directors announced at 15% increase in the Fellowship stipend, bringing the total to $300,000 over the award's four-year term.

“Over the past three decades, the rate of cancer mortality in the U.S. has dropped by a third, saving an estimated 3.8 million lives. This is because of earlier diagnoses, a better fundamental understanding of the genetic changes that take place in a cancer cell, and personalized treatment options like targeted therapy and immunotherapy. Damon Runyon scientists have been a part of each and every one of these advances,” said Yung S. Lie, PhD, President and CEO of Damon Runyon. “We fund the best young talent—risk takers and innovators. I am confident that because of the research being done by our scientists, this trend will continue, such that ultimately cancer will be a fully treatable disease. My optimism is shared by the cancer research community.”

ŷ���ڱ���Ƶ Hoitsma's Research:

Human cells have complex mechanisms to repair DNA damage, such as that caused by exposure to sunlight or chemical substances. If DNA is not properly repaired, however, it can lead to cancer. In fact, faulty DNA repair has been associated with the initiation and progression of all types of cancer and is often targeted in cancer treatment to stop uncontrolled cell growth. A better understanding of how cells naturally defend against DNA damage will allow for the development of better drugs to treat cancer. Dr. Hoitsma aims to investigate specialized proteins, known as chromatin remodelers, that make damaged DNA accessible for repair. This research will provide insight for the development of novel therapeutic strategies to target these critical pathways. Dr. Hoitsma received her PhD from University of Kansas Medical Center, Kansas City and her BS from South Dakota State University, Brookings.

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Dr. Marvin H. Caruthers of the University of ŷ���ڱ���Ƶ, Boulder, has won the inaugural Richard N. Merkin Prize in Biomedical Technology (https://merkinprize.org/) for developing an efficient, automated technology for synthesizing DNA. The chemical reactions that he discovered in the early 1980s to accurately and quickly assemble nucleotides into strands of DNA provided an essential element in the development of modern molecular medicine. Today, scientists use these reactions to produce customizable DNA and RNA molecules that enable genetic sequencing, drug and vaccine development, pathogen tests, cancer diagnostics, and many aspects of basic biomedical research. “I am honored to acknowledge the incredible and transformative impact of Dr. Caruthers’ technology on human health over the last four decades,” said Dr. Richard Merkin, founder and CEO of Heritage Provider Network, one of the country’s largest physician founded and physician owned integrated healthcare systems. “He deserves our support and recognition. I hope this prize not only raises awareness of this work, but underscores and encourages others to realize the broader importance of developing new scientific technologies to transform healthcare.” The Merkin Prize, which recognizes novel technologies that have improved human health, carries a $400,000 cash award. The prize was created by the Merkin Family Foundation and is administered by the Broad Institute of MIT and Harvard. Dr. Caruthers will be honored in a prize ceremony held this fall.

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The biochemistry assistant professor is investigating how inflammatory proteins called NLRs establish the first line of defense against viral infection in bacteria and humans

Aaron Whiteley, an assistant professor in the Department of Biochemistry at the University of ŷ���ڱ���Ƶ Boulder, has been selected to join the Pew Scholars Program in the Biomedical Sciences, the .

“I am truly thrilled to be named a Pew Scholar,” said Whiteley. “Support from this grant will help my lab pursue high-risk/high-reward research on how the immune system recognizes pathogens. I hope one day our findings can inform design of the next generation of vaccines and antiviral treatments.” 

Aaron Whiteley, an assistant professor in the Department of Biochemistry at ŷ���ڱ���Ƶ Boulder, was recently selected to join the Pew Scholars Program in the Biomedical Sciences. Whiteley’s recent research has identified unexpected similarities between how bacteria and human cells fight off viruses. 

This award follows a recent publication from the Whiteley lab in the journal  that identified unexpected similarities between how bacteria and human cells fight off viruses. The article reveals that a part of the human immune system, called “NLRs,” actually originated from bacteria. 

“Like studying a fossil, understanding bacterial ancestors of our NLRs will help us understand the human immune systems,” Whiteley said. 

He added, “One of the most impactful aspects of being a Biomedical Scholar is connection to the fantastic network of Pew-supported scientists from across the country. This award is career milestone—I am grateful for the recognition and opportunity.”

Whiteley is one of 22 early career scientists who will receive four years of funding to spearhead innovative studies exploring human health and medicine. "This award is career milestone—I am grateful for the recognition and opportunity.”

The 2023 class—all early career, junior faculty—joins a rich legacy of more than 1,000 scientists who have received awards from Pew since 1985. Current scholars have opportunities to meet annually with fellow Pew-funded scientists to exchange ideas and forge connections across a wide variety of disciplines.

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The awards are part of $1.88 million in 2023 biomedical research grant funding for ŷ���ڱ���Ƶ researchers 

Halil Aydin is one of three University of ŷ���ڱ���Ƶ Boulder assistant professors who have been named 2023 Boettcher Investigators, each earning $235,000 in grant funding to support up to three years of biomedical research. The 13-year-old program invests in leading ŷ���ڱ���Ƶ researchers during the early stages of their careers, providing support to fund their independent scientific research.

The three ŷ���ڱ���Ƶ Boulder award winners and their fields of study are: 

• Nuris Figueroa, assistant professor, physics; studying the mechanics of mucus organization and transport; 
• Halil Aydin, assistant professor, biochemistry; investigating cellular and molecular mechanisms of mitochondrial form and function in human health and disease; and  
• Nick Bottenus, assistant professor, biomedical, mechanics of materials, and robotics and systems design in the College of Engineering and Applied Science; studying binding kinetics of targeted microbubble agents.

Funding for the awards is made possible in part by the  program, which is administered by the 

“It’s an honor to be acknowledged by a distinguished organization,” Aydin said of the Boettcher Foundation. “The Boettcher Foundation Webb-Waring Biomedical Research Award will grant our laboratory the opportunity to develop novel approaches and push the boundaries of high-resolution imaging and structural cell biology to advance our understanding of how cellular machines function normally, and how they are corrupted by disease. An integrative understanding of how protein machines function has implications for targeting cardiovascular diseases, metabolic disorders, cancers, aging and a wide range of neurodegenerative diseases.” 

Halil Aydin is an expert in membrane biology, cell signaling, proteins and enzymology, molecular biophysics, structural biology, and electron cryo-microscopy (cryoEM).

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With a vote by the ŷ���ڱ���Ƶ Board of Regents, the University of ŷ���ڱ���Ƶ recently recognized Karolin Luger as a Distinguished Professor—the highest honor bestowed upon faculty across the system’s four campuses.  

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Whiteley, assistant professor of biochemistry, has won a NIH Director's New Innovator Award, which is reserved for “exceptionally creative early career scientists proposing innovative, high-impact projects.” It is a $1.5 million, five-year grant.

Whiteley’s research aims to shed light on why variations in bacteria in the gut microbiome correspond to variations in cancer patients’ responsiveness to immunotherapy. The mechanism is not well understood.

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The NIH recently awarded Dr. Joseph Falke with a 5-year MIRA / R35 grant to continue their research on a membrane-based signaling circuit central to leukocyte chemotaxis and many human cancers. The grant ($2.0M total costs) begins January 1, 2022, and the lab looks forward to recruiting new members!

Abstract Text

SUMMARY At the leading edge of a polarized macrophage, a membrane-based chemotaxis pathway directs cell mi- gration up attractant gradients to sites of infection, inflammation, or tissue damage. Upon arrival, a phagocyto- sis pathway controls the formation and internalization of a phagosome in which the pathogens or damaged tis- sue are engulfed and destroyed. Both the chemotaxis and phagocytosis pathways are regulated by PI3K lipid kinases that serve as regulatory hubs by integrating Ca2+, receptor, G protein, and other input signals while phosphorylating substrate lipids to produce output lipid signals. The potent lipid signals, in turn, activate multi- ple downstream protein kinases. In chemotaxis, the lipid signal controls actin and membrane remodeling to drive the leading edge up the attractant gradient. In phagocytosis, the lipid signal controls processing of the phagosome including the production of reactive oxygen species (ROS) to inactivate pathogens. Closely related PI3K pathways regulate other cell processes, notably including cell growth. When dysregulated, PI3K path- ways trigger or exacerbate a wide array of human diseases ranging from cancer and developmental disorders to defects in innate immunity, inflammation or autoimmunity. The two classes of PI3K lipid kinases targeted by this research program are Class 1 PI3-Kinases (PI3K1) that generate the signaling lipid PIP3 at the leading edge membrane of polarized macrophages, and Class 3 PI3-Kinases (PI3K3, specifically PI3K3 Complex II) that produce PI3P on the surface of the phagosome. The proposed research seeks to understand the regulation of both pathways by addressing fundamental, broad questions including: (i) How do PI3K1 and PI3K3 regulatory hubs integrate multiple inputs from Ca2+ channels, receptors, G proteins and other effectors, and do these inputs combine in additive, synergistic, or opposing fashions? (ii) How do the resulting PIP3 and PI3P output lipids activate downstream protein kinases, including some of the most important master kinases in the cell? (iii) How do drugs, potential therapeutics, and disease- linked mutations inhibit or superactivate key components and reaction steps to generate pathway perturbation or dysregulation? To answer these and other questions, the PI's laboratory has developed a unique, two-pronged approach combining innovative, in vitro single molecule methods with live cell imaging studies. The in vitro studies utilize single molecule TIRF to elucidate signaling mechanisms in a subsection of the pathway, or signaling module, that is reconstituted on a supported lipid bilayer under near physiological conditions. The live cell studies em- ploy fluorescent sensors and cell imaging to test key predictions of the in vitro mechanistic model for relevance in the cellular context. The PI has a strong track record and continues to play leadership roles in his research field, as well as the university and scientific communities. Overall, this research program is well positioned to continue generating fundamental advances with significant impacts on signaling biology and medicine.

Public Health Relevance Statement

NARRATIVE This research program focuses on lipid signaling pathways controlled by ubiquitous PI3K lipid kinase enzymes. PI3K lipid signaling pathways play central roles in normal macrophage function during innate immunity and, when dysregulated, trigger an array of human diseases. Research is pursuing the molecular mechanisms of regulation in the normal pathway, as well as the mechanisms of dysregulation triggered by disease-linked mu- tations, and the mechanisms by which drugs and potential therapeutics drive pathway activation or inhibition.

For more information, see the

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