A sampling of the goods created by the Family Crafters
In Brillion, WI, an amazing family works throughout the year to create craft goods to sell at farmers’ markets, craft shows, and grocery stores. Together, they are the Family Crafters, using their time and talents to raise money for cancer research in a unique and creative way. The Family Crafters create a wide variety of items, ranging from hand towels and potholders to coasters and jewelry, and have generously chosen to donate all profits to McArdle. Some popular items such as their grocery bag holders and catch-all bags are staples, but their selection of offerings is constantly rotating as they continually incorporate new types of goods into their arsenal.
The Family Crafters was formed after several members of the family behind the group were diagnosed with cancer. Collectively, they decided that they wanted to do something to make an impact. For the past decade, the members have been creating goods to raise money for national cancer organizations. As their efforts grew, however, they decided they wanted to support cancer research more directly. The Family Crafters chose to begin donating to McArdle two years ago to make sure the money raised through their hard work and dedication reached the cause they cared about and stayed within Wisconsin.
The members of the Family Crafters have found that their local communities are extremely supportive of their efforts. In addition to appreciating the wonderful crafts they make, many of the people they encounter while selling their goods share stories about their own experiences with cancer, encouraging the group to continue their amazing work.
“When we’re selling the products and people as so appreciative of what we are doing, it makes it all worthwhile,” said a member of the Family Crafters. “We hear their stories, and they’re just grateful that we are out there doing what we do, and that we're doing it all non-profit to benefit cancer research.”
Wei Xu, right, with McArdle Director Paul Lambert and Ron and Ruth Niendorf. Mr. and Mrs. Niendorf were friends and neighbors of Marian Burgenske, and helped her establish the endowment for Dr. Xu's professorship.
McArdle is excited to announce that Wei Xu has been named the new Marian A. Messerschmidt Professor in Cancer Research. Dr. Xu, who has been a faculty member with McArdle since 2005, is also a member of the Carbone Cancer Center Genetics Program and the National Institutes of Health Cancer Biomarkers Study Section. The Messerschmidt endowed professorship was originally held by former McArdle director and Department of Oncology chair Norman Drinkwater, now the Associate Vice Chancellor for Research in the Biological Sciences.
Dr. Xu’s research focuses primarily on studying the transcriptional regulation of estrogen receptor signaling in breast cancer, as well as the epigenetic modifications associated with carcinogenesis. Recently, groundbreaking work from her lab studying how the CARM1 methyltransferase protein regulates cancer progression has been published in premier journals including Nature Cell Biology, Nature Communications, and Cancer Cell.
“Curing breast cancer is our mission,” said Dr. Xu of her lab’s work. “However, there are many different subtypes, so we need to know more about the molecular mechanisms for the initiation, metabolism, and metastasis of breast cancer so we can design more personalized treatments.”
The named professorship recognizes Dr. Xu’s dedication to cancer research and her past accomplishments, and provides her financial support to continue her investigation into breast cancer going forward. Proceeds from the endowment will be used both to support Dr. Xu’s salary and provide her lab with additional funding.
The donor of the endowment for Dr. Xu’s professorship, Marian Burgenske, was a lifelong resident of the Madison area. Born in 1906, she graduated from Wisconsin High School and attended the now-defunct Madison Business College. Shortly after graduating, Marian began working at the registrar’s office of Madison Area Technical College, a job she served in for over 45 years.
As she began working, Marian’s father gave her an ultimatum: she could continue living at home, but only if she was responsible with her money. For Marian, it was an easy choice. She decided to continue living with her parents, even after marrying her husband Rodney in 1930. This financial freedom allowed Marian to begin investing her income in stocks and bonds from a young age. She was an extremely organized and shrewd investor, never using a bookkeeper but rather meticulously tracking and recording all of her own investments.
Marian’s own experiences with cancer inspired her to donate the fruits of her hard work, thrift, and prudent investing to supporting cancer research. During her early life, she battled ovarian cancer, and several decades later was diagnosed with breast cancer. Her neighbor and close friend Ron Niendorf suggested that Marian fund an endowment, allowing the impact her donation to continue in perpetuity. She agreed, and the Marian A. Messerschmidt endowment was established in her maiden name, as per her wishes. The Marian A. and Rodney P. Burgenske Chair in Diabetes Research at UW-Madison, currently held by Dr. Vincent Cryns, as well as the Marian Messerschmidt Scholarship for judicial reporting at MATC were also established from her estate.
Dr. Roz Boutwell and Alex Law
On June 6, 2014, Dr. Roswell “Roz” Boutwell gave a talk on McArdle’s early history. Dr. Boutwell had joined McArdle in 1945, and was one of the core faculty members who helped transform McArdle into a leading cancer research institute. His talk highlighted his role along with the role of many of his colleagues during the early years of McArdle, and delved into some of the key discoveries which propelled McArdle’s research.
Dr. Boutwell passed away on August 25, 2017, at the age of 99. He was the last surviving member of McArdle’s early faculty core. Though the original women and men whose work spearheaded McArdle’s growth and development are no longer with us, their legacy persists thanks to their indelible contributions to the University of Wisconsin and basic cancer research.
Below is a reflection by McArdle graduate student Alexandra Law on Dr. Boutwell’s talk, originally published in July of 2014. A memorial to Dr. Boutwell can be read here.
Upon leaving a pleasant community talk by Dr. Roz Boutwell, a longtime Professor Emeritus of Oncology at the McArdle Laboratory for Cancer Research, I couldn’t help but think of a quote made popular by Sir Isaac Newton: “If I have seen further it is by standing on the shoulders of giants.” For Dr. Boutwell had just finished speaking of the early days of McArdle Laboratory and of the “Core” group of individuals involved who played key roles in establishing the first cancer research program at the University of Wisconsin; a program which had its humble beginnings 75 years ago in the year of 1939, and would grow to be recognized around the world as a leading center for basic cancer research.
What was particularly remarkable about this talk was 97-year-old Dr. Boutwell himself. Not only was he still quite energetic and incredibly sharp-minded but, as his age suggests, he was a part of this “Core” group of academics who had such high hopes and ambitions for basic cancer research at the University of Wisconsin. These scientists were staunchly dedicated to initiating and developing a strong cancer research program at a time when there was very little support and funding for it. Dr. Boutwell spent the majority of his talk focusing on this “Core” group of people with their remarkable achievements and contributions to cancer research.
Dr. Boutwell identified the years of 1939-1948, the first years of McArdle Laboratory, as key for the program. He stressed that the work of this “Core” group during this time was instrumental to McArdle’s success many years later. Dr. Boutwell stated that to him, the word “Core” meant “heart.” He was undoubtedly referring to the incredible persistence and determination that this “Core” group of academics had in building a strong cancer research program in Wisconsin and in the US.
Introducing the people that made up the “Core”, Dr. Boutwell started with Dr. Harold P. Rusch. Dr. Rusch, who obtained his college and medical degree from the University of Wisconsin (UW), is easily considered the most influential member of the “Core” because he was the first Director of the McArdle Laboratory and the first key motivator in establishing a cancer research program in Wisconsin. With the help of funds bequeathed by Michael W. McArdle, an attorney and entrepreneur from Door County, Wisconsin, who before his passing from cancer in 1935, requested that his funds be directed towards cancer research in Wisconsin, Dr. Rusch spearheaded the building of a facility on the UW campus to house laboratories solely devoted to cancer research. Dr. Boutwell describes Dr. Rusch as being very optimistic, energetic, easily approachable, and willing to talk to anybody. Dr. Rusch was a leader and having received training in Physiology, became very interested in cancer and implementing the first cancer research on campus. He believed that the field of Biochemistry could reveal many of the unknowns of cancer and hoped to look inside a cell to visualize the mechanisms involved. Dr. Rusch, being the first Director of McArdle, was responsible for successfully recruiting many strong scholars to serve as faculty in the program. These early faculty members proved to be outstanding scholars in their own right and thus comprised the rest of the “Core” group that would propel McArdle forward in cancer research.
Dr. Rusch’s first faculty recruit was Dr. Van R. Potter. Dr. Potter received his undergraduate degree from South Dakota State College and received his Ph.D. at UW. In his book “Something Attempted, Something Done,” Dr. Rusch describes Dr. Potter’s early interest in Enzymology; specifically, comparing enzyme activities in normal and cancerous tissues. Dr. Boutwell emphasized that it was Drs. Rusch and Potter that made up the “heart” of the “Core”. Though they were both studying separate problems, they communicated often and filled the other in on what was and was not working in the lab. They quickly understood that, although they were the first and, for a short time, the only project leaders present in the new program, that by working together they could establish a foundation for cancer research appealing to new faculty recruits who shared their goals.
The next two recruits of the fledgling program were James and Elizabeth Miller who arrived in the program in 1943 and 1945 respectively after completing their graduate training at UW. James, or “Jim” as he was known by his colleagues, was brought in for his expertise in chemical carcinogenesis and Elizabeth, or “Bette” as she was more affectionately known in the department, was sought after for her training in nutritional carcinogenesis. While at McArdle, both published seminal work that Dr. Rusch describes as “classic in its field”. Dr. Rusch states that “[James and Elizabeth] have added more to our basic understanding about how chemical carcinogens induce cancer than anyone else in the world.” Among their many contributions, one of their greatest was recognizing that most chemical carcinogens require metabolic activation to become electrophilic reactants. It is these chemically active compounds that can induce mutations and thereby be carcinogenic. Dr. Boutwell emphasized that though each was a highly proficient scientist in his and her own right, and that while in the department they each had their own studies and lab personnel, the Millers operated often as a team. He stressed that they complemented each other, they were each in tune to the other’s work, and they often relied on the other’s professional expertise. Dr. Boutwell spoke highly of them and considered them to be close colleagues and friends. It was with sorrow that he spoke of their passing from cancer.
Lastly, Dr. Boutwell spoke of himself and his arrival at McArdle in 1945. He received his graduate training in the Biochemistry Department at UW. At that time, Dr. Rusch had been seeking someone with knowledge in nutrition to provide expertise on the effects of diet on cancer formation. Since Dr. Boutwell had developed a strong background in nutrition as a graduate student, Dr. Rusch considered him to be a suitable candidate to provide this expertise. In addition to his work on nutrition and carcinogenesis, Dr. Boutwell made great advances in the field of tumor promotion. He found that some compounds that initiate cancers may not be sufficient to promote tumors, but that these compounds in combination with a tumor promoter can cause cancers. Dr. Boutwell mentioned that it was in these early days that they began to appreciate the power of hormones in carcinogenesis and early questions of the role of hormones in prostate cancer were formed at this time.
In addition to speaking of his previous research, Dr. Boutwell went into detail about the strong relationships he had developed with other faculty members of the program. He told several entertaining stories of those early days, one of which involved him participating in a weekly poker club that these colleagues used to be a part of. While telling these stories, Dr. Boutwell briefly spoke of his personal relationship with his wife, Louise, or “Lou”. In hearing Dr. Boutwell’s stories, it was clear that he treasured the personal and professional relationships he had developed with his family and his colleagues. Accordingly, members of the department have considered Dr. Boutwell to be a particularly special colleague in that whenever a fellow colleague was in need of assistance, he was consistently available to help. His trustworthiness, reliability, and dependence were important contributions that Dr. Boutwell made to the program. Hearing of how Dr. Boutwell is remembered by his colleagues helped me realize that McArdle was built not only by its research but also by its individuals such as Dr. Boutwell who made significant contributions, many of which cannot only be measured by publication success, to the program.
Dr. Boutwell concluded his talk recognizing that an hour was simply not enough to recognize every person involved in the early days who contributed to the success of McArdle and that there were many names that he did not have a chance to introduce. Yet he emphasized that the roles of Drs. Rusch, Potter, James Miller, Elizabeth Miller, and himself were crucial to establishing the program that remains in existence today, 75 years later. Sadly, the sorrow that Dr. Boutwell felt about the Millers also punctuated his talk since of the “Core” members described, he alone survives. Yet he emphasized how grateful he was to have been able to spend much of his career with such remarkable colleagues and was pleased and excited to be able to speak to us at length about them and their contributions to the cancer research program at UW and to the cancer research field. It was upon hearing him that I was reminded of the quote about “… standing on the shoulders of giants.” It was quite a pleasure to be a member of this audience and hear of the magnanimous efforts made by historically important members of McArdle Laboratory to create a strong research program that would provide the highest training for graduate students such as myself. Experiences such as this one help me and other students appreciate being given the opportunity to be a part of this excellent program.
Feature image on home page: Dr. Boutwell (center, in beige jacket) with McArdle faculty after his June 6, 2014 talk.
Prior to 2003, there was almost no multiple myeloma (MM) research ongoing at UW-Madison. However, the Trillium Fund was established that year by several generous patients to support myeloma research at the UW Carbone Cancer Center. In 2004, Dr. Natalie Callander was recruited to the UW-Madison and the Multiple Myeloma Working Group was established. Now, the MM working group is vibrant with physician scientists, pathologists, and basic scientists working together to improve our understanding of the disease and to develop new treatment approaches. Members receive multi-investigator grants from National Cancer Institute and other agencies to support research activities. Since the formation of the MM working group, the members of the group have held many seminar presentations for patients, their family members and friends over the years with topics ranging from basic discoveries to clinical trials to new therapeutic options.
On November 9 this year, the MM working group held “UWCCC Multiple Myeloma Update” seminars for over 200 patient participants with topics including clinical trials update (Dr. Callander), mind-body influences on myeloma (Dr. Constanzo), immunotherapy (Dr. Hall), predicting drug responses (Dr. Miyamoto), anti-myeloma immunity (Dr. Asimakopoulos), minimal residual disease (Dr. Leith), synstatin drugs (Dr. Rapraeger), microbiome influence (Dr. D’Angelo), and novel cell therapies (Dr. Hematti). This morning seminar session was followed by lunch and tours of the bone marrow transplantation clinic (Dr. Hematti) and WIMR labs (Drs. Asimakopoulos and Miyamoto). Many of the participants took the opportunity to take these tours and asked questions regarding basic and clinical research and how their myeloma biopsies and samples are utilized to learn the biology of the disease and to develop new therapeutics. Overall, this public event was highly successful and the MM group is looking forward to continuing to host future events to inform the patients on ongoing multiple myeloma research at UW-Madison and to provide up-to-date information on MM therapy.
-Dr. Shigeki Miyamoto
Feature image on home page: McArdle facuty member Shigeki Miyamoto presents at November 9th's event.
Dr. Xu and her lab group. From left to right: Kristine Donahue, lead author Fabao Liu, author Yidan Wang, Justine Coburn, Carlos Coriano, senior author Wei Xu, Steve Chan, Eui-Jun Kim, and Dominic Dharam. Contributing scientists not pictured: Fengfei Ma, Yuyuan Wang, Ling Hao, Hao Zeng, Chenxi Jia, Peng Liu, Irene M. Ong, Baobin Li, Guojun Chen, Jiaoyang Jiang, Shaoqin Gong, and Lingjun Li.
As cells with a propensity for cancer break down food for energy, they reach a fork in the road: They can either continue energy production as healthy cells, or shift to the energy production profile of cancer cells. In a new study published on Oct. 23, 2017 in the journal Nature Cell Biology, University of Wisconsin–Madison researchers map out the molecular events that direct cells’ energy metabolism down the cancerous path.
The findings could lead to ways to interrupt the process.
“Cancer cells often change their nutrient utilization and energy production, so many efforts are being made to develop drug inhibitors of cancer cell metabolism to starve them,” says senior author Wei Xu, the Marian A. Messerschmidt Professor in Cancer Research at the UW Carbone Cancer Center and McArdle Laboratory for Cancer Research. “We have found that inhibiting a chemical modification of a cancer-associated metabolism protein is enough to inhibit the aggressive nature of cancer cells.”
Cancer biologists have identified nearly a dozen “hallmarks of cancer,” or large-scale changes that send a precancerous cell over the tipping point to become a cancerous one. One hallmark of cancer is the loss of properly regulated energy metabolism, a process referred to as the “Warburg effect” after the Nobel laureate, Otto Warburg, who identified it.
Other hallmarks of cancer include continuous activation of growth pathways, the inability to respond to signals that put the brakes on cell growth, and a gain of invasion and spread to distant organs.
“My lab studies a protein, CARM1, which is associated with worse outcomes in breast cancer patients, though it has also been found expressed in many other cancer types,” Xu says. “CARM1 chemically modifies its target proteins to alter their function, and in doing so directly leads to the activation of several hallmarks of cancer.”
In the study, Xu and her colleagues found that CARM1 protein modifies a cell metabolism protein, PKM2, and changes its function. This drives the Warburg effect, activating a hallmark of cancer. Nearly a decade ago, researchers found that PKM2 was expressed at high levels in cancer cells, but how these levels translated to more aggressive cancers was not known.
So, Xu and colleagues performed a protein interaction assay in a breast cancer cell line and found that CARM1 interacts with and chemically modifies PKM2.
They also assessed whether CARM1-directed modifications of PKM2 might be responsible for leading cells down a cancerous pathway. By engineering cells to express “normal” PKM2 or a mutated form that was not modifiable, the researchers learned that PKM2 appears to be the deciding factor in picking the direction cell metabolism takes at that fork in the road. The CARM1-modified PKM2 shifted cells toward the cancer cell metabolism path while cells with PKM2 that could not be modified took the metabolic path associated with noncancerous cells.
With a clearer picture of how cancer cells shift their metabolism, the researchers next used a mouse model of breast cancer and a competitor drug that prevents CARM1 from effectively modifying PKM2 to test what would happen.
“When we block PKM2 modification by CARM1, the metabolic energy balance in cancer cells is reversed, and we see a decrease of cell growth and cell spreading potential,” Xu says. “This study, then, identifies another therapeutic target to help reverse several hallmarks of cancer.”
In addition to targeting PKM2 modification by CARM1, Xu’s lab is investigating how CARM1 recognizes all of its many target proteins, with the goal of disrupting those protein modifications from driving aggressive cancers.
Xu’s research colleagues include postdoctoral fellow and lead author Fabao Liu, and co-investigators Shaoqin Sarah Gong and Lingjun Li. Gong’s group engineered the unique nanoparticle that allowed for the delivery of the PKM2 competitor, and Li’s group identified where the PKM2 protein was modified by CARM1.
The work was supported by grants NCI R01 CA213293 and R21 CA196653, as well as the UW Carbone Cancer Center core support grant, NIH/NCIP30CA014520.
Slideshow image on home page: Inhibiting PKM2 methylation increases Ca2+ uptake and mitochondrial membrane potential, both important factors for oxidative phosphorylation. The top row images show the co-localization of mitochondrial tracker and Rhod-2 (a Ca2+ indicator) in MCF7 PMK2-KO cells. The bottom row images show Rhod-2-labelled mitochondria in parental MCF7, PKM2-KO, PKM2WT/shPKM1 and PKM2mut/shPKM1 cells. From Liu et al., Nature Cell Biology 2017 Oct 23; 19(11): 1358–1370.
This article was originally published at https://www.med.wisc.edu/news-events/new-study-shows-how-cells-can-be-led-down-non-cancer-path/51459
Expression of both HPV oncogenes E6/E7 and estrogen (E2) alter host gene expression in the cervical stroma. The Venn diagrams and pie charts in this figure show the differential expression of genes in the stroma for E6/E7, E2, and E6/E7+E2 compared to WT mice. From Spurgeon et al., PNAS. 2017 Oct 9; 114(43): E9076-E9085.
Human papillomavirus (HPV) and the hormone estrogen are both linked to the development of cervical cancers, but how they work together has remained unclear. A new study by University of Wisconsin-Madison researchers shows how the combination of two factors influences the local cervical environment and drives the progression of cancer development.
HPV is a virus that infects epithelial cells of mucous membranes such as the vagina, anus or back of the throat. Over 150 strains of HPV are known, ranging from those that cause benign warts to the high-risk strains that cause the majority of all HPV-associated cancers. However, only some high-risk infections progress to cancers, and a better understanding of what factors drive cancer formation should lead to improved therapies.
“Before I started in the Lambert lab, former lab members had discovered that not only is estrogen important in HPV-associated cervical cancers in mice, it is estrogen signaling through the non-cancerous stromal cells, also called the microenvironment, that is important,” said lead author Dr. Megan Spurgeon, an assistant scientist in Dr. Paul Lambert’s lab. “At the same time, Dr. Paul Ahlquist’s lab was looking at human cervical cancer samples and found a role for estrogen signaling through the stroma.
Spurgeon and her research colleagues wanted to know if HPV infection caused the epithelial cells to send a signal that altered the microenvironment, and if the stromal cells in turn sent a signal to the HPV-infected cells that promoted their cancerous growth. So they took a more detailed look at the Lambert lab’s mouse model of cervical cancer. In these mice, high-risk HPV genes are expressed only in cervical epithelial cells; the mice only develop cervical cancer if they are given extra estrogen.
“This model allows us to determine the contribution of HPV alone, estrogen alone, or both together,” Spurgeon said. “And then we used a really precise laser-based dissection tool that allowed us to exactly capture epithelial tissue or stromal tissue and to ask how they each respond to the different factors.”
With the epithelial and stromal tissue precisely separated, the researchers measured changes in total gene expression of the different tissue compartments in response to HPV or estrogen. They compared HPV mice to non-HPV mice, and found hundreds of gene expression differences in the stromal cells.
“The high-risk HPV genes alone were able to reprogram or change gene expression in the nearby stroma, even though HPV genes are not present in the stroma,” Spurgeon said.
Next, they asked how estrogen affected stromal gene expression with or without HPV in the epithelium. They found that estrogen alone causes some changes, as expected. But in the HPV mice treated with estrogen, they found a different set of genes expressed in the stroma than with either factor alone. It was this subset of genes that helped them identify the potential factors involved in crosstalk between the HPV-infected epithelial cells and the estrogen-receptive microenvironment.
Using human cervical cancer cells, they further investigated a class of these genes, the pro-inflammatory chemokines, which are known to move between cells. They grew cells either by themselves or in co-culture with cervical stromal cells, and measured levels of the inflammatory chemokines, and found higher levels in the co-culture.
“The hypothesis now is that those inflammatory chemokines are secreted by the stroma and are feeding back on the epithelial cells or some other cells in the microenvironment to drive cancer development,” Spurgeon said. “The next step is to use our mouse model and genetically engineer it to knock down the chemokine receptors on different cell types or inhibit the chemokine signaling with drugs to see if they are directly contributing to cancer.”
While estrogens are not linked to other HPV-associated cancers, this study highlights how HPV influences the microenvironment to contribute to other cancers.
“The fact that HPV alone was able to reprogram the nearby stroma is an important finding, and suggests that HPV could be conditioning the microenvironment to respond to other factors in other HPV-associated cancers,” Spurgeon said.
The study was published online October 9 in the journal Proceedings of the National Academy of Sciences. It was funded in part by NIH grants CA022443 and P30 CA014520.
Spurgeon is supported by an NIH R50 Research Specialist award (CA211246), a category of new support grants for exceptional scientists who are pursuing research in an existing research program but are not faculty leads themselves. She is the first recipient of such an award at UW; read more about Spurgeon and her R50 award here. Study co-authors include UW Carbone Cancer Center members Lambert, director of the McArdle Laboratory for Cancer Research; Ahlquist, investigator at the Howard Hughes Medical Institute, the Morgridge Institute for Research and McArdle; Dr. David Beebe, director of the UW Microtechnology, Medicine and Biology Lab; and Dr. Avtar Roopra, associate professor of neuroscience.
Conflict of interest statement: Beebe holds equity in Bellbrook Labs LLC, Tasso Inc., Stacks to the Future LLC, Lynx Biosciences LLC, Onexio Biosystems LLC, and Salus Discovery LLC.
Slideshow image on home page: Lead author Megan Spurgeon and principle investigator Paul Lambert.
This article was originally published at https://www.med.wisc.edu/news-events/study-shows-hpv-works-across-cellular-borders-to-drive-cervical-cancer/51428
Dr. Megan Spurgeon, a scientist in Dr. Paul Lambert’s group, is the first recipient at the University of Wisconsin of an R50 Research Specialist Award. This new funding mechanism from the National Cancer Institute seeks to "encourage the development of stable research career opportunities for exceptional scientists who want to pursue research within the context of an existing cancer research program."
The R50, a five-year award, provides the salary for its recipient, allowing the staff researcher some autonomy and alleviating financial strain on their Principal Investigator's budget. The grant also provides a travel allowance for the researcher to attend conferences and research meetings.
Spurgeon initially came to Lambert's lab as a postdoc in 2010, and joined the McArdle staff as an Assistant Scientist in 2014. The R50 grant mechanism came to fruition during her second year as a McArdle staff scientist, and Lambert encouraged her to apply during the grant’s first round of applications.
"I had heard that a grant for staff scientists was in the pipeline, so it was kind of serendipitous that I was a staff scientist in a position to apply by the time that the R50 funding mechanism was introduced," Spurgeon said. "I’m personally honored that my grant application was funded, but I also hope that this grant mechanism helps pave the way for other funding opportunities for staff scientists."
The R50 award was created in part to address the current climate in biomedical research, where a large number of successful postdocs are competing for a very limited number of tenure-track faculty positions. As support from scientists and core facility specialists becomes increasingly important at research institutions, the R50 seeks to help make staff scientist positions more attractive to exceptional researchers like Dr. Spurgeon.
“It is very fitting for Dr. Spurgeon to be awarded the first NIH R50 award here at the University of Wisconsin-Madison," writes Dr. Lambert. "She has contributed greatly to the University’s discussion on the future of biomedical research over the past two years, and is now participating on a campus-wide committee on how the University can provide scientists like her the career security to pursue their life ambition here on campus."
With this award, Spurgeon looks forward to continuing her research within Lambert's lab at McArdle on DNA tumor viruses, including human papillomavirus (HPV) and Merkel cell polyomavirus (MCPyV). On the heels of her recent paper publication in the journal Proceedings of the National Academy of Sciences, she is especially excited about further exploring the pathways by which HPV and the female hormone estrogen affect cell signaling between the epithelium and the microenvironment in HPV-associated cervical cancer.
"I think this new analysis gave us insight into some potential players," Spurgeon said. "We have been chasing after this elusive signaling factor for a long time so now we at least have a sense of where to focus our efforts."
Read more about Spurgeon and the Lambert lab's recent publication here.
Every year, Sun Prairie High School seniors decide on a way they would like to give back to their community before graduation. Two beloved faculty members at Sun Prairie had recently passed away due to cancer, motivating the 2017 graduating class to focus their donation on supporting cancer research at McArdle.
"Every student in our high school had known at least one of the two teachers that passed away and felt the impact that their dedication had on the school," said Justice Hadley, a class co-president and freshman at UW-Madison. "My fellow class officers and I knew that donating to research was something both teachers would have appreciated."
In choosing an institution to give to, the senior class especially valued the local connection with McArdle.
"The class presidents researched different institutes around the country, and we all decided that we wanted to support an institute that was close to home, and whose research would be able to help our families and friends," explained class co-president Nathan Smith, now attending West Point.
The senior class was able to raise money in a variety of ways, ranging from setting aside proceeds from school events like prom to collecting individual student donations. John Barth, a social studies teacher at Sun Prairie, helped facilitate the process, but emphasized that the entire effort was driven and funded by the students.
“Often times young people get a bad reputation of either not knowing or not caring about problems,” Barth said. “We as staff are proud that our kids are so giving, and really want to make their community a better place and pay it forward.”
Director Paul Lambert writes, "We are extremely honored that the students of Sun Prarie High School chose to donate to McArdle. We will use these donations to pursue new discoveries about how cancer arises, and thereby new directions for how we can prevent and treat this human malady.”
The photo for this article was found on http://findorff.com/project/detail/sun-prairie-high-school/
amount of luminescence 13 days after treatment was started. Purple = least luminescence; Red = highest luminescence. From Bilger et al., Oncotarget 2017 Jul 4; 8(27): 44266–44280.
Epstein-Barr virus (EBV) can cause the development of fatal lymphomas in transplant patients. EBV can infect human cells in two different forms: latent infection, in which the virus does not kill the infected cell, but expresses cancer-causing viral proteins; and lytic infection, in which viral proteins are expressed that kill the infected cell. Both the latent and lytic types of infection contribute to the proliferation of infected cells in immunosuppressed patients.
We show that an FDA-approved drug currently used to treat multiple sclerosis, teriflunomide, not only inhibits the growth of latently EBV-infected cells, but also prevents the lytic form of EBV replication. Furthermore, we find that a clinically relevant dose of teriflunomide inhibits the development and growth of EBV-induced lymphomas in two mouse models. Our investigations suggest that teriflunomide (and its prodrug, leflunomide) may be useful for preventing and/or treating both latent and lytic EBV infection in patients who require immunosuppression (such as transplant recipients) and are at high risk for developing EBV-induced lymphomas.
Link to paper in Oncotarget: