Award recognizes her career contributions in research
Physician-scientist Farrokh Dehdashti, MD, the Drs. Barry A. and Marilyn J. Siegel Professor of Radiology and senior vice-chair and director of the Division of Nuclear Medicine at WashU Medicine, is being recognized by the Radiological Society of North America for advancing the radiologic sciences throughout her career in research.
For her scientific accomplishments, she will receive the 2025 Outstanding Researcher award at the society’s annual meeting, Nov. 30-Dec. 4 in Chicago.
The Radiological Society of North America represents professionals spanning the full breadth of radiologic subspecialties in more than 160 countries around the world and publishes six peer-reviewed journals.
Dehdashti is credited with expanding the role of positron emission tomography (PET) imaging in the field of oncology. She conducted some of the first studies in people of several novel PET diagnostic compounds related to several types of cancers, including cervical, breast, pancreatic and prostate cancers. Her other research interests include imaging estrogen receptors and progesterone receptors in breast cancer; Chemokine receptor imaging, such as CCR2 imaging in pancreatic and head and neck cancers; PARP imaging of solid tumors; and imaging tumor proliferation. See her research profile here.
She earned her medical degree from Pahlavi University School of Medicine in Iran in 1977 and completed her radiology residency in 1980 at the same institution. She served as chief resident and then research fellow in PET imaging in the Division of Nuclear Medicine at WashU Medicine before joining the faculty in 1990.
Bennett oversees screening and diagnostic mammography services at Siteman Cancer Center, based at WashU Medicine and Barnes-Jewish Hospital, and is a member of the breast cancer specialist team. As a member of several national panels, she is helping shape national guidelines and policies relating to breast imaging and cancer screening. She is also a co-author on the most recent version of the ACR Breast Imaging Reporting and Data System Atlas, the international standard for breast imaging reporting. Bennett was named chief of breast imaging in 2020.
“We’re forging history and moving forward with new techniques that support women,” said Pamela K. Woodard, MD, the Elizabeth E. Mallinckrodt Professor of Radiology and director of MIR. “Debbie has been a mentor to many residents who have chosen breast imaging as their career.”
A physician committed to providing high-quality care throughout the community, Bennett specializes in the diagnosis of benign breast conditions and breast cancer. Her research focuses on the early diagnosis of breast cancer and the impact of screening mammography on population outcomes, and she is a co-investigator on multiple collaborative research projects focused on mammogram-based risk prediction, risk reduction interventions and use of novel technologies to reduce benign biopsies.
At her installation ceremony, Bennett presented “Building Community Through Breast Imaging,” in which she discussed the evolution of MIR’s breast imaging section. “This is the house that Barbara built,” she said, referring to Barbara Monsees, MD, professor emeritus of radiology, who was the first chief of breast imaging and later the inaugural Ronald and Hanna Evens Endowed Professor of Women’s Health. The impact of her decades-long career is still felt today, with accomplishments including co-developing the Joanne Knight Breast Health Center and launching the mammography van in 1986 — bringing breast cancer screening to underserved areas across the region.
Established in 2004 by The Foundation for Barnes-Jewish Hospital, the Ronald and Hanna Evens Endowed Chair in Women’s Health honors the distinguished career of Ronald Evens, MD, longtime MIR director who oversaw a time of booming growth for the department. He held many other leadership roles, including president and CEO of St. Louis Children’s Hospital, president of Barnes-Jewish Hospital, vice chancellor for financial affairs at WashU and vice president of Washington University Medical Center. Hanna Evens is a 1960 graduate of Barnes Hospital School of Nursing and a former nurse at St. Louis Children’s Hospital.
Bennett was installed in a ceremony held at WashU Medicine. She punctuated the night with the nexus of her medical philosophy: “Always bring it back to the patient.”
Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine is pleased to announce funding for 12 new projects, including four clinical trials. Through this research, investigators aim to improve the understanding of tumor formation and growth, develop safer, more effective therapies, and explore new cancer screening strategies.
The projects will benefit from $2.42 million in new grants awarded through the Siteman Investment Program. The goal of the grants is to support and accelerate the pace of innovation in cancer research. The money awarded comes from a variety of sources, including The Cancer Frontier Fund at The Foundation for Barnes-Jewish Hospital, which includes gifts from Pedal the Cause’s annual bike challenge, the Foundation’s annual Illumination Gala, and donations throughout the year; the Cancer Center Support Grant (CCSG) from the National Cancer Institute; the Alvin J. Siteman Cancer Research Fund; Swim Across America – St. Louis; and various philanthropic gifts.
Please see below for more details on each funded project.
New Clinical Trial Category
Project Title: Phase II Study of Stereotactic Body Radiotherapy plus FAK and RAF/MEK inhibition in Advanced Pancreas Adenocarcinoma
Goal: This is a phase II, single-institution, open-label trial treating patients with borderline resectable (difficult to remove surgically) or locally advanced (cannot be removed by surgery) pancreatic cancer. The hypothesis is that advanced pancreatic cancer patients receiving treatment of adaptive (change the plan each day to adapt to patient’s anatomical changes in bowel and tumor position) stereotactic body radiotherapy (SBRT) plus defactinib + avutometinib at the same time will have more time after treatment during which the cancer will not progress (otherwise known as increased progression-free survival, or PFS) compared to historical PFS rates for patients receiving adaptive SBRT alone.
Project Summary: Pancreatic ductal adenocarcinoma (PDAC) has a five-year survival rate of 12%. The only potential for a cure is surgical removal of the tumor (resection). However, despite 48% of patients presenting with advanced non-metastatic disease, only 10-15% of these patients are surgically resectable. Current standard of care for these locally advanced PDAC (LAPC) patients who are surgically unresectable is chemotherapy followed by consolidation stereotactic body radiation therapy (SBRT). However, more than half of these patients will progress to metastatic disease in one year. Current SBRT strategies infrequently generate sufficient tumor regression to enable a surgical option in LAPC patients. Thus, more effective treatment strategies for LAPC that lead to greater prevention of metastatic disease would directly improve PDAC patient survival. This application seeks to build on exceptional scientific, pre-clinical, clinical and biomarker findings. We will conduct a phase I/II study of SBRT plus FAK inhibition (Defactinib) and a RAK-MEK inhibitor (Avutametinib) in advanced pancreatic cancer patients. Our hypothesis is that this combination will be safe and lead long-term survival through modulation of tumor-intrinsic and immune pathways.
Project Title: Therapeutic RSK1 Targeting in Myeloid Malignancies
Goal: This study investigates a new approach to treating certain types of blood cancers. Currently available treatments for these blood cancers are only partially effective. Thus, there is a desperate need to develop more effective treatments for these diseases. The proposed study involves the repurposing of a treatment that is currently in development for breast cancer. This would be the first study of this treatment in blood cancers. This study hypothesizes that PMD-026, an oral inhibitor of ribosomal protein S6 kinase A1 (RSK1), is safe and well tolerated in participants with MF and MDS/MPN and will improve spleen response, symptom response and bone marrow histopathological response.
Project Summary: Myelofibrosis is a chronic myeloproliferative neoplasm (MPN) characterized by anemia, enlargement of the spleen, bone marrow fibrosis, fever, night sweats, fatigue and weight loss. Life expectancy with MF is limited, with a median survival of only five years. MF exhibits a propensity for transformation to post-MPN secondary acute myeloid leukemia (sAML), for which the prognosis is dismal (median survival < 6 months). Despite vigorous research, therapies capable of effectively treating MF and preventing progression to sAML remain elusive. Thus, there is a pressing need to develop novel therapeutic strategies for patients with these diseases. We initially identified aberrantly increased expression of the phosphatase DUSP6 in CD34+ hematopoietic stem/progenitor cells (HSPCs) from patients with MPNs transformed to sAML. Genetic and pharmacologic inhibition of DUSP6 inhibited MPN cell proliferation and suppressed downstream signaling effectors including phosphorylated RSK1 (pRSK1). To further understand the role of RSK1 (encoded by RPS6KA1), we performed patient-derived xenograft (PDX) experiments with sAML patient CD34+ HSPCs subjected to RPS6KA1 shRNA knockdown. Remarkably, RPS6KA1 knockdown led to near complete elimination of human CD45+ cells in the peripheral blood and bone marrow of engrafted mice. Our clinical trial challenges current treatment paradigms by investigating therapeutic targeting of a novel signaling pathway in myeloid malignancies. This investigator-sponsored study will be the first study with PMD-026 in blood cancers. The study additionally incorporates laboratory correlative studies (RNA-sequencing, mass cytometry, multiplex cytokine profiling, molecular genomics) to characterize how treatment with PMD-026 impacts downstream signaling effectors, inflammatory markers, and molecular response. This proposal leverages novel scientific concepts to address important unmet needs for patients with myeloid malignancies.
Project Title: Phase II Trial of Surgery followed by Risk-Directed Post-Operative Adjuvant Therapy for HPV-Related Oropharynx Squamous Cell Carcinoma: “The Minimalist Trial-2 (MINT-2)”
Goal: To reduce the dose of radiation and chemotherapy a patient receives after undergoing surgery for human papillomavirus (HPV)-related oropharynx squamous cell carcinoma (throat cancer)
Project Summary:
Despite improvements in operative techniques (e.g. transoral robotic surgery, or TORS), which have reduced short-term surgical morbidity for HPV+ oropharyngeal squamous cell carcinoma (OPSCC), otherwise known as throat or tonsil cancer, radiation and chemo after surgery remain a cause of significant long-term morbidity. While surgery is well-tolerated, post-surgery therapy often causes serious acute and chronic adverse events (AEs), including debilitating inflammation of the mucous membranes that line your mouth and GI tract, severe dry mouth, taste disorders and neck fibrosis/scarring among others, potentially resulting in long-term dependence on a feeding tube. Given the overall high rates of cure for HPV+ throat or tonsil cancer, there has been a strong focus on de-escalation of chemoradiation therapy (POACRT) in these patients to improve long-term morbidity. Our prior MINT trial (MINT-1) was a major step forward in de-escalation of HPV+ OPSCC patients. We believe this new proposal will significantly alter the standard of care adjuvant therapy of HPV+ throat and cancer patients and improve the therapeutic potential of current treatments. Importantly, MINT-1 was a non-randomized study; thus, at a minimum, confirming and extending the results of that study through MINT-2 represents a critical advance that is likely to yield adoption of this approach nationally and change the standard of care.
Project Title: A Multicenter Phase II Study of Propranolol for the Treatment of Kaposi Sarcoma in Adults
Goal: This is a phase II, open-label, multicenter, single-arm treatment trial evaluating the use of propranolol (a beta blocker) to treat Kaposi sarcoma (KS), a disease in which cancer cells are found in the skin or lymphatic or visceral sites in the body. The hypothesis of this study is that an overall response rate (ORR = CR + PR rate) of at least 45% (as assessed by the AMC KS response criteria) will be achieved in participants, and that propranolol will be safe and well-tolerated by patients with KS. Our goals are to determine: 1) the safety and response of propranolol for KS, and 2) the effect on KS-associated gene expression.
Project Summary: Infectious agents cause 20% of cancers worldwide. Kaposi sarcoma (KS) is caused by the KS γ-herpesvirus (KSHV). KSHV is also associated with primary effusion lymphoma, a B cell lymphoproliferative, preneoplastic disease, multicentric Castleman’s disease (MCD), and KS inflammatory cytokine syndrome (KICS). Treatment of KS involves immune reconstitution and/or systemic liposomal anthracyclines, taxanes, pomalidomide, or immune checkpoint inhibitors, but most of these therapies are not available low-income countries, and KS is one of the most common cancers in sub-Saharan Africa in HIV-negative or positive individuals.
Although remissions are obtained in most patients, complete remissions are rare, and continuous therapy is required. Propranolol is an inexpensive, globally available beta blocker, which is highly effective therapy for infantile hemangioma, and other vascular lesions and anecdotal reports describe successful treatment of KS with oral propranolol. Therefore, it is logical to assess the safety and activity of propranolol in a prospective clinical trial, and identify biomarkers of response. Single cell transcriptomics (scRNAseq) provides in-depth data about KS interactions with the tumor microenvironment, which will be utilized with baseline and on-treatment biopsies. We are uniquely qualified for this project given our extensive KS biological, pathological, epidemiological, translational and clinical experience.
Up to 25 eligible patients will be enrolled in a 2-stage phase 2 clinical study (18 at Washington University and 7 at the Kenya Medical Research Institute), with different KS subtypes, and treated with up to 20 weeks of propranolol. Successful completion of this study trial may provide a new, inexpensive, well-tolerated, globally available therapy for KS, and identification of biomarkers of response. This should prompt an assessment of beta blockers in other malignancies.
Team Science
Project Title: Elucidating Mechanisms and Translational Strategies to Enhance Therapeutic Anti-Tumor Immunity
Goal: The Cancer Immunity Team Science group is a translational, interdisciplinary research program with the overarching goal to develop new forms of immunotherapy that enhance a patients’ anti-tumor T cell immunity by design and thereby improve clinical outcomes or achieve cure.
Project Summary: The Cancer Immunity program is a group of physicians and scientists united in the goal of discovering new strategies that initiate or promote a patient’s own T cells to destroy their cancer. These discoveries will then be translated into multiple novel treatment strategies that may have a broad impact on multiple cancer types. The projects utilize solid tumor (sarcoma) and blood cancer (lymphoma) immunocompetent mouse models to evaluate these new ideas, with translational relevance enhanced by confirming findings within lymphoma patient samples. The first project established these two cancer models in mice, defined key cancer cell proteins (neoantigens) targeted by T cells, developed neoantigen vaccines to initiate cancer immunity, and discovered a new CD4+ Tr1 cell that suppresses effective CD8+ T cell responses to these malignancies. This project serves as an integrative hub for the other projects. A second project investigates how chimeric antigen receptor (CAR) T cells bring about cancer immunity, and correlates key findings in samples from patients undergoing CAR T cell therapy. The third project defines the ability of CAR natural killer (NK) cells to increase anti-tumor immunity by enhancing neoantigen release via direct killing, dendritic cell localization and maturation, antigen presentation and T cell localization. Concepts discovered will be confirmed in humanized mouse models. The fourth project advances CAR dendritic cells, evaluating mechanisms to promote robust cancer immunity through epitope spreading, and combining with strategies that target suppressive cells, including Tr1 cells. The projects are highly integrated by evaluating Tr1 cells in each strategy, performance of inter-project experiments to address resistance to a single immunotherapy, and have shared model profiling that evaluates Tr1, T cells, NK cells and DCs across projects. The projects will be supported by research cores that facilitate uniform immunology and informatics analysis, biostatistics and shared mouse modeling, in a planned extramural team science program application.
Pre-R01 Category
Project Title: Optimizing Targeted Alpha-Emitter Radiopharmaceutical Therapy for Intraperitoneal Carcinomatosis
Collaboration with University of Missouri – Columbia
Goal: This proposal aims to develop a safer, more effective radiotherapy treatment for patients with advanced colorectal cancer that has spread to the abdomen — helping improve both survival and quality of life.
Project Summary: Colorectal cancer often spreads to the lining of the abdomen, forming small tumors called peritoneal metastases. These tumors are especially hard to detect and treat and current therapies like systemic chemotherapy offer only limited benefit. There is a critical need for more effective and targeted treatments. This project explores a promising new strategy called intraperitoneal targeted alpha therapy (IP TAT). This approach delivers powerful cancer-killing radiation — known as alpha particles — directly into the abdominal cavity, where it can precisely target cancer cells while minimizing damage to healthy tissue. Alpha-emitters deliver extremely potent radiation and are increasingly being used in cancer patients, often successfully treating tumors for which other therapies have failed.
In the first part of this study, we will test a group of specially designed radioactive drugs that are made to seek out and attach to colorectal cancer cells. These agents are developed by our collaborators at the University of Missouri, who bring expertise in radiochemistry and tumor biology. By comparing different versions, we aim to find the one that most effectively reaches and sticks to tumors and stays in place long enough to be effective. In the second part of the project, we will use advanced imaging techniques and computer modeling—developed by the physicists and radiobiologists of the Washington University team — to precisely measure where the radiation accumulates and how much radiation the tumors receive. This will help us determine how best to eliminate cancer cells while avoiding harmful side effects.
Project Title: Diet-Related Therapies to Enhance Radiation Anti-Tumor Responses and Minimize Toxicity
Goal: The primary objective of this proposal is to investigate how cellular processes, such as autophagy and the activation of specific metabolic pathways, may enhance the effects of radiation therapy on tumors and protect the heart from radiation-induced damage. Our goal is to develop treatments that improve radiation’s helpful effects on cancer and reduce its harmful effects on the heart.
Project Summary: Radiation therapy (RT) is an important component of modern cancer treatment; it is received by over half of all patients with cancer. Despite recent advances, RT does not cure all patients, and some experience harmful side effects — especially to the heart when the chest is treated. This highlights the need for new strategies to improve RT. We recently demonstrated that intermittent fasting (IF), a dietary approach that alternates periods of fasting with normal eating, enhances RT’s ability to kill tumors and also protects against RT-induced heart damage in animal models. IF can cause a wide range of effects, including increased cycling of a process called autophagy, which is linked to health and aging, as well as altered tumor metabolism. Our preliminary data from pre-clinical laboratory models suggest that IF and RT alter autophagy in tumors and the heart, which may lead to the favorable effects of combining IF and RT. Our metabolomics and other data from pre-clinical models suggest that regulation of branched-chain amino acid metabolism may also mediate the enhanced anti-tumor effects of IF on radiation. Our objective in this proposal is to use innovative preclinical techniques to determine how IF and RT impact autophagy and branched-chain amino acid metabolism in preclinical models of cancer and heart damage using RT. Our findings have the potential to identify translatable interventions that replicate the beneficial effects of IF, thereby enhancing radiation outcomes in patients with cancer. For instance, approved drugs used for other conditions may mimic IF, potentially improving RT efficacy in patients. These studies may lead to clinical trials and ultimately improved outcomes for patients with cancer.
Collaboration with University of Missouri – Columbia
Goal: The long-term goal of this project is to develop a new treatment for glioblastoma (GBM) by leveraging the immune-boosting effects of a safe and weakened version of a bacterium, Brucella melitensis, which we call SPIKE1.0.
Project Summary: A major challenge in the treatment of patients with GBM is that patients’ immune systems do not attack the tumor. The tumor suppresses the number and function of immune cells around it. Researchers from the laboratories of Drs. de Figueiredo (University of Missouri) and Chheda (Siteman Cancer Center/Washington University) are working together on a new strategy using a safe, genetically modified bacterium that carries activating molecules, to lure and unleash anti-tumor defenses to attack and clear the tumor. Before moving to treatment in humans, they will rigorously test the hypothesis that this new treatment will improve the anti-tumor immune response in mice bearing brain tumors and significantly increase their survival. Upon successful completion of the specific aims of the project, the investigators will have the necessary preliminary data for an R01 proposal in which they will delve deeper into how this treatment works and develop even better therapeutic interventions. If successful, this research will eventually lead to a new treatment for glioblastoma patients that will improve their quality of life and help them live longer.
Project Title: Adapting a Multi-Level Intervention to Increase Lung Cancer Screening and Reduce Rural Cancer Disparities
Goal: To change practice, increase lung screening, and reduce the elevated rates of lung cancer mortality in rural southern Illinois
Project Summary: Many rural communities, including those in the Siteman catchment area, experience persistently elevated rates of cancer and cancer mortality compared to more urban areas. This holds true for lung cancer. Low-dose CT (LDCT) scans are recommended for adults aged 50 to 80 years who have a 20 pack-year smoking history and currently smoke or have quit within the past 15 years. Less than 1 in 5 eligible adults are up to date with lung cancer screening, and rates are lower in rural areas. Rural southern Illinois is no exception to this trend and has areas that are health professional shortage areas and experience longer distances to care, persistent poverty and higher rates of tobacco use. We must find effective ways to increase lung cancer screening rates. Our team collaborated with Southern Illinois Healthcare, a rural health system, to develop, implement, and test a bundle of multi-level interventions (a “toolkit”) to increase colon cancer screening. We successfully partnered with providers to distribute patient education, deliver provider nudges, make systems changes and, and provide community awareness. In clinics that participated in the intervention, the likelihood of patients being screened for colon cancer was increased. We now propose to collaborate similarly to increase lung cancer screening. To transition this work to a successful NCI R01 trial, our toolkit must be substantially revised. As such, for this pre-R01 Siteman Investment Program study, we propose: Aim 1 — Identify primary care providers’ challenges in lung screening and preferences for intervention support. We will conduct interviews and site visits at primary and specialty care, to examine the context and challenges of lung cancer screening and identify provider-proposed strategies to increase screening. We will interview patients to identify potential areas of hesitance or needs for support. Aim 2 — Build on prior work and Aim 1 findings to create a toolkit to help primary care providers increase lung cancer screening. We will adapt our existing materials, while bringing in new LDCT specific elements. Aim 3 — Prepare for successful R01 by completing two key foundational steps: (1) Begin adaptation of health maintenance page in EHR to make screening easier to find and (2) add lung cancer screening materials to SIH’s community outreach. We will observe and investigate perceptions of these materials for improvement in our trial. This work is necessary for our future R01 and will directly lead to a stronger NCI application. Our likelihood of success with NCI funding is better if we have developed these components, which we feel we can do with this SIP research. We plan to submit the R01 in 2026.
Project Title: Characterizing Hepatocellular Carcinoma (HCC) Tumor Immune Microenvironments to Inform Rationale Combination of Y-90 Radioembolization and Immune Checkpoint Inhibitors through Spatial Transcriptomics
Goal: To identify predictive biomarkers of treatment response and resistance, supporting future precision strategies to optimize the use of Y-90-RE and ICIs in early and intermediate stage hepatocellular carcinoma, a type of liver cancer
Project Summary: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death globally, with increasing incidence in the United States driven by metabolic-associated steatotic liver disease (MASLD, or fatty liver disease) and alcohol-related liver disease. While Yttrium-90 radioembolization (Y-90-RE) is a highly effective liver-directed therapy capable of achieving complete tumor response in early-stage HCC, a substantial proportion of patients, particularly those with more advanced disease, experience recurrence due to minimal residual disease (MRD). This failure to eradicate all viable tumor cells is likely driven by underlying differences between tumor cells, such as the presence of treatment-resistant cancer cells and the ability to avoid detection by the immune system. Although immune checkpoint inhibitors (ICIs) have shown promise in advanced-stage HCC, their use in early and intermediate HCC stages in combination with Y-90-RE is currently empirical and lacks molecular guidance. This proposal aims to identify molecular and tumor immune microenvironment (TME) features associated with response or resistance to Y-90-RE, and to determine which patients may benefit from the addition of ICIs. Using a unique biobank of pre-treatment biopsies and explant specimens from HCC patients treated with Y-90-RE with or without ICIs, we will analyze how genes are active in different parts of the tumor using advanced spatial mapping technology called Xenium.
Project Title: Targeting c-Myc Transcriptional Stress in Cancer
Goal: To understand the workings of a specific pathway (RNF113A-ASCC) that maintains genome stability and is lethal to cells with the c-Myc oncogene, a gene that plays a crucial role in cell growth and cancer proliferation
Project Summary: The main goal of this proposal is to understand the mechanism of a specific pathway that maintains genome stability and is lethal to cells with the c-Myc oncogene, a gene that plays a crucial role in cell growth, proliferation, and cancer metabolism. Our team discovered a new signaling pathway that starts when cells face damage to their DNA and RNA bases, a common effect of cancer treatments. This pathway involves two key proteins, RNF113A and SMYD3, which help bring repair enzymes to the damaged DNA. We’ve found that RNA signaling is crucial for activating this repair pathway. Our findings suggest that a certain protein (known as ASCC3 helicase) helps separate the spliceosome from the DNA, which is important when there’s increased stress from high c-Myc activity. We believe this pathway works during active RNA transcription and processing, which makes targeting it in tumors with high c-Myc levels a promising strategy. In this proposal, we plan to inhibit the RNF113A-ASCC pathway using genetic tools and existing drugs that act as inhibitors of SMYD3 to see if it can effectively fight small cell lung cancer (SCLC), a deadly cancer often linked to c-Myc amplification. We will also study how this pathway helps manage stress from high transcription to prevent harmful DNA-RNA structures and replication issues (Aim 2). This research aims to enhance our understanding of genome stability and its application in cancer treatment.
Project Title: Functional Impact and Clinical Application of DNA Methylation Epimutations in Acute Myeloid Leukemia
Goal: To define the changes in DNA methylation (chemical changes in DNA) that occur in acute myeloid leukemia and leverage these insights to improve our understanding of the way the disease forms and our ability to predict its potential return after treatment
Project Summary: Acute myeloid leukemia (AML) is a lethal hematologic malignancy characterized by mutations in hematopoietic (blood) stem cells. Prior research has shown that AML can develop from pre-existing clonal bone marrow diseases, including clonal hematopoiesis (CH) and myelodysplastic syndromes (MDS), and there is extensive overlap in the mutational spectrum across these conditions. In some CH and MDS patients, transformation to AML can occur with little change in the genetic composition of the cancerous cells, indicating a role for other contributing factors. DNA methylation is a chemical change in DNA that is essential for normal tissue development and is universally abnormal in AML patients. Recent studies by our lab have used new methods to directly sequence native DNA molecules without modifying them first, which improves our ability investigate changes in DNA methylation as a potential source of novel contributing factors to AML development. This approach identified specific regions in the DNA of patients with AML where DNA methylation was different between the maternal and paternal copies of specific genes that are important for blood cell function. These methylation patterns stayed the same in samples from the same patients at the start of their illness as when the illness came back, and they were also seen in these patients when they did not have active disease but still had signs of cancer cells based on genetic tests. Many of these “methylation spots” were recurrent across multiple patients and affected how easily parts of the DNA could be accessed, and they affected genes that control how stem cells grow and renew themselves, including a gene called GATA2 that is known to be very important for blood cell development.
Based on this evidence, we hypothesize that specific changes in DNA methylation represent clonal “epimutations” that can disrupt normal gene regulation and be selected for during the formation of leukemia. We further hypothesize that epimutations create a unique pattern in leukemia cell populations, which means they could help detect leftover leukemia cells when patients are in remission. In this proposal, we will study how DNA methylation epimutations affect the GATA2 gene by closely examining the structure of the chromatin in leukemia cells. After that, we will create a new testing method to detect both genetic mutations and these epimutations. This test will help us find remaining leukemia cells in patients who seem cured after chemotherapy. Overall, these studies will help us understand how DNA methylation epimutations impact the GATA2 gene in leukemia and offe
For something so simple, there can be something surprisingly enjoyable about a cold drink on a hot day.
It can quench our thirst, cool us down and just taste great.
And during these warm months when we need to drink more than usual to stay hydrated, it’s important to choose drinks that we like, but it’s also important to choose drinks on the healthier side.
Figuring out which drinks hit that sweet spot, though, isn’t always easy. To help with that, I spoke with Yikyung Park, a nutrition researcher and professor in the Division of Public Health Sciences at WashU Medicine, for her insight on which popular summer drinks are easy to say “yes” to — and which ones we should try to limit.
Plain water. “The best choice!” she said. Zero calories and refreshing, with nothing extra. From the kitchen tap or bottle filling station, it’s basically free — and easy to find. Keep a reusable, plastic-free bottle in your pack or on your desk, so water’s always in easy reach.
Fizzy water. “As good as plain water.” It can cost more but also be a nice twist on plain water. Choose unsweetened versions.
Iced tea and iced coffee. “A good choice, but avoid drinking too much.” There can be some health benefits from drinking coffee, but caffeine can be a problem with both tea and coffee. And try to keep milk, cream and sugar to a minimum. The calories and saturated fat can add up quickly.
Coconut water. “It has electrolytes, which can be helpful when we’re sweating a lot, but choose those with no added sugar.”
Fruit juice. “Good option, but be sure to choose 100% fruit juice, not a fruit-flavored drink.” And even for 100% juice, it’s best to drink it only once in a while. While 100% juice has some vitamins and minerals, it also has about as much sugar as soda.
Lemonade. “Very refreshing — and a summer classic — but watch out for sugar content.” Like juice, it can have as much or more than soda. So, it’s best to have it only sometimes.
Sugary soda, energy drinks and sports drinks. “These types of sugary beverages are not a good option. They’ve been linked to an increased risk of weight gain, diabetes and other chronic diseases. Many sodas and energy and sports drinks also contain a high amount of caffeine, which can be problematic for many people, especially children.” Combined with the warm temperatures of summer, the caffeine can also lead to dehydration. Sugary drinks are popular, but they’re best to avoid, particularly for kids.
Diet soda. “Since there’s no sugar in diet soda, it seems a better option than sugary drinks, but that’s not the case.” It’s best to limit them as well. Diet sodas contain caffeine and artificial sweeteners, which have been linked to poor health outcomes in some studies.
Blended coffee drinks. “These are an unhealthy combination of sugar and caffeine, plus they can be very high in calories!” Iced coffee or cold brew with just a splash of milk is a healthier alternative.
Bubble tea. “A fun drink for summer, but best to limit. It contains a high amount of caffeine and calories.”
Beer, hard seltzers and other alcohol. “Alcoholic beverages can lead to dehydration — and they have other well-known, serious health effects.” Alcohol increases the risk of cancer as well as injury, suicide, liver disease, mental illness and even infectious disease. As much as beer and other drinks can be a traditional part of summer celebrations, the healthiest approach is not to drink. Try nonalcoholic beer for a better option that tastes like the real thing.
Enjoying our favorite drinks with family and friends — or in a quiet moment alone — can be a special part of summer. Day-to-day, though, try to choose healthier drinks overall. It’s the best way to stay hydrated and can give a real boost to our long-term health.
“Except for plain water, it’s best to drink all other beverages in moderation or less,” Park concluded. “Most we shouldn’t drink every day.”
New understanding of how mutations interact could pave way for early detection, prevention strategies
As we age, our cells replicate, and the DNA in these cells can acquire mistakes — or mutations — every time the sequence is copied. Most newly acquired mutations are harmless, but some can tip the balance toward cancer development later in life.
Now, a new study led by researchers at Washington University School of Medicine in St. Louis shows that such newly acquired mutations interact with our inherited mutations — those passed down by our parents — in important ways that influence a person’s lifetime cancer risk. Understanding such interactions could guide development of new methods for early detection and prevention of cancer.
The research, published in Nature Genetics, focused specifically on the risk of blood cancers such as acute myeloid leukemia (AML), although interactions between inherited and acquired mutations likely have roles in other types of cancer.
Inherited mutations are carried in the egg and sperm and are therefore present in every cell starting at birth, whereas acquired mutations accumulate gradually with age in different cells. Led by Kelly Bolton, MD, PhD, an assistant professor of medicine in the Division of Oncology at WashU Medicine and the study’s senior author, the research team set out to understand how interactions between these two types of mutations influence a person’s risk of developing blood cancer.
In particular, they focused on a blood condition called clonal hematopoiesis that is known to increase a person’s risk of developing blood cancer. Clonal hematopoiesis is caused by a mutation in blood stem cells — cells that give rise to all the different cell types in the blood — that gives those cells a slight survival advantage over the normal stem cells. Such stem cell clones multiply more and are at risk of transforming to blood cancer.
“Most people with clonal hematopoiesis never develop blood cancer,” said Bolton, who treats patients at Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine. “To a certain extent, it’s a normal aging process. However, we think that many if not all individuals who develop blood cancer pass through a phase of clonal hematopoiesis at some point. We are still in the early stages of trying to figure out which individuals with clonal hematopoiesis will go on to develop blood cancer and which will not.”
Studying genomic data of more than 730,000 people, including from blood samples, the researchers found that clonal hematopoiesis was more common among those with inherited mutations in certain genes already known to increase the risk of cancer. They also found that such inherited mutations had an impact on patterns of newly acquired mutations that cause clonal hematopoiesis. If stem cell clones go on to acquire just a handful more harmful mutations, the clonal hematopoiesis can transform into a blood cancer, such as AML, in which the cells stop doing their jobs and multiply until they crowd out healthy cells.
With the goal of finding ways to detect and eliminate pre-cancerous cells in people at high risk of blood cancer, Bolton and her colleagues found that among individuals with clonal hematopoiesis, those who had inherited mutations that predispose to clonal hematopoiesis had a higher risk of developing blood cancer than those without inherited mutations.
“Our study is a first look at the inherited genetic background that is providing the soil, so to speak, and we’re seeing what undesirable seeds that are acquired later in life are more or less likely to grow from that soil,” Bolton said. “The goal is to stamp out the weeds early, before they can take root and become full-blown cancer.”
Though clonal hematopoiesis is part of normal aging, certain factors such as smoking or prior exposure to radiation or chemotherapy can speed up the process and increase the risk of it transforming into cancer. Still, some people progress to cancer without major environmental risk factors, and the new study suggests that the interaction of their inherited genome with newly acquired mutations plays an important role in this cancer progression.
The study’s first author Jie Liu, a graduate student in Bolton’s lab, noted: “It’s exciting to see how combining large-scale genomic data can reveal how inherited and acquired mutations work together to influence cancer risk. These insights move us closer to identifying high-risk individuals before cancer develops. Our work shows that it’s not just the mutations you’re born with or those you acquire later in life, it’s the interaction between them, and we can now measure that.”
Earlier intervention
Bolton said being able to detect and measure both inherited cancer risk and clonal hematopoiesis would likely be a powerful way to identify individuals who would benefit most from early prevention strategies, such as targeted therapies for the most damaging mutations. At present, clonal hematopoiesis is difficult to identify without specialized blood tests that are not given as part of routine care. Even though such individuals already have clones taking up a greater proportion of their blood stem cells, they can still show normal blood cell counts as part of blood tests typically given at an annual well visit, for example.
In theory, if scientists know what gene mutations to look for, they could develop new blood tests to identify such individuals before any evidence of a problem could be detected with routine blood screening tests. The new study singles out many genes of interest that could be key in the future development of such a blood test.
“Because leukemia is so hard to treat, we hope to find ways to intervene early — when it’s still pre-cancerous — so we can stop clonal hematopoiesis from transforming into leukemia,” Bolton said. “We would want to start with preventive clinical trials for people who have certain inherited mutations and who already have evidence of clonal hematopoiesis, such as one or two clones expanding in their blood.”
Researchers at Siteman are now conducting clinical trials investigating whether specific drugs called IDH1 and IDH2 inhibitors can stop the expansion of certain types of blood stem cell clones before they become cancer. For now, such trials only include people who could be identified as having clonal hematopoiesis because they already had progressed to having abnormal blood cell counts, placing them on the cusp of full-blown leukemia.
“We are hopeful about the prospects of these preventive treatments, but we would like to have tools to identify these individuals even earlier, before their blood cell counts become abnormal,” Bolton said. “There are a lot of targeted therapies that are being developed right now and new approaches researchers are looking at for this purpose.”
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Liu J, Tran D, Xue L, Wiley BJ, Vlasschaert C, Watson CJ, MacGregor HAJ, Zong X, Chan ICC, Das I, Uddin MM, Niroula A, Griffin G, Ebert BL, Mack T, Pershad Y, Sharber B, Berger M, Sehir A, Ptashkin R, Levine RL, Papaemmanuil E, Joseph V, Gao T, Kemel Y, Mandelker D, Stopsack KH, Pharoah PDP, Mukherjee S, Ding L, Cao Y, Walter MJ, Blundell JR, Chatterjee N, Offit K, Godley LA, Link DC, Stadler ZK, Bick AG, Natarajan P, Bolton KL. Germline genetic variation impacts clonal hematopoiesis landscape and progression to malignancy. Nature Genetics. July 15, 2025. DOI: 10.1038/s41588-025-02250-x.
This work was supported by the National Institutes of Health (NIH), grant numbers R01HL148050, R01HL168894, DP5 OD029586, R01AG088657 and R01AG083736; the MDS Foundation; the Children’s Discovery Institute; a Prostate Cancer Foundation Challenge Award; the Edward P. Evans Foundation; the SciLifeLab & Wallenberg Data Driven Life Science Program, grant number KAW 2020.0239; the Swedish Cancer Foundation, grant numbers 22.0577JIA and 22.2362Pj; the Swedish Research Council, grant number 2023-03131; a Burroughs Wellcome Fund Career Award for Medical Scientists; a Pew Charitable Trusts and Alexander and Margaret Steward Trush Pew-Stewart Scholar for Cancer Research Award; and a Hevolution/AFAR New Investigator Award in Aging Biology and Geroscience Research. The study was conducted using the U.K. Biobank Resource and data provided by patients and collected by the National Health Service. It was also conducted using data from the All of Us Research Program of the National Institutes of Health. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
Software developed at WashU Medicine on accelerated path to approval
A new technology that harnesses AI to analyze mammograms and improve the accuracy of predicting a woman’s personalized five-year risk of developing breast cancer has received Breakthrough Device designation from the Food and Drug Administration (FDA). Developed by researchers at Washington University School of Medicine in St. Louis, the software has been licensed to Prognosia Inc., a WashU startup company.
The system analyzes mammograms to produce a risk score estimating the likelihood that a woman will develop breast cancer over the next five years. The technology is compatible with both types of mammogram imaging available: the four 2D views of the breast produced by full-field digital mammography and the synthetic 3D view of the breast produced by digital breast tomosynthesis.
Importantly, the system produces an absolute five-year risk that makes it possible to compare a woman’s risk to an average risk based on national breast cancer incidence rates. This provides a meaningful estimate that is aligned with the U.S. national risk reduction guidelines, so that clinicians will know what steps to take next if a woman’s risk is elevated.
The FDA Breakthrough Device designation provides an expedited review process for full market approval in an effort to give patients and clinicians accelerated access to new medical devices. Products that receive the designation have already undergone rigorous testing and shown excellent promise in their potential to improve treatment or the diagnosis of debilitating or life-threatening conditions.
The software package, called Prognosia Breast, was developed by Graham A. Colditz, MD, DrPH, the Niess-Gain Professor of Surgery at WashU Medicine and associate director of prevention and control at Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine; and Shu (Joy) Jiang, PhD, an associate professor of surgery in the Division of Public Health Sciences in the Department of Surgery at WashU Medicine. Colditz and Jiang co-founded Prognosia in 2024 in collaboration with WashU’s Office of Technology Management (OTM) and BioGenerator Ventures, the latter of which provided both financial support and business strategy expertise from Entrepreneur-in-Residence David Smoller, PhD.
The software is a pre-trained machine learning system that analyzes mammogram images and provides an estimate of how likely a patient is to develop breast cancer over the next five years, based solely on images and a woman’s age. According to the developers, Prognosia Breast estimates a person’s five-year risk of developing breast cancer 2.2 times more accurately than the standard method, which is based on questionnaires that consider factors such as age, race and family history. The system was trained on past mammograms from tens of thousands of individuals who underwent breast cancer screening through Siteman Cancer Center. Some of them went on to develop cancer, teaching the system what to look for in the earliest stages of tumor development. Such early signs of disease can’t be perceived even by a well-trained human eye.
“We’re excited about the potential of this technology to improve risk prediction and prevention of breast cancer broadly, no matter where a woman is getting screened,” Colditz said. “The long-term goal is to make this technology available to any woman having a screening mammogram anywhere in the world. No matter the type of imaging they receive, our data show the software’s potential to identify women at increased risk of developing breast cancer over the next five years, providing them with opportunities to take targeted steps to reduce that risk.”
The new device could have a large impact on risk prediction because the infrastructure is already in place to begin immediately using the software anywhere mammography is provided. Furthermore, many women already receive regular mammograms. According to 2023 survey data from the Centers for Disease Control and Prevention, more than 75% of women ages 50 to 74 reported having received a mammogram in the past two years.
Even with widespread screening, about 34% of breast cancer patients in the U.S. are diagnosed at later stages of the disease. According to the investigators, being able to assess risk up to five years in advance of the onset of cancer is likely to improve early detection, reducing the number of late-stage cancers diagnosed. Early detection has been shown to make treatment more effective and reduce deaths from breast cancer.
“Receiving a Breakthrough Device designation is a powerful validation of the extraordinary dedication and vision of this research team to improve breast cancer diagnosis and care,” said Doug E. Frantz, PhD, vice chancellor for innovation and commercialization at WashU. “It takes years of concerted effort to produce software that could quickly be integrated into the workflow of any mammography center, significantly enhancing the clinical value of routine mammograms no matter where they are provided. This is a prime example of the vital role of entrepreneurship and commercialization at WashU in transforming cutting-edge research into real-world technologies that improve patient care.”
The device produces a five-year risk score that is intended to complement, not replace, the analysis provided by radiologists, who will continue to review the mammograms following standard protocols. According to the American Society of Clinical Oncology and the U.S. Preventive Services Task Force, a five-year risk score of 3% or higher is considered elevated. According to guidelines from these organizations, women with elevated scores should be referred to specialists who can further advise them on their options for additional screening and prevention strategies.
About one in eight women in the U.S. will be diagnosed with breast cancer in their lifetime. Those found to be at elevated risk of this cancer have the option to receive more frequent screening — which may include other types of imaging, such as MRI — and in some cases may choose to take a type of chemotherapy called tamoxifen or endocrine therapy as preventive treatments. With such options available, identifying women at high risk is important so they have access to specialists who can help guide them in making these important choices.
The developers are planning a clinical trial at Siteman Cancer Center that will apply the risk score from Prognosia Breast in combination with the standard mammography screening protocols. Standard screening protocols include the review of mammograms and measures of breast density already provided to all patients. Individuals found to be at elevated risk will be referred to Siteman’s breast health specialists, who focus on helping individuals navigate the options they have for managing high breast cancer risk.
“Despite the sophistication of today’s breast imaging and its broad use for identifying existing tumors, today’s risk prediction for breast cancer is still questionnaire-based and not very good at estimating future risk,” Jiang said. “Our work has focused on filling that need for better methods. Moving to image-based risk prediction — which our studies have shown is much more accurate — has the potential to be revolutionary for patient care.”
The current FDA designation applies to the software’s analysis of mammogram images taken at a single time point. In the future, the researchers plan to update Prognosia Breast to analyze several years of mammograms from the same individual, which may further improve the accuracy of the prediction.
ASTRO counts 10,000 members worldwide, including physicians, physicists and cancer biologists, whose work advances care, education, professional development and research in the radiation oncology field. Only 541 of ASTRO’s members have been named fellows since the program began in 2006.
This year, De Los Santos and Hugo are among 43 members to receive the ASTRO Fellow (FASTRO) designation. They will be recognized Sept. 30 at an awards ceremony during ASTRO’s 67th Annual Meeting in San Francisco.
“These distinguished leaders embody ASTRO’s core principles of excellence, innovation and unwavering dedication to improving patients’ lives through radiation oncology,” said Howard M. Sandler, MD, chair of the ASTRO Board of Directors. “On behalf of ASTRO, we celebrate their elevation to FASTRO status and their meaningful contributions to cancer care.”
De Los Santos and Hugo are affiliated with Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine, where De Los Santos treats patients at the Head and Neck Tumor Center. Her research interests include the development of paradigm-shifting treatment approaches across several cancer sites, and translational work to define populations who may successfully proceed with these approaches.
Hugo is vice chair of the Medical Physics Division in the Department of Radiation Oncology at WashU Medicine His research interests include image-guided adaptive radiotherapy particularly for lung cancer, image registration and analysis, and the use of machine learning in radiation oncology.
They join other recently named fellows, including WashU Medicine professors and radiation oncologists Clifford Robinson, MD, and Julie Schwarz, MD, PhD, who were appointed last year. Radiation oncologist Jeff Michalski, MD, MBA, the Carlos A. Perez Distinguished Professor at WashU Medicine, is the immediate past chair and a past president of the ASTRO Board of Directors.
Nationally recognized clinical trials expert, also known for outstanding patient care
Premal H. Thaker, MD, MS, a physician-scientist recognized for her expertise in conducting clinical trials, authoring numerous medical and scientific publications and outstanding patient care, has been named chief of the Division of Gynecologic Oncology at WashU Medicine. In this role, she oversees a continuum of research and clinical approaches aimed at improving the treatment of ovarian, cervical, endometrial and other gynecologic cancers at Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine.
A member of WashU Medicine’s faculty since 2006, Thaker has served as interim director of the division for the past 17 months. She also is the David G. and Lynn Mutch Distinguished Professor of Obstetrics and Gynecology and director of Gynecological Oncology Clinical Research at WashU Medicine. As a surgeon, she is a member of the multidisciplinary teams at Siteman that provide personalized care incorporating the specific needs of each patient.
“I am honored and humbled to lead such a great team of physicians, nurse practitioners, nurses, scientists and staff who are committed to excellent patient care and cutting-edge research in gynecologic malignancies,” Thaker said. “I am excited by the opportunity to continue to expand our service line both locally and regionally to help more patients receive care from Wash U Medicine and Siteman Cancer Center.”
She succeeds Matthew A. Powell, MD, the Ira C. and Judith Gall Professor of Obstetrics and Gynecology, who served as chief of the Division of Gynecologic Oncology from 2015-2024.
The division’s mission is to improve care through exceptional clinical service, research, education and community engagement. Specialties within the division include advanced minimally invasive benign gynecologic surgery and gynecologic oncologic surgeries, fertility-sparing medical and surgical options for gynecologic oncology diseases, and reconstructive surgery. Pediatric, adolescent and young adult gynecologic care is also offered.
Thaker earned her undergraduate degree in biology from Villanova University in Villanova, Pa., and her medical degree from Allegheny University of the Health Sciences in Philadelphia through a prestigious six-year BA/MD program. She completed her residency in obstetrics and gynecology at the Hospital of the University of Pennsylvania, also in Philadelphia, and her fellowship in gynecologic oncology at the University of Texas MD Anderson Cancer Center in Houston. She also holds a master’s degree in cancer biology from the University of Texas Graduate School of Biomedical Sciences, also in Houston.
Additionally, Thaker received training in laparoscopic lymph node dissection at Charité – Universitätsmedizin Berlin in Germany.
In recognition of her outstanding patient care, she has been consistently named to the St. Louis Magazine and Castle Connolly Top Doctors lists since 2013 and 2021, respectively.
Thaker also is an accomplished clinical investigator in translational research and is recognized for her expertise in conducting clinical trials. She has co-led a collaborative R01 program that explored biobehavioral influences such as social isolation on ovarian cancer progression. This work began during her fellowship at MD Anderson and resulted in a landmark publication in 2006 in Nature Medicine titled, “Chronic stress promotes tumor growth and angiogenesis in a mouse model of ovarian carcinoma.” This collaborative research has resulted in more than 24 articles in such journals as Cancer, the Journal of Clinical Oncology and Brain, Behavior, and Immunity.
She also has been part of WashU Medicine and Siteman’s endometrial Specialized Program of Research Excellence (SPORE), first received in 2009, evaluating ERK signaling in endometrial cancer and its potential for therapeutic targeting. Thaker continues to engage in translational research evaluating stress on ovarian cancer immunology, with her colleague Melanie Flint, PhD, at the University of Brighton in the United Kingdom. This work was published by their mutual graduate student Marta Falcinelli, PhD, in Brain, Behavior and Immunity in 2023. Thaker has published more than 200 peer-reviewed manuscripts, nine reviews and 11 chapters. See her research profile here.
Under Thaker’s leadership, WashU Medicine has been named among the top five sites for patient accrual for Lead Academic Participating Site (LAPS) and GOG Partners clinical trials. She has been the national principal investigator of two GOG Foundation clinical trials, four national pharmaceutical trials and three investigator-initiated trials. Thaker also serves on several Data and Safety Monitoring Boards for clinical trials. She has chaired the Early Business Development Subcommittee for GOG Partners since 2021 and has led efforts of the Association of Community Cancer Centers to educate the greater medical oncology community about ideal ovarian cancer care, leading to a white paper in Cancer in 2022. Thaker also represents Siteman Cancer Center on the ovarian cancer guidelines committee of the National Comprehensive Cancer Network (NCCN), an alliance of 33 leading cancer centers that convenes world-renowned experts to create national clinical practice guidelines.
Since joining the WashU Medicine faculty, Thaker has shown a strong commitment to education and has mentored many medical students, residents, fellows and faculty members. She also contributes to continuing medical education programs locally, nationally and internationally.
Food sizzling on the grill is one of the classic sounds of summer — right up there with kids splashing in sprinklers and the crack of a bat at the ballpark.
That sizzling can also be a good stand-in for how we might feel outside on a sweltering day.
With a little planning, though, we can make our time in the sun feel cooler and more comfortable — and much better for our skin.
“Any amount of tan, and certainly sunburn, represents damage to the DNA of our skin cells,” said Dr. Aubriana McEvoy, a dermatologist at WashU Medicine in St. Louis. “And the more sun people get over their lives, the more of a chance there is for damaged cells to turn into skin cancer, which can affect our quality of life and, in some cases, the length of our lives.”
Too much sun can also lead to wrinkles, coarse skin and discoloration, making our skin look older than it is, she added.
Some simple steps can go a long way toward lowering the risk of skin cancer while keeping our skin looking healthier as well. And everyone can benefit, from those with fair skin to those with darker skin.
Sunscreen is a great place to start. Choose one with Sun Protection Factor (SPF) 30 or higher and be sure to use a generous amount, about an ounce for an adult at the pool — reapplying every couple hours. There are a lot of sunscreen options these days, so try out a number of them to find one you and your family like.
“My favorite sunscreen is the one you will wear,” McEvoy said.
Clothes are another way to stay sun-safe. Long-sleeved shirts, pants and wide-brimmed hats do a great job covering skin and don’t need to be reapplied like sunscreen. And there are many inexpensive, lightweight options that are specifically made to protect from the sun and that have their own rating, called Ultraviolet Protection Factor (UPF). As with sunscreens, the higher the UPF number, the greater the protection.
The combination of clothes and shade from trees or sun shelters can be particularly important for kids. Sunscreen is not recommended for children under 6 months old. And older kids can be so active that it can be hard to keep them well-covered in sunscreen, McEvoy added.
Shade and lightweight, loose-fitting clothes can also help with staying cool and feeling good on a hot day summer day. And it’s hard to overstate the importance of drinking enough water. It can be easy to get behind on our hydration, especially on a fun-filled outing with family and friends. Try to keep a bottle close by filled with plain water or low-sugar sports drink mix. Make it as easy as possible for you and your family to stay hydrated.
For many of us, summer is the best time of year, in no small part because we get to spend so much time enjoying long days and warm weather outside. And that’s an important part of life, McEvoy feels. Also important, of course, is doing so safely and healthfully.
When asked for one of her favorite tricks for staying cool and sun-safe in summer heat, she replied:
“If I’m at the playground or park with my kids, I’ll wear a sun-protective shirt and just wet it down. That keeps me way cooler and protects me from the sun.”
Immunotherapy Improves Survival of Patients with Locally Advanced Head and Neck Cancer
The Food and Drug Administration (FDA) has approved a new standard of care for certain locally advanced head and neck cancers — the first change in standard-of-care therapy for affected patients in more than two decades. This follows the promising results of clinical trials first launched at Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine in 2013.
The drug, pembrolizumab (brand name Keytruda), has revolutionized care for melanoma since it was first introduced more than a decade ago. On June 12, 2025, the FDA approved the immunotherapy as part of a new standard of care for certain adults with resectable locally advanced head and neck squamous cell carcinoma (HNSCC).
An international phase 3 clinical trial co-led by WashU Medicine physician-scientists at Siteman showed that such patients benefited from the addition of the immunotherapy drug to the previous standard-of-care therapy. They saw greater tumor shrinkage prior to surgery and, on average, survived cancer-free almost two years longer than did patients who received only the previous standard of care.
“It’s exciting to see our ideas move toward clinical practice with such impressive and potentially life-changing results,” said Douglas R. Adkins, MD, a professor of medicine and director of the Section of Head and Neck and Thyroid Medical Oncology at WashU Medicine who has co-led the clinical trials at Siteman and elsewhere.
Head and neck cancers include tumors of the mouth, sinuses, nose and throat. Smoking and other tobacco use as well as human papillomavirus (HPV) infection increase the risk of such cancers.
Specifically, affected patients are those with resectable locally advanced HNSCC whose tumors express PD-L1 [Combined Positive Score (CPS) ≥1] as determined by an FDA-approved test, as a single agent as neoadjuvant treatment, continued as adjuvant treatment in combination with radiotherapy (RT) with or without cisplatin after surgery, and then as a single agent.
Pembrolizumab is what’s known as an immune checkpoint inhibitor, meaning that it works by skirting roadblocks that keep the body’s own immune cells from destroying tumor cells. One of these roadblocks is a protein on the surface of tumors called PD-L1. By circumventing PD-L1, pembrolizumab allows the patient’s own immune cells to attack and kill tumor cells. The FDA approved the therapy for advanced melanoma in 2014. It has since been approved for many other cancers, including advanced lung cancer, colorectal cancer, cervical cancer and lymphoma. In 2016, it was approved for recurrent and metastatic head and neck cancer.
The proposal to evaluate pembrolizumab in locally advanced head and neck cancer originated at WashU Medicine and formed the basis of an earlier phase 2 clinical trial that began at Siteman in 2013. The findings from that study led directly to the international phase 3 trial that the FDA considered in its recent approval.
The FDA decision also was the first approval of a therapy for HNSCC in six years and the first overall perioperative approval for locally advanced HNSCC.
“The survival benefit we’ve seen in adding pembrolizumab to the previous standard-of-care therapy is clinically meaningful and groundbreaking,” said Adkins, who treats patients at the Robert Ebert and Greg Stubblefield Head & Neck Tumor Center, which he co-leads at Siteman.
He reported findings from the international phase 3 clinical trial, funded by Merck, at this year’s annual meeting of the American Society of Clinical Oncology (ASCO). His co-investigator, Ravindra Uppaluri, MD, PhD, of Dana-Farber Brigham Cancer Center, presented related findings at the American Association for Cancer Research (AACR) annual meeting.
