It’s never too late for those with cancer to quit smoking

Smoking cessation program developed by WashU Medicine researchers at Siteman Cancer Center is more effective at prolonging life than some chemotherapies

Around 25% of people with cancer in the U.S. are active smokers when they are diagnosed, and studies have found that many of them continue to smoke during treatment. This may be due in part to a common misconception — even among some doctors — that quitting won’t help much if a person already has cancer, particularly if it’s at an advanced stage.

Now, a study led by Li-Shiun Chen, MD, MPH, ScD, a professor of psychiatry at WashU Medicine in St. Louis, shows that kicking the habit after starting cancer treatment is well worth it — and what’s more, smokers with the most advanced cancers glean the biggest benefit from quitting, more than doubling their survival time.

Patients in Chen’s study had help quitting through a smoking cessation program developed and administered at Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine. The program offers a unique approach to cancer care by integrating smoking cessation interventions into patients’ cancer treatment plans. Delivering all treatment on-site eliminates hurdles involving time and transportation.

Chen’s findings were published Oct. 9 in the Journal of the National Comprehensive Cancer Network.

“WashU Medicine and Siteman are the leading frontier to ensure every cancer patient is offered tobacco treatment as part of their cancer care, using a novel, informatics-enabled, point-of-care model,” said Chen, who also directs the Tobacco Treatment Program at Siteman. “By showing that it’s never too late, even for the sickest patients, we hope to inspire all cancer centers and patients to include smoking cessation support as part of routine cancer care to improve survival.”

In the study, Chen and her collaborators followed 13,282 adults who received outpatient oncology care during a six-month period at Siteman. The team recorded each participant’s smoking status at their initial visit, then tracked cessation rates over the next six months along with survival over the next two years. Of 1,725 patients who reported at their first visit that they smoked, about one-fifth of them quit within the following six months.

Across all cancer types and stages, the researchers found that the probability of survival two years after patients’ initial oncology visit was 74% among those who continued smoke, versus 85% among those who quit. This benefit was driven mainly by patients with late-stage cancers (stage 3 or stage 4), among whom quitting was associated with a bigger increase in survival rate over this time period compared to people with early-stage cancer (stage 1 or stage 2).

Examining the results another way, the researchers found that for patients with stage 3 or 4 cancer who kept smoking, 85% were alive at 210 days. In comparison, of those who quit, 85% were still alive at 540 days. That’s nearly a year of additional days of life.

“Advanced-stage cancer patients often feel hopeless,” said first author Steven Tohmasi, MD, a resident in the Department of Surgery at WashU Medicine. “If they feel they have limited time, some doctors might not actively encourage patients to quit smoking or may prioritize patient comfort over cessation efforts.

But when we’ve shown patients our data, it gives them hope and motivates them to want to quit. An extra year of life is a long time for patients who may have been told they only had months to live.”

The Fourth Pillar of Treatment

Siteman’s team-based approach to tobacco care was developed as part of the National Cancer Institute’s Cancer Center Cessation Initiative, which is focused on helping NCI-designated cancer centers incorporate evidence-based tobacco treatments into clinical care. The goal, in essence, is making smoking cessation “the fourth pillar of cancer treatment, alongside surgery, radiation and chemotherapy,” Tohmasi explained.

Siteman’s smoking-cessation program uses electronic health records to identify patients who smoke and gauge their interest in quitting. A nurse or medical assistant then offers assistance with quitting during their visit, such as access to phone- or text-based counseling, an app designed to help them quit, referral to a smoking-cessation group, and medications to support quitting.

In earlier research, Chen showed that the program helped more cancer patients quit successfully than previous methods had. In a related study, Chen also found evidence that quitting smoking could improve treatment efficacy and boost survival rates. But Chen said she faced some professional pushback at the idea of following that research thread further.

“People told us that we were wasting time — that we should work on smoking cessation in patients who aren’t already so sick,” Chen said. “Smoking is also highly addictive, and it’s hard for people to quit. So we needed to be sure the effort would be worthwhile for patients and for their care teams.”

In the new study, Chen and Tohmasi analyzed the outcomes of all Siteman patients seen over the designated six-month period — a group that included patients with all kinds of cancers at all stages who came from across the St. Louis metro area and southern Illinois, representing an array of demographic backgrounds. This differentiated the study from some previous research on smoking cessation in cancer patients that focused only on certain cancer types and never examined the benefit of smoking cessation on survival in people with advanced cancers.

By linking cancer survival to tobacco use for all cancer patients across severity levels and including patients who were never, former or current smokers, Chen and Tohmasi were able to gain a broad perspective on smoking cessation and the important role of Siteman’s integrated treatment program.


The program has been scaled and adapted for several of Siteman’s partner health centers. Based on the program’s success, the model was implemented in 14 clinics affiliated with Siteman Cancer Center across eastern Missouri and southern Illinois starting in July 2025. Nationally the program has been disseminated through EpicShare, where it continues to prove both cost-effective and successful in supporting smoking cessation.

Starting in September 2025 with the support of a $1.6 million NCI grant, Chen and colleagues Alex Ramsey, PhD, an associate professor of psychiatry at WashU Medicine, and Ross Brownson, PhD, the Steven H. and Susan U. Lipstein Distinguished Professor in WashU’s School of Public Health, launched a pragmatic clinical trial on tobacco treatment, including smoking cessation. The trial aims to compare how different care models can scale and sustain tobacco use treatment among cancer survivors in different care settings serving cancer survivors across eight states. The trial will be conducted with research partners at four regional hubs: WashU, the University of Pennsylvania, Vanderbilt University Medical Center and the St. Louis VA Medical Center.

Learn more about smoking cessation tools available to Siteman patients and members of our community.

Eberlein named President-Elect of American College of Surgeons

Timothy J. Eberlein, MD, FACS, director of Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine, has been elected president-elect of the American College of Surgeons (ACS). The three-year commitment includes one-year terms each as president-elect, president and immediate past-president.

Eberlein began his term as president-elect after ACS’s annual meeting this month in Chicago. With more than 90,000 members, the organization is dedicated to improving the care of surgical patients and safeguarding standards of care.

“It is an honor to be elected to the leadership of the ACS by my national peers,” said Eberlein, who also is the Spencer T. and Ann W. Olin Distinguished Professor and senior associate dean for cancer programs at WashU Medicine and Barnes-Jewish Hospital. “In this position, I will continue to work tirelessly to help the College and its Fellows in our shared mission to care for patients and advance surgical care.”

Eberlein has been active within the ACS for many years, including as an ACS Fellow since 1988 and a member of the Board of Regents from 2015-2024. He served as chair of the board from 2022-2023. Since 1995, Eberlein has been a member of the Commission on Cancer, an ACS-founded consortium of professional organizations dedicated to improving survival and quality of life for patients with cancer. He also served as editor-in-chief for the Journal of the American College of Surgeons from 2004-2024.

For his numerous achievements, Eberlein received the Rodney E. and Thomas G. Sheen Award from the New Jersey Chapter of the ACS and the ACS Owen H. Wangensteen Scientific Forum Award.

Eberlein also has held leadership positions at the American Board of Surgery, Advisory Committee to the Board for Surgical Oncology, Board of the National Comprehensive Cancer Network, Society of Surgical Oncology, American Surgical Association and the National Cancer Institute.

Dehdashti honored by Radiological Society

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.

Dehdashti also is co-leader of the Oncologic Imaging Program at Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine, medical director of PET imaging at the Center for Clinical Imaging Research and a member of the leadership team at Mallinckrodt Institute of Radiology.

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.

1,000th patient treated at Siteman with AI-enabled radiation therapy system

Combining artificial intelligence (AI) with advanced imaging, the technology supports more precise, personalized daily treatments by WashU Medicine physicians

Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine has treated its 1,000th patient using state-of-the art radiation therapy technology that allows physicians to update a patient’s treatment plan on each day of treatment.

Called adaptive technology, the system incorporates slight changes in tumor shape, size and location, as well as the movement of surrounding healthy organs and tissue, to adjust a patient’s daily radiation therapy treatment plan for the best possible outcome.

The system is used to treat a range of tumors, including head and neck, central nervous system, thoracic, abdominal and pelvic cancers.

“We are pleased to offer this advanced technology to our patients — from the first person we treated with this system in 2020, to the 1,000th person in August 2025,” said WashU Medicine radiation oncologist Hyun Kim, MD, associate professor of radiation oncology and chief of Adaptive Radiation Therapy at WashU Medicine and Siteman.

“The milestone of 1,000 patients treated on this platform is literally the result of thousands of hours dedicated by our faculty and staff to personalize treatment every day for every patient,” he said.

Also known as online adaptive radiation therapy, it requires a team of expert physicians, physicists and radiation therapists to develop and review a treatment plan after the patient’s arrival — all within minutes after the patient is positioned to receive treatment.

In addition to the AI component and machine learning, the platform is equipped with cone-beam computed tomography (CT). Cone-beam CT quickly provides high-quality images and leads to better visualization of the tumors and surrounding healthy organs and tissue, allowing the physician to develop even more accurate, personalized treatment plans than with some older radiotherapy platforms.

In clinical trials incorporating the new technology, patients experienced decreased times to treatment and, in some cases, improved cancer control with less damage to surrounding healthy organs and tissue.

For some gynecologic cancers, treatment can involve imaging the ovaries of pre-menopausal patients. As a result, some patients have experienced premature ovarian failure and early menopause when treated with older radiotherapy technologies. WashU Medicine physician-scientists are conducting an ongoing clinical trial using the new technology with the hope that they can spare these organs.

Known as Ethos, the platform is manufactured by Varian Medical Systems, which also makes the cone-beam CT imaging component, called HyperSight.

Working together, cells extend their senses

New research from Amit Pathak’s lab has implications for tracking cancer

The story of the princess and the pea evokes an image of a highly sensitive royal young woman so refined, she can sense a pea under a stack of mattresses. When it comes to human biology, it also takes an abnormal individual to sense far beyond its surroundings, in this case, a cancer cell. Now, researchers also know that normal cells can pull a similar trick by working together.

Research published in the journal PNAS from engineers at Washington University in St. Louis offers a clearer picture of how cells can sense beyond their direct environment. The research can help further the understanding of how cancer moves and points to potential targets to stop that migration.

Amit Pathak, PhD, a professor of mechanical engineering and materials science at the McKelvey School of Engineering and a research member of Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine, explained that “depth mechano-sensing” is how cells sense beyond what they are attached to. In previous research, he and colleagues discovered that abnormal cells with a “high front-rear polarity” (indicative of migrating cells) can sense the farthest depth, up to 10 microns beyond their adhered environment.

Part of that sensory ability has to do with how the cell deforms the surrounding fibrous collagen to reach out into extracellular matrix (ECM) and “feel” the next layer, whether that’s a hard tumor, soft tissue or bone just around the bend. The single abnormal cell can “feel” the stiffness of the ECM and set its course based on that input.

The new research shows that a collective of epithelial cells, found on the surface of tissue, can do the same and then some, working together to muster enough force to “feel” through the fibrous collagen the layer as far as 100 microns away.

“Because it’s a collective of cells, they are generating higher forces,” said Pathak, who authored the research along with PhD student Hongsheng Yu.

According to their models, this occurs in two distinct phases of cell clustering and migration. What those clustering cells “feel” will impact migration and dispersal.

The extra sensing power of cancer cells means that they can get out of the tumor environment and evade detection, migrating freely thanks to their enhanced sense of what’s ahead, even in a soft environment. Researchers’ next step will be understanding how that works, and if certain regulators allow for the range. Those regulators could be potential targets for cancer therapy. If a cancer cell can’t “feel” its way forward, its toxic spread may be put in check.

# # #

Hongsheng Y, Pathak A. Emergent depth-mechanosensing of epithelial collectives regulates cell clustering and dispersal on layered matrices. PNAS, Sept. 11, 2025. DOI: https://doi.org/10.1073/pnas.2423875122

Funding for this research was provided by the National Institutes of Health (NIH) (R35GM128764) and National Science Foundation, Civil, Mechanical and Manufacturing Innovation (2209684).

Siteman investment program awards $2.42 million for cancer research

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

H Kim
Hyun Kim, MD

Principal Investigator: Hyun Kim, MD

Co-PIs: Patrick Grierson, MD, PhD, and David DeNardo, PhD

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

Stephen T. Oh Md Phd
Stephen Oh, MD, PhD

Principal Investigator: Stephen Oh, MD, PhD

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)”

Puram Sid 2023 2 280x386
Sidharth Puram, MD, PhD

Principal Investigator: Sidharth Puram, MD, PhD

Co-PI: Douglas Adkins, MD

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

Lee Ratner Md Phd
Lee Ratner, MD, PhD

Principal Investigator: Lee Ratner, MD, PhD

Co-PI: Thomas Odeny, MD, MPH, PhD

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

Todd Fehniger Md Phd
Todd Fehniger, MD, PhD

Principal Investigator: Todd Fehniger, MD, PhD

Project Leads: Carl DeSelm, MD, PhD; Robert Schreiber, PhD; Nathan Singh MD, MS

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

Remco Bastiaannet Phd
Remco Bastiaannet, PhD

Principal Investigator: Remco Bastiaannet, PhD

Co-PI: David Bauer, PhD (MU)

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

Carmen Bergom Md Phd
Carmen Bergom, MD

Principal Investigator: Carmen Bergom, MD

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.

Project Title: Bacteria to Treat Brain Tumors

Paul De Figueiredo Phd
Paul de Figueiredo, PhD (MU)

Principal Investigator: Paul de Figueiredo, PhD (MU)

Co-PI: Milan G. Chheda, MD

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

Aimee James Phd Mph
Aimee James, PhD, MPH

Principal Investigator: Aimee James, PhD, MPH

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

Christopher Malone Md
Christopher Malone, MD

Principal Investigator: Christopher Malone, MD

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

Nima Mosammaparast Md Phd
Nima Mosammaparast, MD, PhD

Principal Investigator: Nima Mosammaparast, MD, PhD

Co-PI: Hani Zaher, PhD

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

Principal Investigator: David Spencer, MD, PhD

David Spencer Md Phd
David Spencer, MD, PhD

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

AI-Based Breast Cancer Risk Technology Receives FDA Breakthrough Device Designation

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.

Image 1

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.

Genetic study suggests ways to catch blood cancer earlier

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.

Bennett named Evens Professor of Women’s Health

WashU Medicine breast cancer imaging specialist Debbie L. Bennett, MD, chief of breast imaging at Mallinckrodt Institute of Radiology (MIR), was installed Aug. 14 as the Ronald and Hanna Evens Endowed Chair in Women’s Health at Barnes-Jewish Hospital.

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 recruiting participants for multi-cancer detection tests

National study aims to detect disease before symptoms appear

Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine is recruiting participants for a national study of a new type of blood test aimed at detecting several types of cancer before symptoms appear. The tests could identify the presence of ovarian, pancreatic, bladder and other cancers that currently have no recommended screenings, as well as more common cancers that do.

WashU Medicine researchers at Siteman are recruiting people ages 45 to 75 who haven’t been diagnosed with cancer in the past five years to participate in the study. A blood draw is the most invasive part of participating, though additional time for follow-up is also required. There is no cost for participating in the study.

“We’re building the evidence on how these tests will perform: how they’re experienced by people, their potential benefits and more,” said Aimee James, PhD, MPH, MA, a WashU Medicine cancer prevention and control researcher at Siteman. “This could open up access to screenings for cancers we don’t already have screening options for — including stomach, esophageal and liver cancer.”

Multi-cancer detection tests are designed to detect biological substances that cancer cells release into the bloodstream, information that can even indicate where the cancer originated. The tests in this study, a national effort known as the Vanguard Study, also will screen for cancers that already have recommended screenings, including breast, colorectal, lung and prostate cancers.

The Vanguard Study is an important preliminary step in a larger plan to evaluate how well such tests work for reducing cancer deaths. The study will:

  • Provide information on how the tests work as cancer screening tools
  • Explore the decisions that participants and care providers make based on the results

The tests under review are expected to detect cancer in fewer than 5% of participants. If cancer is indicated, a nurse navigator will work with study participants to find appropriate follow-up care.

To enroll in the study or to learn more, call 314-362-5539 or visit https://publichealthsciences.wustl.edu/csrn.