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.

AI-driven blood test could aid earlier detection of brain cancer

WashU Medicine physician-researchers at The Brain Tumor Center at Siteman Cancer Center have co-developed an innovative approach that uses artificial intelligence (AI) to detect brain cancer, potentially leading to earlier diagnoses. Siteman is based at Barnes-Jewish Hospital and WashU Medicine.

The process incorporates a noninvasive blood test and machine learning that analyzes the blood sample for evidence of brain cancer – specifically, circulating DNA patterns associated with brain tumors. It then identifies repeating genomic patterns that indicate the presence of brain cancer. Such tests have already shown success in the earlier detection of lung cancer.

“We now have a method that detects brain cancer based on its unique characteristics, including DNA fragmentation and immune responses,” said WashU Medicine neurosurgeon Dimitrios Mathios, MD, who developed the test with Victor E. Velculescu, MD, PhD, co-director of the Cancer Genetics and Epigenetics Program at Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins.

“The signals we detect come from both the tumor itself and the immune system’s reaction to it,” said Mathios, an assistant professor of neurosurgery and director of the Lab for Molecular Neuro-oncology at WashU Medicine and a Siteman research member.

Mathios and Velculescu published their work April 29 in Cancer Discovery.

Detecting brain cancer before symptoms appear is challenging, often leading to diagnoses at more advanced stages when tumors are larger and located in high-risk areas. This complicates treatment, making it both riskier and less effective. The blood-brain barrier, which protects the brain, also prevents biomarkers — signs of cancer — from entering the bloodstream, further complicating early detection.

Using their new approach, the researchers successfully detected brain cancer in approximately 75% of cases from a cohort of 505 patients in the U.S. and South Korea, according to their paper, and validated their results in a separate group of 95 patients in Poland. In contrast, traditional blood-based liquid biopsy methods have detected brain cancer in fewer than 10% of cases.

A key factor in this success is the detection of immune system changes associated with brain cancer. Brain cancer often leads to immune suppression and alters the immune cell profile in the blood. These immune changes occur throughout the body, bypassing the blood-brain barrier and making them detectable, Mathios said.

In a simulation, the researchers modeled the potential benefits of using their method to screen the 10 million patients who visit emergency rooms or primary care clinics annually due to headaches. Normally, these patients are only referred for brain imaging if a physician suspects a problem. However, the simulation showed that incorporating blood-based liquid biopsy results could help identify nearly 1,700 additional cancer cases in the U.S.

The next step for the team is to conduct a larger prospective trial to confirm these findings in a broader population at higher risk for brain cancer.

Innovative immunotherapy shows promise against aggressive T cell cancers

WashU startup’s “off-the-shelf” CAR-T cell therapy evaluated in international clinical trial

A new type of immunotherapy that targets aggressive blood cancers shows promising results alongside manageable side effects, according to the results of an international phase 1/2 clinical trial led by WashU Medicine researchers at Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine.

The clinical trial evaluated the safety and efficacy of an innovative CAR-T cell immunotherapy that is specifically designed to attack cancerous T cells. Participants in the trial had been diagnosed with rare cancers — T cell acute lymphoblastic leukemia or T cell lymphoblastic lymphoma — and had run out of treatment options after standard therapy proved ineffective for them. With the new immunotherapy, most of the patients in the study who received the full dose of cells achieved full remission of their cancer.

The trial’s results were published May 30 in the journal Blood.

“For patients with these rare and aggressive cancers, who have no other options, this has the potential to become a transformative advance in the field,” said senior author John F. DiPersio, MD, PhD, the Virginia E. & Sam J. Golman Professor of Medicine at WashU Medicine, who first developed the therapy in his lab at WashU Medicine. “The trial demonstrated a high likelihood of response to the therapy and even remission. This CAR-T cell treatment shows promise in becoming a ‘bridge-to-transplant’ therapy for patients who would otherwise not be eligible for stem cell transplantation, which is the only potentially curative treatment for these blood cancers.”

Larger studies with more patients and longer follow-up are necessary before the researchers can determine whether this new therapy could be curative on its own.

The current trial included 28 adult and adolescent patients with T cell acute lymphoblastic leukemia and T cell lymphoblastic lymphoma that either returned after several lines of therapy or that never responded to treatment. About 1,000 people are diagnosed with these cancers annually in the U.S. If the cancer does not respond to treatment or returns after initial treatment, patients survive only six months, on average, and less than 7% are still living at the five-year mark.

The therapy, called WU-CART-007, was developed by Wugen, a WashU biotech startup company founded by DiPersio and other WashU Medicine investigators, including Matthew Cooper, PhD, who co-founded the company when he was on the WashU Medicine faculty and now serves as Wugen’s chief scientific officer. The clinical trial was conducted in Australia, Europe and multiple sites across the U.S. For the St. Louis site, the trial was conducted at Siteman Cancer Center.

The trial design included a dose-escalation phase, which determined the recommended dose of therapeutic cells that patients would receive for the second phase of the trial. Dose escalation helps determine the largest dose of CAR-T cells that patients can receive and still have manageable side effects. Thirteen patients received the full dose of 900 million CAR-T cells after undergoing a procedure to clear the patients’ own immune cells. This procedure — called lymphodepletion — reduces immune cells, making room for the new therapeutic T cells to establish themselves and expand in number. Two of these patients died from their cancer or treatment complications, such as infection, during the study period.

Of 11 patients who could be evaluated after treatment, the overall response rate was 91%, meaning 10 patients either showed no signs of cancer after treatment or their cancer cell burden was reduced significantly. Eight out of 11 patients (72.7%) achieved complete remission. At the study’s data cut off, six who underwent a transplant remain in remission, with no evidence of disease, six to 12 months later.

“These response and remission rates — ranging from 70%-90% of patients — are much higher than we would expect from standard-of-care for this cancer type, which typically leads to remission in only 20%-40% of patients,” said first and corresponding author Armin Ghobadi, MD, a professor of medicine and clinical director of the Center for Gene and Cellular Immunotherapy at WashU Medicine. “These responses are remarkable because the patients in this trial had run out of options. They had very aggressive cancers return after several lines of therapy, including several who relapsed after an earlier stem cell transplant.”

Most patients (88.5%) experienced cytokine release syndrome as a side effect of the immunotherapy, and these cases were predominantly mild or moderate. Cytokine release syndrome is a common side effect of CAR-T cell therapy that occurs when large numbers of immune cells release chemicals that cause a full-body inflammatory response. About 19% of the patients experienced more-severe cytokine release syndrome. A small number of patients experienced rarer side effects, such as neurotoxicity syndrome and low-grade graft-versus-host disease. Adverse events were managed with additional therapies.

Off-the-Shelf Cell Therapy

The immunotherapy evaluated in the trial is considered a “universal” CAR-T cell therapy because — harnessing CRISPR gene editing technology — it can be produced from cells donated by any healthy individual and used to treat any patient with a T cell cancer. In contrast, approved CAR-T cell therapies are adapted from the patient’s immune cells. The cells must be collected from the patient and shipped to a manufacturing facility to be made and then shipped back, a process that typically takes three to six weeks. In contrast, universal CAR-T cell therapies can be made ahead of time, stored frozen and be readily available “off-the-shelf,” greatly reducing the wait time before therapy can begin.

Using CRISPR gene editing tools, the production process deletes the T cell receptor from the donor cells, greatly reducing the risk of graft-versus-host disease, in which donor T cells attack healthy tissue. Removing another key antigen also prevents the CAR-T cells from attacking one another. The types of rare cancers in this study presented a unique challenge: the therapeutic cells and the cancer cells are both T cells, so steps must be taken to prevent the therapeutic T cells from mistaking one another for the cancer and causing CAR-T cell fratricide. All other approved CAR-T cell therapies target B cell cancers, which do not have this T cell self-targeting complication. After using CRISPR gene editing to modify the CAR-T cells to prevent these harmful side effects, the cells are further engineered to target a protein called CD7 on the surface of cancerous T cells to then destroy the cancer.

“A larger international clinical trial of this therapy is already underway,” DiPersio said. “We must complete this larger trial first, but we are hopeful this universal CAR-T cell therapy can become an approved treatment for patients with deadly T cell cancers.”

# # #

Ghobadi A, Aldoss I, Maude SL, Bhojwani D, Wayne AS, Bajel A, Dholaria B, Faramand R, Mattison RJ, Rijneveld A, Zwaan CM, Calkoen F, Baruchel A, Boissel N, Rettig M, Wood B, Jacobs K, Christ S, Irons H, Capoccia B, Masters D, Gonzalez J, Wu T, del Rosario M, Hamil A, Bakkacha O, Muth J, Ramsey B, McNulty E, Baughman J, Cooper ML, Davidson-Moncada J, DiPersio JF. Phase 1/2 trial of anti-CD7 allogeneic WU-CART-007 in patients with relapsed/refractory T cell malignancies. Blood. May 30, 2025.
Ghobadi has provided consulting for Wugen. Wugen’s founders include members of Washington University physicians who are colleagues of Ghobadi. Several co-authors are employees of Wugen and some hold shares in the company. DiPersio is a co-founder of Wugen and holds equity-ownership in the company.
This trial was funded by Wugen; and by the National Cancer Institute (NCI) of the National Institutes of Health (NIH), through an NCI Outstanding Investigator Award, grant number R35CA210084; an NCI Leukemia SPORE, grant number P50CA171963; and an NCI Research Specialist Award, grant number R50CA211466.

Brain pathway links inflammation to loss of motivation, energy in advanced cancer

Study in mice shows motivation can be restored with targeted treatments

The fatigue and lack of motivation that many cancer patients experience near the end of life have been seen as the unavoidable consequences of their declining physical health and extreme weight loss. But new research from Washington University School of Medicine in St. Louis challenges that long-held assumption, showing instead that these behavioral changes stem from specific inflammation-sensing neurons in the brain.

In a study published April 11 in Science, the researchers report that they identified a direct connection between cancer-related inflammation and the loss of motivation characteristic of advanced cancer.

Studying mice with cancer-linked cachexia, a condition typical of the disease that leads to muscle wasting and weight loss, they discovered a previously unrecognized pathway in the brain. This pathway senses inflammation and actively suppresses dopamine — a key driver of motivation — resulting in apathy and loss of drive.

Blocking the pathway restored motivation, even though the cancer and weight loss continued. This indicates that apathy can be treated separately from the disease itself.

“The implications of the research are profound,” said the study’s lead author, Adam Kepecs, PhD, professor of neuroscience and of psychiatry at WashU Medicine. “We’ve uncovered a direct brain mechanism through which inflammation drives apathy in cancer, and we were able to restore normal motivation in mice with cachexia, despite ongoing inflammation as cancer progressed.”

About 70% of patients with advanced cancer experience cachexia. In addition to physical decline, patients often suffer from severe fatigue, apathy and a lack of motivation that affect their overall quality of life.

To understand whether these psychological symptoms are side effects that emerge from physical deterioration or whether they arise from distinct biological mechanisms, the research team, including Marco Pignatelli, MD, an assistant professor of psychiatry at WashU Medicine, and Tobias Janowitz, MD, PhD, an associate professor at Cold Spring Harbor Laboratory, turned to a well-validated mouse model of cancer cachexia. They focused specifically on behavioral symptoms, which had not previously been investigated, and mapped the brain regions involved.

They discovered that a structure in the brainstem, a part of the brain that controls vital functions such as breathing and heart rate, acts as a sensor for inflammatory signals in the bloodstream, particularly a molecule called interleukin-6 (IL-6), which is elevated in cancer cachexia. When IL-6 levels rise, neurons in this region of the brainstem transmit a signal through a defined pathway that suppresses dopamine release in a part of the brain called the nucleus accumbens, which is key for motivation and reward. The resulting drop in dopamine had the effect of making the mice less motivated to exert themselves to complete activities.

To see if interfering with this response could treat the lack of motivation and apathy, Kepecs and his colleagues tried two different approaches: they boosted dopamine levels and blocked inflammation-sensing neurons in the brainstem. Both approaches eliminated or reduced apathy in the mice. Treating the mice with an IL-6 antibody similar to an existing FDA-approved drug for rheumatoid arthritis, an inflammatory condition, also restored the animal’s motivation, a finding that points to a potential treatment for the psychological symptoms associated with advanced cancer.

“What’s remarkable is that motivation was restored even in late-stage disease,” said Pignatelli. “It suggests we may be able to improve quality of life by targeting the brain circuit.”

For acute illnesses such as infections, this inflammation-driven reduction in motivation may be adaptive, helping the body conserve energy to fight off disease, Kepecs explained. But in chronic conditions such as cachexia, prolonged apathy — including a reduced drive to eat, move or engage socially – can become harmful, worsening health and quality of life. Because IL-6 — the inflammatory molecule driving this effect — is elevated in many other conditions, and the brain regions involved are central to motivation, this same circuit likely contributes to apathy across a range of chronic illnesses.

“This gives us a new way to understand apathy in advanced cancer,” said Kepecs. “It’s not just a byproduct of physical decline, but a direct response to inflammation in the brain. That means we can potentially target the underlying biology to improve motivation and quality of life — even when the cancer itself is no longer treatable.”

# # #

Zhu XA, Starosta S, Ferrer M, Hou J, Chevy Q, Lucantonio F, Muñoz-Castañeda R, Zhang F, Zang K, Zhao X, Fiocchi FR, Bergstrom M, Siebels AA, Upin T, Wulf M, Evans S, Kravitz AV, Osten P, Janowitz T, Pignatelli M, Kepecs A. A neuroimmune circuit mediates cancer cachexia-associated apathy. Science.

April 11, 2025. DOI: 10.1126/science.adm8857

This research was funded by the National Institute of Child Health and Human Development of the National Institutes of Health (NIH) grant P50 HD103525, Deutsche Forschungsgemeinschaft grant DFG -STA 1544, LaCaixa, the Mark Foundation for Cancer Research grant 20-028-EDV, the Simons Foundation, Cancer Grand Challenges, NIH grant 1OT2CA278690-01, CRUK: CGCATF-2021/ 100019, and NIH/National Cancer Institute grant R37CA286477-01A1, Cancer Center Support grant 5P30CA045508, NIMH grant MH130610, the Taylor Family Institute for Innovative Psychiatric Research, the Hope Center Pilot Grant, the McDonnell Center for Systems Neuroscience Small Grant, and the NARSAD Young Investigator Grant 27102 and P&S Fund, a WUSTL BJC investigator award and NIH grant DP1 MH14002. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

Study sheds light on how inherited cancer mutations drive tumor growth

Findings could help predict cancer risk over a person’s lifetime, develop prevention strategies

Most cancer genome studies have focused on mutations in the tumor itself and how such gene variants allow a tumor to grow unchecked. A new study, led by researchers at Washington University School of Medicine in St. Louis, takes a deep dive into inherited cancer mutations measured in a healthy blood sample and reports how those mutations might take a toll on the body’s cells starting at birth, perhaps predisposing a person to develop cancers at various stages of life.

The authors analyzed the inherited genomes of more than 1,000 cancer patients and determined how inherited mutations — also known as germline variants — result in malfunctioning proteins, which in turn can impair physiological activities. The findings have implications for determining an individual’s inherited cancer risk and informing potential new strategies for prevention, early detection and treatment.

The study appears April 14 in the journal Cell.

“This is important foundational work for the field,” said senior author Li Ding, PhD, the David English Smith Distinguished Professor of Medicine at WashU Medicine. “We need to know how the germline variants — rare or common — potentially impact the protein machinery that makes our bodies work and what those impacts might mean for cancer development over the lifespan.”

The study represents a key milestone in the work of the Clinical Proteomic Tumor Analysis Consortium, a nationwide effort supported by the National Cancer Institute of the National Institutes of Health (NIH) that aims to define the roles of all cellular proteins involved in cancer development and progression. Everyone is born with germline variants — some consequential, some inconsequential, and many uncertain — and over the lifespan, different tissues pick up their own mutations. Tumors almost always have a set of new mutations that has been the focus of most clinical research. In this new study, the focus is on the inherited germline variants, rather than those acquired later.

Physicians can offer people with certain inherited mutations — such as those in two BRCA genes, which are known to increase breast cancer risk — options to reduce their risk of developing cancer. These interventions include more frequent breast cancer screening, preventive chemotherapy and surgeries.

The new study builds on the utility of knowing cancer risks generated by germline mutations by analyzing the genomes of healthy cells from more than 1,000 cancer patients.

The team, co-led by first author Fernanda Martins Rodrigues, PhD, a postdoctoral researcher in Ding’s lab, analyzed the proteins associated with the inherited genomes of 1,064 individuals with 10 cancer types. The researchers identified 119 rare, cancer-causing genetic variants and additional common variants in cancer genes that may affect the structure, abundance and stability of key proteins involved with these cancer types. They also identified new, rare mutations strongly associated with cancer as well as common variants that, in concert, may tip the scales toward disease.

“What is new here is this study expands our knowledge beyond the inherited rare cancer-causing variants that we understand well, such as mutations in the BRCA genes,” said Ding, also a research member of Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine. “This analysis now adds more common variants that may not cause cancer individually but appear to function as a group to influence important pathways involved in cancer.”

To determine the collective effect of all the variants they identified that could affect cancer risk, the researchers calculated what’s called a polygenic risk score for each patient. Such a score can estimate the combined cancer risk based on all the mutations taken together. If a person just has one or two cancer-predisposing inherited variants, that might not have a large effect. But inheriting multiple such variants could result in a higher risk.

The researchers found that patients with the deadly brain cancer glioblastoma, pancreatic cancer or an aggressive form of lung cancer had significantly higher polygenic risk scores than did healthy people or even people who developed other types of cancer. For patients with any cancer type, those with higher polygenic risk scores had more aggressive disease.

Based on their protein analysis, Ding and her colleagues found that multiple inherited risk variants, while seemingly independent, had downstream effects that converged on some biological process, such as certain aspects of immune function and protein stability.

One of the particularly insightful aspects of the study was the authors’ examination of how inherited mutations can affect structural alterations that proteins can undergo after they are assembled. Two of these important modifications involve small molecular tags being added to a protein in certain places.

These tags can have tremendous impact on how a given protein functions, such as determining when and where the protein is active or not.

Genome sequencing alone — and not precisely matching germline mutations to the consequences they have on proteins, as Ding and her coauthors did — will miss these important modifications. This type of study adds new knowledge about the genetic factors that increase cancer risk, which could help improve the accuracy of polygenic risk scores in the future.

# # #

Rodrigues FM, Terekhanova NV, Imbach KJ, Clauser KR, Selvan ME, Mendizabal I, Geffen Y, Akiyama Y, Maynard M, Yaron TM, Li Y, Cao S, Storrs EP, Gonda OS, Gaite-Reguero A, Govindan A, Kawaler EA, Wyczalkowski MA, Klein RJ, Turhan B, Krug K, Mani DR, da Veiga Leprevost F, Nesvizhskii AI, Carr SA, Fenyo D, Gillette MA, Colaprico A, Iavarone A, Robles AI, Huang K, Kumar-Sinha C, Aguet F, Lazar AJ, Cantley LC, Marigorta UM, Gumus ZH, Bailey MH, Getz G, Porta-Pardo E, Ding L, Clinical Proteomic Tumor Analysis Consortium. Precision proteogenomics reveals pan-cancer impact of germline variants. Cell. April 14, 2025.

This work was supported by the National Cancer Institute (NCI) Clinical Proteomic Tumor Analysis Consortium (CPTAC) under award numbers U24CA210955, U24CA210985, U24CA210986, U24CA210954, U24CA210967, U24CA210972, U24CA210979, U24CA210993, U01CA214114, U01CA214116, U01CA214125, U24CA210972, U24CA210979 and U24CA270823; and contract GR0012005; the Spanish Ministry of Science, under grants RYC2019-026415-I, PID2019-107043RA-I00, RYC2019-026415-I, PID2019-107043RA-I00, RYC2020-030632-I, PID2019-108244RA-I00); the Fundación Cris Contra el Cáncer (PR TPD 2020-19). This research has been conducted using the UK Biobank Resource under Application Numbers 54343 and 74382. Data used in this publication were generated by the National Cancer Institute Clinical Proteomic Tumor Analysis Consortium (CPTAC), access through dbGaP accession numbers phs000892.v6.p1 (“CPTAC Proteogenomic Confirmatory Study”) and phs001287.v17.p6 (“CPTAC Proteogenomic Study”). This project has been funded in part with federal funds from the National Cancer Institute, National Institutes of Health, under Contract No. HHSN261201500003I, Task Order No. HHSN26100064.

The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

Q&A: Jennifer De Los Santos, MD, highlights head and neck cancer

April is Head and Neck Cancer Awareness Month, an opportunity to highlight a set of cancers that 60,000 Americans will be diagnosed with in 2025, according to the American Cancer Society. These cancers most commonly include those of the tongue; tonsils and throat behind the mouth; and gums, floor of the mouth and other parts of the mouth.

Remembering the recent passing of actor Val Kilmer due to laryngeal cancer, Jennifer De Los Santos, MD, a WashU Medicine radiation oncologist at Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine, talks about warning signs and raising awareness.

Tell us a little about these cancers and symptoms and other information we should be aware of.

Dr. De Los Santos: Head and neck cancers, including laryngeal cancer, can present with symptoms of sore throat, hoarse voice, ear pain and a mass in the neck. These cancers, which affect the throat, voice box and mouth, are often delayed in detection, as symptoms are often attributed to an upper respiratory infection. If patients do not have insurance or a primary care provider, diagnosis can be delayed even further.

What is laryngeal cancer?

Dr. De Los Santos: Laryngeal cancer is a type of cancer that develops in the larynx, also known as the voice box. The larynx is a part of the throat located between the back of the mouth and the trachea (windpipe) at the level of the thyroid cartilage (sometimes called the Adam’s apple). It plays a crucial role in breathing and speaking because it houses the vocal cords.

What are some risk factors for this cancer?

Dr. De Los Santos: The most common ones include:

  • Tobacco use – Smoking cigarettes, cigars or pipes is the single largest risk factor for laryngeal cancer. Both smoking and chewing tobacco can increase the risk.
  • Alcohol consumption – Heavy drinking of alcohol, particularly when combined with smoking, significantly raises the risk of laryngeal cancer. Alcohol can irritate the lining of the larynx and make it more susceptible to the carcinogenic effects of tobacco.
  • Exposure to certain chemicals – Occupational exposure to industrial chemicals such as asbestos or sulfuric acid has been linked to an increased risk of laryngeal cancer.
  • Marijuana use – New data suggest that marijuana use may also be associated with the development of head and neck cancer.


WashU Medicine’s Department of Radiation Oncology is at the forefront of the fight against head and neck cancers. Could you elaborate on some of the leading-edge treatments you’re working on?

Dr. De Los Santos: Absolutely. Our department is proud to be pioneering several promising treatment options. In particular, radiation therapy, immunotherapy and targeted treatments have made huge strides in improving outcomes for our patients. Tailoring radiation therapy to each patient can help control or even eliminate cancer cells while minimizing damage to surrounding healthy tissue. Immunotherapy is also showing great promise, particularly in helping the immune system recognize and fight cancer. Targeted therapies, which focus on specific genes or proteins involved in cancer growth, are another exciting area.

That’s amazing progress. Please talk about the importance of preserving patients’ voices, especially for those undergoing procedures like laryngectomy, and how technology is playing a role.

Dr. De Los Santos: For many patients, especially those with laryngeal cancer, losing the ability to speak is a devastating consequence. One of our main goals is not only to combat the cancer but also to preserve the patient’s quality of life. With advances in artificial intelligence (AI) and other technologies, we are investigating tools that can help patients communicate more effectively after procedures like a laryngectomy. AI-driven devices are being developed to create more natural-sounding speech, and they hold tremendous potential for improving a patient’s ability to engage in day-to-day life. This technology is transformative, offering an option that may both improve communication and preserve the patient’s natural voice.

It sounds like there’s so much hope on the horizon. How can people help support the critical research and advances you’re making at WashU Medicine and Siteman Cancer Center?

Dr. De Los Santos: Some of the best ways to support our work is through advocacy and spreading awareness. This includes promoting early detection – for example, by encouraging people with ongoing symptoms to seek follow-up care if antibiotics don’t help. The second is by recognizing the real difference that breakthrough discoveries can make. Val Kilmer’s legacy of advocacy is a powerful example of how one person’s story can inspire change, and we hope that this month, and beyond, people will join us in our mission to improve outcomes for patients battling head and neck cancers. Together, we can make a significant difference.

Learn more about multidisciplinary care and research at the Head and Neck Tumor Center at Siteman.

Jennifer De Los Santos, MD Professor of Radiation Oncology

Jennifer De Los Santos, MD

WashU Medicine radiation oncologist at Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine

WashU advances in STAT Madness

Two Washington University research projects – including a breast cancer vaccine launched at Siteman Cancer Center – have advanced to Round 2 of STAT Madness. The annual bracket-style contest highlights scientific and medical advances.

Vote for Washington University School of Medicine research here. A free account is required. Round 2 voting continues until 3 a.m. Central time on March 17.

The breast cancer vaccine, spearheaded by William Gillanders, MD, the Mary Culver Distinguished Professor of Surgery at Washington University, has shown promising results in a small clinical trial. Learn more.

The other Washington University research project involves psilocybin and its effect on brain function. Learn more.

WashU experts to present at NCCN annual conference

NCCN 2025 Annual Conference will feature findings from Jessica Vanderlan, PhD; Laura Bierut, MD; and Saiama Waqar, MD.

Washington University clinician-researchers at Siteman Cancer Center will highlight their work at the NCCN 2025 Annual Conference, March 28-30 in Orlando and virtually.

Hosted by the National Comprehensive Cancer Network, the conference convenes multidisciplinary expertise in the treatment of various cancers, as well as patient access to care, mental health and more.

The Washington University presenters are:

  • Jessica Vanderlan, PhD, manager of the Siteman Psychology Service, who will deliver part of the opening plenary, “Addressing Mental Health in Cancer Care: Optimizing Interdisciplinary Psychosocial Support,” at 8:35 a.m. Eastern time on Friday, March 28.
  • Laura Bierut, MD, who will present during the “Smoking Cessation for Patients with Cancer: State of the Evidence” session at 10:55 a.m. Eastern time on Saturday, March 29.
  • Saiama Waqar, MD, who presents an online, on-demand educational session, “Treatment Updates for Small Cell Lung Cancer.”

Learn more on the conference website. Follow the meeting on X, LinkedIn, Facebook and Instagram using #NCCN2025.

Vote for WashU research in STAT Madness contest

A breast cancer vaccine launched at Siteman Cancer Center is one of two Washington University research projects featured in this year’s STAT Madness, a bracket-style competition of academic research institutions.

Vote for Washington University School of Medicine here. A free account is required. Round 1 voting continues until 3 a.m. Central time on March 10.

The breast cancer vaccine, spearheaded by William Gillanders, MD, the Mary Culver Distinguished Professor of Surgery at the School of Medicine, has shown promising results in a small clinical trial. Following treatment, 14 of 18 patients showed immune responses to the vaccine and, after three years, 16 patients remained cancer-free. Learn more.

The other Washington University research project featured in the contest involves psilocybin, the psychedelic compound produced by “magic” mushrooms, that can affect brain function. Researchers report that the compound destabilizes a critical network of brain areas involved in introspective thinking. The findings provide a neurobiological explanation for the drug’s mind-bending effects. Learn more.

Experts to highlight blood cancer research and therapies at Tandem meetings

The multidisciplinary event – a joint meeting of ASTCT and CIBMTR – will feature findings from physicians, researchers and administrators

One of the largest scientific conferences dedicated solely to cellular therapy, the Tandem Meetings of the American Society for Transplantation and the Cellular Therapy (ASTCT) and Center for International Blood and Marrow Transplant Research (CIBMTR), takes place Feb. 12-15 in Honolulu. Presenters include physicians, researchers, nurse and research administrators and others affiliated with Siteman Cancer Center and/or Barnes-Jewish Hospital or Washington University School of Medicine.

They are advancing cellular and gene therapies through numerous studies across various subspecialities, sharing their research and clinical findings related to in vivo gene therapy, CAR T-cell therapy, stem cell transplantation and more. In total, affiliated clinicians, researchers and administrators are involved in 17 presentations.

Learn more.

Follow and tag Siteman at the meeting on X (@sitemancenter) or Bluesky (@sitemancenter.bsky.social). The conference hashtag is #Tandem25.