<![CDATA[Psychiatrists debunk 10 common antidepressant myths—placebo claims, addiction fears, suicide risk, overuse, and withdrawal—offering evidence-based guidance.]]>
Integrated bulk, single-cell, and spatial transcriptomic analyses prioritize NOTCH1 as a candidate gene associated with neurovascular and immune-related alterations in Parkinson’s disease
IntroductionParkinson’s disease (PD) is classically defined by dopaminergic neurodegeneration in the substantia nigra, yet how immune activation is linked to neurovascular dysfunction in the diseased brain remains incompletely understood.MethodsHere, we integrated bulk substantia nigra microarray expression datasets with single-cell and spatial transcriptomic data to delineate disease-associated neurovascular and immune-related transcriptomic programs in PD.ResultsAcross three independent human microarray cohorts, differential expression and weighted gene co-expression network analyses identified PD-associated genes enriched for synaptic processes together with immune, adhesion, and vascular-related pathways. Network topology analysis and machine-learning feature selection prioritized a five-gene candidate panel, among which NOTCH1 showed the most consistent cross-dataset association and external directional support. Importantly, quantitative real-time PCR (qRT-PCR) validation in the substantia nigra of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model mice further supported dysregulated Notch1 expression. Single-cell mapping placed NOTCH1 expression within neurovascular and glial cellular contexts, including pericytes and endothelial cells, while CellChat and NicheNet analyses nominated transcriptome-derived ligand-receptor relationships involving NOTCH-related, vascular, inflammatory, extracellular-matrix, and growth-factor-associated programs. Spatial transcriptomics from mouse 6-hydroxydopamine (6-OHDA) substantia nigra sections provided model-based anatomical context for spatial proximity between pericyte and microglial signatures, without establishing direct functional communication. In parallel, exploratory in silico perturbation and docking-based screening generated hypotheses regarding the NOTCH1-associated regulatory context and compounds with predicted docking affinity toward NOTCH1.DiscussionCollectively, these analyses prioritize NOTCH1 as a reproducible PD-associated candidate gene and suggest that NOTCH1-related signals may be embedded within broader neurovascular, glial, inflammatory, extracellular-matrix, and immune-associated transcriptomic alterations. These findings provide a computational prioritization framework for future experimental validation rather than evidence of a defined NOTCH-driven mechanism.
Polypill for heart failure with reduced ejection fraction: the POLY-HF randomized trial
Nature Medicine, Published online: 02 July 2026; doi:10.1038/s41591-026-04504-5
In an open-label randomized trial, a polypill containing three types of heart failure medication (metoprolol, spironolactone and empagliflozin) improved left ventricular ejection fraction and resulted in a smaller number of heart failure hospitalizations or emergency room visits at 6 months, as compared to enhanced usual care.
Awareness, Educational Needs, and Curriculum Preferences Regarding AI and Medical Big Data Education Among Clinical Medicine Undergraduates: Cross-Sectional Survey Study
Background: The rapid integration of artificial intelligence (AI) and medical big data into health care is transforming diagnosis, treatment planning, and research. However, formal education in these areas remains limited in undergraduate medical curricula, particularly in China. Objective: This study aimed to investigate clinical medicine undergraduates’ familiarity with AI and medical big data, their perceived need for related courses, and their preferred curriculum design and assessment methods. Methods: A cross-sectional, web-based survey was conducted at Zunyi Medical University, Guizhou, China, from January 10 to 17, 2025. In the institutional context of this study, “clinical medicine” included related clinical-track specialties such as pediatrics and psychiatry. All eligible students (N=1094) were invited, and 871 (79.6%) were included in the final analysis. The self-administered questionnaire was developed based on a literature review and expert consultation, with content validity quantified using the content validity index. Descriptive statistics were used to summarize response distributions. For ordinal outcomes (items 1-14), adjusted ordinal logistic regression models were applied, with gender and grade as predictors and major as a covariate. Given the small number of third- and fourth-year students, grade was modeled as an ordered trend variable. For nominal outcomes (items 15-16), group differences were assessed using chi-square tests or Fisher exact tests, as appropriate. Results: A total of 871 students were analyzed, of whom 62.6% (n=545) were women. Overall familiarity with AI and medical big data was limited: 34.8% (303/871) agreed or strongly agreed that they were familiar with the topic, and only 33% (287/871) reported having at least some prior learning experience. In contrast, the perceived educational need was high: 94% (819/871) considered such a course at least somewhat necessary, 57% (497/871) reported that the course was needed or very needed, 75.5% (658/871) indicated that they would likely or definitely enroll, and 56.5% (492/871) reported that they would likely or definitely engage in self-directed learning. Personalized teaching based on textbooks (566/871, 65%) or open-book examinations (633/871, 72.7%) was the most preferred instructional and assessment format. Preferences for course materials and assessment methods differed by grade but not by gender. Conclusions: Early-stage clinical medicine undergraduates demonstrated limited familiarity with AI and medical big data but expressed a strong demand for related education. Students preferred structured yet flexible instructional formats and open-book assessments. Although the findings are based predominantly on first- and second-year students, they support the development of staged, practice-oriented AI and medical big data curricula tailored to the needs of early-stage clinical medicine undergraduates.
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Biological aging might help to explain the rising risk of early-onset cancer
Nature Medicine, Published online: 01 July 2026; doi:10.1038/s41591-026-04517-0
Cancers have risen rapidly in younger adults in recent generations. Analyzing large population-based cohorts, we found that recent generations exhibited signs of faster biological aging than older ones, and that systemic and organ-specific aging markers were associated with an increased risk of early-onset solid cancers.
The Microbiome’s Growing Role in Cancer Immunotherapy
Much of cancer research and therapy focuses on the direct impacts on cancer cells. However, understanding the broader context of cancer as a component of a patient, rather than an isolated invader, has opened a variety of insights and treatments for patients with cancer. Investigations of how the microbiome impacts cancer and immunotherapy was the prime focus of the second session on June 23, 2026 at the Frontiers in Cancer Immunotherapy Symposium hosted by The New York Academy of Sciences.
GVHD and the microbiome
Opening the discussion, Marcel van den Brink, MD, PhD, president of City of Hope Los Angeles and City of Hope Medical Center spoke about the role of the intestinal microbiome in cancer immunotherapy.
He began by describing the history of graft versus host disease (GVHD), pointing out that while early work from the 1970s suggested that germ free mice had reduced instance of GVHD following transplants, more current work has pointed to the intestinal microbiome as an immune system modulator.
“Protection of the commensal anaerobes is beneficial,” he said. He explained that Enterococcus has a habit of dominating a population with reduced diversity, pointing out that it “happens very frequently within the context of allogenic transplant, and again is linked with graft versus host [disease].”
“So we try to understand how that happens, why do you get that domination?” van den Brink described how damage to the internal lining of the gut by chemotherapy or XRT conditioning can lead to alloreactivity of immune cells. Damaged enterocytes are less able to produce lactase, leading to increase in lactose availability, which can help drive the growth of Enterococcus species, including E. faecillis—a primary species found in patients who develop GVHD. Concurrently, bile acids can have an immune suppressive effect.
He went on to share results of two published studies exploring the role of immune cells in this cycle and potential interventions. He summarized this work saying, “The protection of the commensal anaerobes is critical.
“That’s probably the easiest point that I can make, if you think about using the gut microbiome as a target to improve outcomes for cancer patients.”
As the gut is a complicated ecosystem, and there are many angles of research, the van den Brink lab is also now exploring other avenues of research that do not involve antibiotics in addition to their work with antibiotics and other therapies.
Probiotic engineering
The second talk in this session, presented by Nicholas Arpaia, PhD, associate professor of microbiology and immunology at Columbia University, explored the possibility of personalized cancer immunotherapy with the use of engineered probiotics.
His work has focused on exploring the interactions between bacteria and the tumor microenvironment (TME) and how bacteria can act as a sort of Trojan horse to access the inner tumor environment.
In terms of cancer immunotherapy, Arpaia began by saying, “hopefully I’ll be able to convince you that utilizing bacteria is a potential path forward.” Bacteria, he argues, have a bright future in the field with a strong and growing research background based on the publications, companies formed, and clinical trials over the last 20 to 30 years.
He continued describing the wide scope of the field, both in how bacteria are engineered, and in how those bacteria are delivered. While the immune-oncology space has tended towards engineering payloads that modify the TME or deliver neoantigens, there are other approaches aimed at delivering toxins or modifying the metabolism within the TME. Further, Arpaia shared details on the differences between intravenous (IV), intratumor, or oral delivery. He pointed out that bacteria injected intravenously have been found in the cores of tumors. “It’s been speculated that this occurs because of the amenable conditions within the tumor.”
The question then arises, how can this behavior be beneficial to cancer therapy? “Features of bacteria themselves can activate the innate immune system,” Arpaia said. “If you then couple that with something that’s going to help activate the adaptive immune system, it gives us all the signals we need to really get long-term durable and effective responses.”
While many bacterial strategies involve the bacteria bringing specific payloads to the TME, much of his work explores a strategy of quorum-based lysis or a synchronized lysing circuit.
“Essentially what we should observe is that there’s growth, they hit a quorum threshold, so this synchronized lysis event occurs, a few of the bacteria remain, and the entire population undergoes these cyclic events again.”
Following the lysis event, what remains is “just a massive bag of innate immune stimulatory ligands.” The payload is released over and over through this synchronized lysis of the bacteria. Arpaia summed the process: “They grow, they undergo a lytic event, they grow back, and the entire process again occurs again and again.”
Tumor-associated bacteria in space
The final talk seamlessly transitioned from the discussion of bacterial lysis deep within the tumor to a discussion on how the location of tumor-associated bacteria within the TME can impact therapy approaches.
Susan Bullman, PhD, associate professor of immunology at the University of Texas MD Anderson Cancer Center began her discussion by taking a step back from cancer. “What I’m going to talk about is the native colonization of tumors by bacteria, by members of our microbiome,” she said.
She explained that her group is “particularly interested in oral gastrointestinal cancers and understanding how microbes disseminate from our microbiome and can infiltrate human tumors to modulate the TME.”
Bullman described how certain bacterial that or typically restricted to the oral cavity can migrate and infiltrate cancers throughout the gastrointestinal (GI) tract. She focused specifically on Fusobacterium nucleatum, which not only has been consistently identified in GI tract tumors, but has also been found to negatively impact patient outcomes.
“When this microbe is enriched in the tumor, patients tend to have an increased risk for relapse, metastases and overall poor prognosis,” she said. Bullman explained that there is variability between tumor types and likelihood of tumor infiltration by microbes—with GI tract tumors having a higher instance of bacterial infection. Further, there is a heterogenous distribution of the bacteria within the tumor itself and while this bacterium is not the only microbe within the tumor tissue, her work aims to understand how this species modulates the TME.
She asked, “When these microbes get into a tumor tissue or infiltrates the tumor tissue, what exactly are they doing?” She pointed out that in healthy tissue, bacteria will interact with epithelia cells and interact with the immune system, but it’s unclear what they do within the TME.
Through the use of sequencing of both tumor and bacterial cells, her lab was able to identify details on the genetic expression of tumor cells and have a better understanding of the TME. They found that just the mere presence of bacteria at all in the tumor also has a physical impact on the tumor. The bacteria have been shown to impact tumor cell density, increasing space between the human tumor cells. As a result, these cells become stressed and stay in temporary quiescence until the bacteria are removed.
“This is interesting for a range of perspectives, from an immunotherapy perspective and an immunology perspective,” she shared.
“We see that these quiescent cells, they reduce metabolism, they reduce gene expression, and they have reduced antigen presentation. So when the cancer epithelial cells are pushed into this dormant state, they become somewhat invisible to the immune system.”
From a chemotherapy perspective, this was an interesting discovery. “We know that many anti-metabolite chemotherapies that are used in the clinic, they are targeting hyperproliferative cells,” she explained.
Currently, the team is working to map the host-bacterial interactions within the TME, looking for co-localization of cells and function to better understand how the tumor responds to bacterial infection. While they are still trying to understand the mechanisms, Bullman is encouraged by the current data.
“There [are] hints towards impacts of microbes, the amount, the load of these microbes, the immune cells, the monoid cells that they’re recruiting, and their impact on immune checkpoints within the tumor microenvironment.”
The post The Microbiome’s Growing Role in Cancer Immunotherapy appeared first on Inside Precision Medicine.
Alzheimer’s Targets Spotted in Circulatory System
Several genes relating to plasma proteins—particularly those involved in the immune system—have been linked for the first time with Alzheimer’s disease.
The proteome-wide association study (PWAS) strengthens the link between dementia and the immune system.
It also highlights potential therapeutic targets outside the traditional confines of the central nervous system (CNS) brain and spinal cord.
Genes relating to both the innate and adaptive immune system were linked with the neurodegenerative disease in the Science Translational Medicine study.
“The present PWAS, which modeled circulating protein abundance, identified potential candidate genes, many of which are expressed broadly or predominantly outside the CNS,” reported Keenan Walker, PhD, from the National Institute on Aging in Baltimore.
“These genes exhibited a higher enrichment for adaptive immunity compared with GWAS [genome-wide association study] candidates, implying distinct mechanistic pathways operating outside the CNS.”
Data on the plasma proteome and protein quantitative trait loci (pQTLs)—genetic variants that control the expression of proteins—are increasingly becoming available.
These offer the opportunity to identify disease-related genes through their effect on protein levels. Proteins are highly relevant to diseases and the development of therapeutic targets, given their role as effectors of cellular biology.
Walker and team compared genetic and proteomic changes associated with Alzheimer’s disease by studying GWAS results from tens of thousands of cases of Alzheimer’s disease, related dementias and control individuals.
They then compared this information with genetic models of 1348 circulating proteins derived from European Americans and 1385 circulating proteins from African Americans.
Plasma cis-pQTL data identified genes associated with the neurodegenerative disease through the cis regulation of plasma protein abundance. It also highlighted several plasma proteins with potential links with dementia.
The research revealed 18 genes with potentially causal relationships with the risk of Alzheimer’s disease among people with European ancestry, six of which had not been previously identified through GWAS.
Leukocyte immunoglobulin-like receptor (LILR)B1 and signal regulatory protein alpha (SIRPA), two immunoregulatory proteins not previously implicated in GWAS, showed the strongest mechanistic link to Alzheimer’s disease in the European Americans.
“We demonstrated that a subset of the plasma proteins encoded by PWAS candidate genes may function as biomarkers, given their association with dementia risk over 8- and 20-year follow-up periods, as early as middle adulthood,” the researchers reported.
“These same plasma proteins were associated with biomarkers of [Alzheimer’s disease] pathology and a broad set of cerebrospinal fluid (CSF) proteins enriched for immune and metabolic processes relevant to [Alzheimer’s disease].
“The present PWAS, which modeled circulating protein abundance, identified potential candidate genes, many of which are expressed broadly or predominantly outside the CNS.
“These genes exhibited a higher enrichment for adaptive immunity compared with GWAS candidates, implying distinct mechanistic pathways operating outside the CNS.”
The post Alzheimer’s Targets Spotted in Circulatory System appeared first on Inside Precision Medicine.
CAR T Cells Simultaneously Target Glioblastoma and Immune Cells
Scientists have identified a new molecular target for CAR T-cell immunotherapy to attack both glioblastoma cells and tumor-supporting macrophages at once. A study published today in Nature shows promising preclinical results that could allow this approach to overcome the limitations of previous attempts to target glioblastoma with CAR T cells.
“Our approach targets both the tumor and the environment that allows it to thrive,” said Sheila K. Singh, MD, PhD, professor of neuro-oncology and neurosurgery at King’s College London and McMaster University. “Instead of treating glioblastoma as only a mass of cancer cells, we need to think of it as a connected tumor-immune ecosystem. By going beyond the cancer cells alone, we are also targeting immune cells that help shield the tumor from treatment.”
Glioblastoma is an aggressive and lethal form of brain cancer where current treatments, including surgery, radiation and chemotherapy, only provide temporary benefits and are rarely able to prevent recurrence. Past attempts to develop CAR T therapies for glioblastoma have failed to produce sustained responses due to a number of challenges such as heterogeneous antigen expression, antigen loss, and microenvironmental barriers that treatments solely focusing on targeting the tumor cells have not been able to surmount.
In particular, tumor-associated macrophages have been shown to be key contributors to glioblastoma progression. While macrophages normally play an important role in the immune response against infections, glioblastoma can recruit and reprogram these immune cells to promote tumor growth, suppress the immune system, and resist treatment.
“CAR T therapy has been effective in some blood cancers, but translating that success to brain tumors has been difficult,” said Shan Grewal, an MD/PhD candidate at McMaster and co-lead author of the study. “Most approaches have focused on killing cancer cells alone. Our work suggests we may also need to dismantle the immune support system that helps glioblastoma survive.”
Using patient tumor samples, Singh’s team conducted multi-omic profiling studies that led to the identification of a promising target present both in glioblastoma cells and tumor-associated macrophages, called glycoprotein non-metastatic melanoma protein B (GPNMB). By engineering CAR T cells to target GPNMB, the researchers were able to attack glioblastoma tumors on two fronts and show potent antitumor activity in several preclinical models including patient-derived xenografts.
While more work will be needed before this strategy can be evaluated in clinical trials, the study introduces a new framework to identify immunotherapy targets that could potentially be applied to a wide range of solid tumors beyond glioblastoma.
Supporting this concept, a team at the University of Calgary has simultaneously published results in Nature Cancer from a first-in-human study using a similar approach in relapsed alveolar soft-part sarcoma (ASPS) and translocation renal cell carcinoma, two types of cancer that stably express GPNMB. In these patients, a CAR T-cell therapy directed against GPNMB was found to be safe and induced stable disease for up to three months, providing early clinical evidence supporting the feasibility of this therapeutic approach.
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Highly Sensitive ctDNA Test Improves Detection of Residual Pancreatic Cancer
A highly sensitive blood test that detects traces of tumor DNA in patients with localized pancreatic cancer identified substantially more patients with residual disease than conventional liquid biopsy testing, according to a prospective study published in Clinical Cancer Research. The findings suggest that more sensitive detection of circulating tumor DNA (ctDNA) could improve risk stratification after chemotherapy and surgery and help identify patients who remain at high risk for recurrence despite reassuring imaging results.
Researchers at Northwestern Medicine evaluated digital droplet polymerase chain reaction (ddPCR), a liquid biopsy approach that detects specific KRAS mutations, against standard next-generation sequencing (NGS), which surveys hundreds of cancer-associated genes but with lower sensitivity. Because KRAS mutations drive more than 90% of pancreatic cancers, the investigators hypothesized that focusing on this single, biologically important target would allow detection of extremely low levels of circulating tumor DNA that broader sequencing approaches often miss.
“We’re able to detect very high sensitivity in the blood for pancreas cancer,” said senior author Akhil Chawla, MD, clinical associate professor of surgery at Northwestern University Feinberg School of Medicine and a complex surgical oncologist at Northwestern Medicine. “We’re looking for extremely low levels of the DNA in the plasma.”
The prospective study followed 106 patients with localized pancreatic cancer from diagnosis through chemotherapy and surgical resection. Blood samples were collected before treatment, after chemotherapy, and following surgery to determine whether changes in KRAS ctDNA reflected treatment response and predicted patient outcomes.
At diagnosis, ddPCR detected tumor-derived KRAS DNA in 65% of patients, compared with just 17% using conventional NGS. The differences became even more striking after treatment. Following chemotherapy, ddPCR detected ctDNA in 60% of patients, while NGS detected it in only 5%. After surgery, ddPCR remained positive in 56% of patients compared with 9% using standard sequencing.
“What this publication is going to show is that yes, we can detect it with both, but we are missing a significant number of patients with standard sequencing,” Chawla said.
According to the study, patients whose disease was detected only by ddPCR represented a previously hidden intermediate-risk group. These patients had a median overall survival of 27 months after diagnosis, compared with 41 months among patients who tested negative by both assays. The findings suggest that standard liquid biopsy testing may underestimate the presence of minimal residual disease in many patients who appear to have responded well to therapy.
“We’re missing up to 60% of patients,” Chawla said. “Even at the time of diagnosis, and after treatment—particularly where we think it looks like on a CT scan after a patient’s undergone chemotherapy and had their surgical resection—everything looks great, and even the blood test that looks at ctDNA looks great. In sixty percent of patients we were still able to detect low levels.”
He adds, “Our goal is to get rid of that disease forever. Unfortunately, even with the work that we’ve done, we’ve shown that 60% to 70% of patients have recurrence of that disease after chemotherapy and surgery.”
The study also demonstrated that ctDNA dynamics over the course of treatment carried important prognostic information. Rather than relying solely on whether ctDNA was present or absent, investigators found that changes in ctDNA levels reflected treatment response.
“We’ve been able to see it even with chemotherapy and surgery,” Chawla said. “Patients that have that significant decline in the marker—not just the presence or absence, but even if they go from a high level to a medium to low level—those patients actually are benefiting from that treatment.”
Conversely, patients whose ctDNA levels remained stable or increased during treatment experienced substantially worse outcomes.
Unlike broad NGS panels, which search for hundreds of genetic alterations simultaneously, ddPCR focuses on a limited number of mutations with far greater analytical sensitivity. Chawla emphasized that the innovation was not a new laboratory technology but rather a new application of an established one.
“DDPCR can detect a single mutation with 1,000 times more sensitivity,” he said. “When we do that deep dive in pancreas cancer, what we’re really trying to do is identify whether this biomarker can, number one, be detectable in a high percentage of patients; number two, is it prognostic… and number three, can it really tell us how well a treatment is working?”
Because the assay targets the same KRAS mutations that are the focus of emerging targeted therapies, Chawla believes the approach could become increasingly valuable as those therapies enter clinical practice.
“I think there’s a lot of value in this test, particularly as we enter the age of KRAS-targeted treatments,” he said. “Our biomarker actually targets the exact same gene.”
Currently, surveillance after surgery relies primarily on CT imaging performed every few months, leaving clinicians with limited tools for detecting microscopic residual disease before recurrence becomes radiographically apparent.
“What the standard of care today is, is we just get CT scans every three months to give us an idea of when this comes back—we’re just kind of sitting on our hands and waiting,” Chawla said. “This blood test gives us an opportunity to be more active in that surveillance, potentially be more adaptive in our treatment.”
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Stockholm3 Blood Test Detects More High-Risk Prostate Cancers Early
A new blood test may help address one of the key challenges in prostate cancer detection—identifying aggressive forms of the disease early on. According to research led by a team at Karolinska Institutet, the Stockholm3 blood test detected more clinically significant cancer cases than the well-established, but problematic, Prostate Specific Antigen (PSA) screening test.
The study appears in the Annals of Internal Medicine. Swedish researchers collaborated with teams from Europe and the U.S. on this work.
Prostate cancer is one of the top cancers among men globally, with an estimated 1.5 million new cases and 397,000 deaths annually. PSA testing has long been used for early detection. But, although PSA is prostate-specific, it is not cancer-specific. Elevated PSA levels can be caused by benign conditions as well as cancer and up to 50% of diagnosed aggressive prostate cancers are in men with low PSA values—below today’s cutoffs of PSA 3 ng/ml or PSA 4 ng/ml.
“There are a number of tests in development to improve on PSA alone. A lot of them, like Stockholm3, are fairly ingenuous and do a good job,” Mark Pomerantz told Inside Precision Medicine. He is a medical oncologist at the Dana-Farber Cancer Institute in Boston. Until one of these newer tests emerges as a winner, though, MRI is the gold standard for evaluating men with high PSA. “With MRI we can see the prostate in some detail,” Pomerantz said, “But it is expensive.”
The Karolinska-led researchers analyzed data from 12,670 men aged 50–74 from the population-based STHLM3-MRI study, which compared MRI-targeted and standard biopsy in men with elevated PSAs. In this more recent Annals study, the men were tested first with both PSA and Stockholm3 and followed for two years via national cancer registries, which allowed researchers to also identify cancer cases missed during the initial screening.
Stockholm3 detected 90 percent of aggressive cancer cases, compared to 74 percent for PSA.
“The test incorporates plasma protein biomarkers, genetic risk information from a polygenic risk score, and clinical factors such as age, family history, and prior biopsy history,” the study’s lead author Thorgerdur Palsdottir, told Inside Precision Medicine. Palsdottir is a researcher at the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet.
He added, “Together, these components provide a more comprehensive estimate of a risk of harboring clinically significant prostate cancer than PSA alone.”
The components, he explained, map onto distinct biological axes rather than a single one. The kallikreins (PSA, free PSA, hK2) reflect prostate epithelial and tumor secretory activity, and the free-to-total PSA relationship helps separate benign enlargement from cancer. The polygenic score and family history capture inherited susceptibility—a man’s baseline predisposition—rather than anything about a tumor. GDF-15 is a stress-response marker that has been associated with more aggressive disease across several cancers.
During the study follow-up, 443 men were diagnosed with clinically significant, i.e. aggressive, prostate cancer. Stockholm3 missed significantly fewer serious cancer cases than PSA, while the proportion of men incorrectly classified as high-risk was similar between the tests.
“These results point toward a potential change in how prostate cancer screening can be conducted. A more precise blood test could enable earlier detection of aggressive disease while reducing the number of unnecessary follow-up examinations and procedures,” said Palsdottir.
He adds that longer-term follow-up is needed to fully assess the effects on mortality and long-term outcomes. “The next important step is to evaluate longer-term outcomes, including disease progression, metastatic disease, and prostate cancer mortality.”
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