The research team, led by investigators at Hangzhou Hospital of Traditional Chinese Medicine in China, mined the National Health and Nutrition Examination Survey, or NHANES, a continuous program run by the U.S. National Center for Health Statistics that assesses the health of the civilian population through stratified, multistage probability sampling. From an initial pool of 76,496 individuals spanning survey cycles from 2005 through 2020, the investigators retained 37,139 adults aged 20 or older after excluding those lacking data on depressive symptoms or heart attack history. Within that final sample, 1,574 participants reported having had a myocardial infarction.

Depression was quantified with the nine-item Patient Health Questionnaire, or PHQ-9, a widely validated instrument administered in person at mobile examination centers. Each of its nine items captures how often a respondent has experienced a given depressive symptom over the preceding two weeks, scored from zero for “not at all” to three for “nearly every day,” yielding a total between 0 and 27. Participants were grouped into four severity bands: no depression (0 to 4), mild (5 to 9), moderate (10 to 14) and severe (15 to 27). A total score of 10 or higher, which previous studies have shown to achieve roughly 88 percent sensitivity and specificity for diagnosing depression, served as the study’s clinical threshold.

The heart attack outcome came from the survey’s Medical Conditions Questionnaire, in which participants were asked whether a doctor had ever told them they had a heart attack. Crucially, because NHANES employs a complex survey design, the researchers applied the appropriate sample weights, strata and primary sampling units so that their estimates represent the entire non-institutionalized U.S. adult population rather than merely the tens of thousands who walked into the examination centers.

The gradient that emerged was striking. The prevalence of myocardial infarction rose progressively across depression severity categories, from 2.89 percent among participants with no depressive symptoms to 4.39 percent with mild, 5.80 percent with moderate and 7.08 percent with severe depression, a pattern that was statistically robust at p < 0.001. In the unadjusted logistic regression model, every one-point increase in PHQ-9 score corresponded to a 6.2 percent increase in the odds of having had a heart attack, with an odds ratio of 1.062 and a 95 percent confidence interval of 1.047 to 1.077. Participants with severe depression faced approximately 2.56-fold higher odds of myocardial infarction compared with those without depressive symptoms.

Critically, the association survived increasingly aggressive statistical adjustment. The researchers built three logistic regression models: the first unadjusted, the second controlling for sex, age and race/ethnicity, and the third adding education, marital status, poverty income ratio, body mass index, systolic and diastolic blood pressure, triglycerides, total cholesterol, LDL-C, HDL-C, uric acid, smoking, alcohol use, vigorous or moderate physical activity, congestive heart failure, coronary heart disease and hypertension. Even under this fully saturated model, the link between depressive burden and heart attack history remained significant. To probe whether the relationship might bend at higher symptom levels, the team employed restricted cubic spline regression, a technique that fits flexible curves across the exposure range. No significant nonlinearity appeared in any model, supporting an approximately linear dose-response pattern between depression scores and heart attack odds.

Not every subgroup told the same story, however. The association was directionally consistent across most population strata, including those defined by sex, race, education, income, body mass index, smoking, drinking and hypertension, with no significant statistical interactions. But the researchers detected significant interactions for three variables: congestive heart failure, coronary heart disease and vigorous or moderate physical activity, all with interaction p-values below 0.05. In participants with pre-existing heart failure or coronary disease, and in those who engaged in higher levels of moderate-to-vigorous activity, the apparent association between depression and myocardial infarction was attenuated. The authors suggest that in people already carrying high baseline cardiovascular risk, the incremental signal attributable to depression may be diluted, while regular physical activity may buffer some of the inflammatory and autonomic consequences of depression.

Those buffering hypotheses point to the biological machinery that plausibly connects mood and myocardium. Depression is known to activate the hypothalamic–pituitary–adrenal axis and the sympathetic nervous system, elevating blood pressure and heart rate and thereby increasing cardiac workload. It also drives systemic low-grade inflammation, reflected in elevated C-reactive protein and interleukin-6, promotes endothelial dysfunction and platelet hyperreactivity, all of which accelerate atherosclerosis and plaque destabilization. Meta-analytic evidence cited by the authors shows that coronary patients with comorbid depression exhibit both higher inflammatory markers and lower heart rate variability, a signature of vagal withdrawal that heightens vulnerability to events. Emerging work also implicates the tryptophan–kynurenine pathway as a metabolic bridge linking neuroinflammation to coronary pathology, while platelet activation markers such as soluble P-selectin are elevated in coronary artery disease populations, lending biological plausibility to a depression-driven prothrombotic mechanism. Even the gut–heart axis may participate: microbial metabolites such as trimethylamine N-oxide and short-chain fatty acids can modulate immune and neuroendocrine pathways in ways that influence both atherosclerosis and depressive phenotypes.

Behavioral pathways likely compound the biology. In the study’s baseline data, rising depression severity tracked with higher body mass index, higher triglycerides, lower HDL cholesterol, more smoking, less physical activity and lower income, a cluster of shared vulnerabilities that simultaneously raise the probability of depressive symptoms and cardiovascular events. The authors are careful, though, about what their design cannot show. Because the analysis is cross-sectional, it cannot establish causation or temporal order. The PHQ-9 captures symptoms over just the prior two weeks, whereas the myocardial infarction outcome is a lifetime self-report, so reverse causation, particularly the well-documented phenomenon of post-heart-attack depression, cannot be excluded. Self-reported outcomes also introduce recall, misclassification and survival bias, and despite exhaustive adjustment, residual confounding from factors such as medication adherence, psychosocial stress and cardiac rehabilitation remains possible.

The broader context sharpens the urgency. Between the 2005–2006 and 2017–2020 survey cycles, the prevalence of myocardial infarction, depression, and their co-occurrence nearly doubled, a parallel secular trend that, while not itself evidence of individual-level association, mirrors a wider global rise in depression-related cardiovascular mortality. Clinical literature consistently finds depression in 20 to 40 percent of patients with coronary heart disease or heart failure, and recent observational work has linked depression in cardiac patients to a three- to five-fold higher risk of major adverse cardiovascular events within a year. Yet whether treating depression improves hard cardiovascular endpoints remains unresolved; some reviews note that antidepressants and exercise improve mood without proven survival benefits, while other data suggest that the persistence or worsening of depressive symptoms over time is more closely tied to adverse outcomes than any single snapshot of symptom severity.

The study’s authors argue their findings support integrating routine depression screening, using tools as simple as the PHQ-9, into both general and high-risk cardiovascular care, alongside holistic mind–body management that addresses physical activity, smoking and metabolic risk in patients with depression. They also stress the need for prospective cohort studies and interventional trials to clarify temporal sequence, test whether modifying depression can genuinely reduce heart attack risk, and validate whether the linear relationship observed here holds across diverse populations and health care systems. For now, the message from this nationally representative sample is clear: the burden on the mind and the burden on the heart rise together, and ignoring one may mean underestimating the other.

A routine blood count could contain a surprisingly broad warning signal for metabolic syndrome, according to a large analysis of U.S. health data. Researchers examining 15,846 adults who participated in the National Health and Nutrition Examination Survey, or NHANES, from 2013 through 2020 found that people with higher pan-immune-inflammation values were more likely to have metabolic syndrome. The association persisted after the investigators adjusted for a wide range of demographic, lifestyle and clinical factors, suggesting that the relationship was not explained simply by age, sex or body weight. Metabolic syndrome is not a single disease but a cluster of abnormalities—including abdominal obesity, elevated blood pressure, high blood sugar, high triglycerides and reduced levels of protective HDL cholesterol—that together raise the risk of cardiovascular disease, stroke and type 2 diabetes. Of the participants included in the analysis, 3,845 met the study’s definition of metabolic syndrome.

The biomarker at the center of the study, known as the pan-immune-inflammation value, or PIV, is designed to combine information from several types of blood cells into one numerical estimate of systemic inflammatory activity. It is generally calculated using platelet, neutrophil, monocyte and lymphocyte counts: platelet count multiplied by neutrophil count and monocyte count, divided by lymphocyte count. Each component reflects a different aspect of the body’s immune and inflammatory state. Neutrophils and monocytes are innate immune cells that can rise during inflammation, while lymphocytes represent an important arm of adaptive immunity. Platelets participate in clotting but also interact with immune cells and blood-vessel walls. By integrating these measurements, PIV may capture a more complex biological pattern than any one cell count or a simpler ratio such as the neutrophil-to-lymphocyte ratio.

The new analysis does not show that inflammation causes metabolic syndrome, nor does it establish that PIV can diagnose the condition. Instead, it identifies a statistical association in a nationally representative, cross-sectional dataset. The researchers divided participants into four groups, or quartiles, according to their PIV values and compared the prevalence of metabolic syndrome across those groups. They then used weighted statistical models designed to account for the complex sampling structure of NHANES, which combines interviews, physical examinations and laboratory measurements to represent the civilian U.S. population. The investigators applied multivariable logistic regression, sensitivity analyses, subgroup comparisons and restricted cubic spline modeling to explore whether the relationship remained after accounting for potential confounding factors and whether it followed a straight-line pattern.

Across four increasingly adjusted statistical models, higher PIV was consistently linked to greater odds of metabolic syndrome. In the least adjusted model, each increase in the analyzed PIV measure was associated with an odds ratio of 1.19, with a 95 percent confidence interval from 1.13 to 1.26. After additional variables were introduced, the association remained statistically significant: the odds ratios were 1.17, 1.19 and finally 1.12 in the most fully adjusted model. The last estimate had a 95 percent confidence interval of 1.04 to 1.19 and a P value of 0.002. An odds ratio above one indicates higher odds of the outcome, although it should not be interpreted as a direct increase in an individual’s absolute risk. The confidence intervals also indicate uncertainty around each estimate; because they did not cross one, the researchers considered the associations statistically significant.

The pattern was not perfectly linear. Restricted cubic spline analysis, a flexible statistical technique that allows the data to curve rather than forcing them into a straight line, detected a nonlinear relationship between PIV and metabolic syndrome, with a P value of 0.044 for nonlinearity. This suggests that the change in metabolic-syndrome odds may not be identical at every point on the PIV scale. In biological terms, inflammation could have different implications at relatively low, intermediate or very high levels, or the association could reflect interactions with obesity, insulin resistance, liver dysfunction, kidney disease or medication use. The analysis found a positive relationship across the PIV range, but the detailed shape of that relationship would need to be tested in prospective studies before it could guide clinical thresholds.

To examine whether the result was being driven by specific types of participants, the researchers performed stratified analyses across subgroups. The positive association between PIV and metabolic syndrome remained broadly consistent, rather than disappearing in one particular demographic or clinical category. The investigators also repeated the analysis after excluding people taking fibrates or omega-3 products, which can affect blood lipids, as well as medications used to lower blood glucose or blood pressure. In that restricted sample, the association became stronger, with an odds ratio of 1.73 and a 95 percent confidence interval from 1.26 to 2.38. This finding may indicate that treatment-related changes in metabolic measurements or blood-cell profiles had partly obscured the relationship in the full dataset, although it could also reflect differences between people who do and do not receive those medications.

The researchers tested additional definitions and methods to assess the robustness of their findings. PIV remained significantly and positively associated with metabolic syndrome when the condition was defined using the Harmonized criteria, an internationally developed approach that brings together several commonly used diagnostic thresholds. Missing data were also addressed using random forest imputation, a machine-learning method that estimates absent values from patterns in the observed data. With that approach, the association remained stable in the first three models but weakened in the most fully adjusted model. Such attenuation is important: it shows that the strength of the association can depend on how missing information and potential confounders are handled, even when the overall signal remains suggestive.

Metabolic syndrome has long been linked to chronic, low-grade inflammation. Excess visceral fat—the metabolically active fat stored around internal organs—can release inflammatory signaling molecules and attract immune cells. These signals may interfere with insulin action, promote abnormal lipid metabolism and impair the function of the vascular endothelium, the cell layer lining blood vessels. Insulin resistance can lead the pancreas to produce more insulin to maintain normal blood glucose, while the liver may continue releasing glucose and producing triglyceride-rich particles. At the same time, inflammation and oxidative stress can alter platelet activity and leukocyte behavior. A composite measure such as PIV could therefore reflect several biological processes that overlap with the development or expression of metabolic syndrome, although it cannot reveal which process comes first.

The potential appeal of PIV is practical as much as biological. Platelet and white-cell counts are routinely included in complete blood counts, making the components relatively inexpensive and widely available compared with specialized inflammatory assays. If future research confirms that PIV adds meaningful information beyond waist circumference, blood pressure, glucose and lipid measurements, it could become a supplementary risk marker for identifying people who warrant closer metabolic evaluation. But the current study is not sufficient to support that use. NHANES provides a powerful population snapshot, yet its cross-sectional design measures exposure and outcome at roughly the same time. The data cannot establish whether elevated PIV precedes metabolic syndrome, results from it, or is influenced by an unmeasured factor such as infection, smoking, diet, medication, chronic disease or socioeconomic conditions.

The authors, led by Qian Dai and colleagues at Shanghai Fifth People’s Hospital affiliated with Fudan University and Fudan University’s Center for Community-Based Health Research, conclude that higher PIV is positively associated with the presence of metabolic syndrome among U.S. adults. They emphasize that prospective cohort studies in diverse populations are needed to determine whether the biomarker can predict future metabolic syndrome and whether it offers advantages over established measures of inflammation and insulin resistance. Clinical trials would also be needed to learn whether changing PIV through lifestyle or medical treatment changes metabolic outcomes, rather than merely accompanying them. For now, the study adds PIV to a growing list of inflammation-related indicators connected with cardiometabolic health. Its most important message is not that a single blood index can replace standard screening, but that the immune system, blood cells and metabolism may be more tightly intertwined than conventional checkups reveal.

This research is particularly timely given the growing global prevalence of diabetes, which has led to an increase in related complications such as diabetic kidney disease and diabetic retinopathy. Diabetic kidney disease significantly amplifies the risk of developing retinopathy, a condition that can lead to blindness if left unchecked. The role of endothelial activation in these processes is an important area of focus, as it serves as a key mediator of vascular dysfunction. The findings suggest that observing endothelial activation more closely can aid healthcare providers in identifying patients at higher risk for developing diabetic retinopathy.

The NHANES database provided an extensive wealth of health data, allowing researchers to conduct a robust analysis. This dataset encompasses a representative sample of the U.S. population, making the findings particularly relevant. The study utilized complex statistical methodologies to assess the relationships between endothelial activation, the stress index, and diabetic retinopathy outcomes among individuals with diabetic kidney disease. This diligent approach enables a deeper understanding of how chronic conditions interplay and elevate the risk of serious complications.

At the core of the study lies the evaluation of endothelial biomarkers, which are indicative of vascular health. The researchers determined that elevated levels of these biomarkers corresponded with heightened stress indexes, culminating in increased occurrences of diabetic retinopathy in the patient cohort. Their conclusions underscore the importance of monitoring these biological markers not just for diabetic kidney disease, but also as predictive indicators for other potential diabetic complications.

Impressively, the study identifies a stark correlation wherein patients exhibiting signs of endothelial dysfunction also reported exacerbated symptoms of diabetic retinopathy. This insight pinpoints endothelial activation as a fundamental pathophysiological mechanism linking these two prevalent diabetic complications. Consequently, early intervention strategies aimed at modulating endothelial health could serve as critical preventive measures in clinical practice, potentially staving off the onset of retinopathy, which complicates existing diabetic conditions significantly.

Additionally, the investigation highlights the pressing need for clinicians to consider stress levels in their assessments of patient health. Many healthcare settings overlook the impact of psychological and physiological stress on chronic diseases; however, these factors can substantially influence disease progression and the development of complications. By recognizing stress as a contributing factor, healthcare professionals can better tailor their approach to patient management and potentially improve outcomes.

The implications of the study extend beyond immediate clinical applications; they also touch on public health strategies aimed at reducing the burden of diabetic complications. As the prevalence of diabetes continues to rise, public health initiatives should encompass education on managing stress and promoting endothelial health, particularly within vulnerable populations. By addressing these aspects holistically, public health campaigns can contribute to enhanced overall health outcomes.

The research team concludes that further investigations are warranted to establish causative pathways that link endothelial activation with diabetic retinopathy and to explore potential therapeutic interventions. These insights could inform future research directions, paving the way for innovative treatment options that target endothelial dysfunction as a mechanism for preventing diabetic complications. The urgency of these explorations is amplified given the increasing global burden of diabetes and its associated conditions.

Among the study’s nuanced findings, the researchers advocate for integrating endothelial biomarker screening into routine clinical practice for patients with diabetic kidney disease. They argue that such measures could serve as a proactive approach to identifying those at risk of developing retinopathy and implementing early interventions to mitigate further complications. Importantly, these insights pave the way for a paradigm shift in how diabetic complications are approached in clinical settings.

Furthermore, the study opens dialogue about the necessity of interdisciplinary approaches in dealing with diabetes-related complications. Urologists, endocrinologists, and ophthalmologists must collaborate to develop holistic treatment strategies that encompass various aspects of patient health. The interconnectedness of diabetes-related complications necessitates a multifaceted approach to care that may involve lifestyle modification, medications targeting endothelial function, and ongoing monitoring of stress levels.

As the research gains traction within the medical community, it has the potential to inform clinical guidelines and recommendations, ultimately lowering the incidence of diabetic retinopathy among at-risk populations. The need for continuous research and public health focus on this topic cannot be understated, given that diabetic retinopathy remains a significant cause of visual impairment worldwide.

In conclusion, the investigation illuminates the vital connections between endothelial activation, stress indices, and the risk of diabetic retinopathy in patients with diabetic kidney disease. These findings not only contribute to the existing body of knowledge but also present a compelling call to action for healthcare providers and policymakers alike. By harnessing these insights, the healthcare community can work towards reducing the burden of diabetes and its myriad complications, enhancing the quality of life for millions around the world.

Understanding and addressing the myriad factors influencing diabetic complications can open new doors in diabetes management. By increasing awareness of endothelial activation and its associations, this study lays a foundational stone in the quest to combat the debilitating effects of diabetes. The ongoing discourse around this research can ultimately shape the future of diabetes care, integrating new strategies that proactively tackle these challenges head-on.

Subject of Research: The relationship between endothelial activation, stress index, and diabetic retinopathy in diabetic kidney disease patients.

Article Title: Association between endothelial activation and stress index and diabetic retinopathy in patients with diabetic kidney disease: a cross-sectional study based on NHANES database.

Article References: Liu, J., Yan, D., Wang, X. et al. Association between endothelial activation and stress index and diabetic retinopathy in patients with diabetic kidney disease: a cross-sectional study based on NHANES database. BMC Endocr Disord 25, 228 (2025). https://doi.org/10.1186/s12902-025-02054-4

Image Credits: AI Generated

DOI: https://doi.org/10.1186/s12902-025-02054-4

Keywords: Diabetic kidney disease, endothelial activation, diabetic retinopathy, stress index, NHANES, vascular health.

For years, vitamin D has been widely regarded as a potential protective agent against various forms of cancer, including prostate cancer. Its fluctuating role in cell differentiation, immune modulation, and apoptosis suggested that higher levels might suppress tumor growth. However, this latest investigation complicates the narrative by demonstrating a positive association between elevated serum 25(OH)D concentrations and prostate cancer prevalence, marking a significant departure from earlier hypotheses.

This study meticulously analyzed health data from 17,989 American men aged 40 years and older, with an average age of 61.1 ± 12.8 years. Utilizing multivariate logistic regression models to control for confounding variables, the researchers observed that men with higher serum 25(OH)D concentrations had increased odds of being diagnosed with prostate cancer. Statistically, every 10 nmol/L increase in 25(OH)D corresponded to a 7% rise in the likelihood of prostate cancer, underscoring a dose-response relationship.

The data also revealed that 3.3% of participants were diagnosed with prostate cancer during the surveyed period. Notably, the average serum 25(OH)D concentration among the study population was 68.3 ± 23.3 nmol/L, falling within ranges generally considered insufficient or borderline sufficient by endocrinological standards. The linear association between increasing vitamin D levels and prostate cancer prevalence persisted even after extensive sensitivity analyses, reaffirming the robustness of these findings.

One of the most compelling aspects of the study involves the interplay between cardiovascular disease (CVD) and vitamin D status. Stratified analyses indicated that men with pre-existing cardiovascular conditions exhibited an even stronger positive correlation between serum 25(OH)D levels and prostate cancer incidence. Specifically, this subgroup demonstrated an odds ratio (OR) of 1.16, with a 95% confidence interval of 1.08 to 1.24, signaling a significant interaction effect. This finding suggests that cardiovascular health may modulate the biological mechanisms through which vitamin D influences prostate carcinogenesis.

The researchers employed a sophisticated curve fitting approach to visualize the relationship, revealing a consistently linear pattern across the entire spectrum of vitamin D concentrations. This contradicts earlier theories suggesting a U-shaped or threshold model, where both low and high levels in vitamin D could be detrimental. Instead, this study posits that increased vitamin D levels, as measured by serum 25(OH)D, are directly proportional to prostate cancer prevalence.

Importantly, these results emerged from a large, nationally representative cohort, enhancing the generalizability of the conclusions to the wider population of American men aged 40 and above. The cross-sectional nature of NHANES data, however, limits causal inference — a caveat that the authors acknowledge while emphasizing the public health significance of their findings.

The potential biological mechanisms underpinning this association remain speculative but warrant further exploration. Vitamin D’s role as a secosteroid hormone implicates it in cellular proliferation and differentiation pathways, possibly influencing prostate epithelial cells differently at varying concentrations or in the presence of comorbidities like cardiovascular disease. Another hypothesis involves alterations in vitamin D receptor (VDR) expression or function in prostate tissue, which might mediate these unexpected effects.

From a clinical perspective, the study raises crucial questions about vitamin D supplementation guidelines, especially in populations at risk for prostate cancer. Given that vitamin D supplementation has surged worldwide due to its perceived health benefits, these findings call for a cautious reevaluation of optimal serum concentrations to avoid unintended pro-oncogenic effects.

Moreover, the interaction between cardiovascular disease and vitamin D status highlights the need for a more nuanced approach when considering supplementation in patients with complex health profiles. Cardiovascular disease is known to affect systemic inflammation and metabolic functions, which may alter vitamin D metabolism or its downstream effects on cancer development.

This research also underscores the importance of personalized medicine, where one-size-fits-all recommendations for vitamin D intake might be inadequate or even harmful. Future clinical trials focusing on stratified patient groups will be essential to determine safe vitamin D thresholds that minimize cancer risk without compromising other physiological benefits.

Despite its compelling insights, the study is limited by its cross-sectional design, which precludes establishing temporal or causal relationships between vitamin D levels and cancer onset. Longitudinal studies and randomized controlled trials are necessary to validate these associations and to dissect the molecular pathways involved.

Furthermore, the reliance on serum 25(OH)D as a sole biomarker of vitamin D status might inadequately capture the complex metabolism of this hormone, including active metabolites like 1,25-dihydroxyvitamin D and variations in binding protein levels. Incorporating such parameters could refine understanding of vitamin D’s role in prostate cancer etiology.

The findings pivot the spotlight onto the paradoxical effects of vitamin D in cancer biology and advocate for integrating clinical, biochemical, and epidemiological data to formulate evidence-based public health recommendations. This line of research could potentially revolutionize screening protocols and preventive strategies in urologic oncology.

As prostate cancer remains one of the leading malignancies among men globally, elucidating modifiable risk factors such as serum vitamin D levels becomes vital in curbing disease incidence and mortality. This study contributes a critical piece to the puzzle, challenging assumptions and inviting a reevaluation of nutritional guidelines for aging populations.

Clinicians and researchers alike must now grapple with the complexity of vitamin D’s influence on prostate carcinogenesis, balancing its well-known benefits against potential risks illuminated by this investigation. The question remains: how can vitamin D be optimally managed to promote overall health without inadvertently increasing cancer susceptibility?

Ultimately, these insights propel the medical community toward more tailored interventions that consider individual risk profiles, co-existing conditions, and environmental factors. As data accumulate, hope emerges for nuanced strategies that harness the positive aspects of vitamin D while mitigating its adverse implications for prostate cancer.

In conclusion, this extensive population-based study establishes a positive, linear relationship between serum 25(OH)D concentrations and prostate cancer prevalence among middle-aged and elderly American men. It highlights the modifying influence of cardiovascular disease and underscores the urgent need for further research to translate these findings into clinical practice, ensuring safer and more effective vitamin D recommendations in cancer prevention.

Subject of Research: Association between serum 25-hydroxyvitamin D levels and prostate cancer prevalence in middle-aged and elderly Americans

Article Title: Association between serum 25-hydroxyvitamin D and prostate cancer in middle-aged and elderly Americans: a national population-based analysis of NHANES 2001–2018

Article References:
Zhang, G., Guo, X., Zhu, C. et al. Association between serum 25-hydroxyvitamin D and prostate cancer in middle-aged and elderly Americans: a national population-based analysis of NHANES 2001–2018. BMC Cancer 25, 1014 (2025). https://doi.org/10.1186/s12885-025-14360-0

Image Credits: Scienmag.com

DOI: https://doi.org/10.1186/s12885-025-14360-0