BACKGROUND:Cancer prevention represents a key pillar of oncological care. In addition to genetic predispositions and lifestyle factors, carcinogenic substances from environmental and occupational exposures play a significant role. However, information about their occurrence and relationship to specific tumor types is often difficult to access in clinical practice. Physicians increasingly encounter patients who came in with incomplete or inaccurately interpreted information from media about carcinogenic risks, which can lead to unnecessary concerns and difficult communication. Although authoritative international databases exist, particularly International Agency for Research on Cancer (IARC) evaluations, their use is limited by complex structure and difficult accessibility. AIM:The aim of this article is to present the interactive OncoVis dashboard, which clearly structures data on carcinogens based on IARC classification and enables quick and intuitive searching for clinical practice needs. The dashboard serves as a practical tool for physicians in prevention, patient education, and orientation in environmental and occupational carcinogenic risks. RESULTS:OncoVis is a web application hosted at oncovis.eirene.eu. Data are primarily derived from official IARC monographs and additionally validated. The dashboard enables dynamic searching in two ways - by selecting a specific carcinogen or by selecting an organ location. For each substance, it displays the IARC classification group (1, 2A, 2B, 3), main exposure sources, exposure routes, and associated tumor locations. The application has a responsive design adapted for various devices (desktop, tablet, mobile). The dashboard is regularly updated according to new IARC monograph releases, and its long-term sustainability is ensured through the EIRENE.eu research infrastructure. CONCLUSION:The OncoVis dashboard represents a practical tool for orientation in carcinogenic substances in clinical practice. It bridges the gap between complex scientific databases and physicians' needs when communicating with patients about environmental and occupational risk factors for cancer. The tool is freely accessible and can contribute to strengthening the preventive role of oncologists.
Smoking is responsible for approximately 25-30% of all oncological diseases. The link with lung cancer, which is the strongest, and is therefore well known, has been demonstrated first. Unfortunately, smoking also contributes to other types of cancer, practically all kinds except endometrial cancer. However, due to the carcinogenic and other toxic effects of several thousand substances in tobacco smoke, smoking has been increasingly replaced in recent years by smoke-free forms of nicotine. Nicotine itself is not carcinogenic; on the contrary, some forms of nicotine replacement therapy are among the World Health Organization's essential medicines.
BACKGROUND:Physical activity (PA) is an important part of comprehensive prevention and treatment of cancer and has a significant impact on the quality of life of cancer patients. Current international and national recommendations support the inclusion of PA in all stages of cancer care. AIM:The aim of this paper is to summarize current knowledge about the effects of PA in cancer patients, describe the principles of its prescription, safety aspects, and possibilities for implementation into clinical practice. The text is based on a review of the professional literature and consensus recommendations focused on PA in cancer care. Regular PA has a proven positive effect on reducing fatigue, improving quality of life, cardiovascular fitness, and mental health, including reducing anxiety and depressive symptoms. For certain diagnoses, particularly breast, prostate, and colorectal cancer, PA has also been shown to reduce overall and cancer-specific mortality. The prescription of PA must be individualized concerning the type of tumor, stage of disease, selected oncological therapy, and its side effects, especially cardiopulmonary, neurological, and metabolic complications. PA can be safely included in the pre-rehabilitation phase, during active treatment, and in long-term follow-up care. CONCLUSION:PA is an effective and safe non-pharmacological tool in the care of cancer patients. Its wider implementation in clinical practice is limited mainly by organizational factors and low patient adherence, which emphasizes the need for interdisciplinary collaboration and systematic support for exercise programs.
BACKGROUND:Obesity is a major and modifiable risk factor influencing both the incidence and prognosis of malignant tumors. AIM:This review aims to summarize current evidence on the relationship between obesity, metabolic syndrome, and cancer risk, with a focus on underlying pathophysiological mechanisms, epidemiological data, and potential interventions. According to the International Agency for Research on Cancer, obesity is causally linked to at least 13 types of cancer, with risk increasing in proportion to body fat. Key mechanisms include chronic inflammation, hormonal activity of adipose tissue, hyperinsulinemia and insulin resistance, and alterations in adipokine profiles, all of which contribute to a tumor-promoting microenvironment. We discuss diagnostic criteria for metabolic syndrome and highlight the concept of metabolically healthy obesity, which carries a lower - but not negligible - risk of malignancy and represents a dynamic state that can progress to metabolically unhealthy obesity. Evidence also indicates that obesity negatively affects cancer recurrence and long-term outcomes, particularly in breast, endometrial, and colorectal cancers. Achieving sustainable, long-term weight reduction is challenging and requires a multidisciplinary strategy, incorporating pharmacotherapy, structured physical activity, behavioral interventions, and individualized nutritional counseling. Successful weight loss not only reduces the risk of developing cancer but may also improve prognosis and decrease the likelihood of recurrence. Therefore, integrating obesity management strategies into both primary and secondary cancer prevention, as well as survivorship care, should be considered a critical component of comprehensive oncology care.
BACKGROUND:Screening programmes are a key component of secondary prevention, with the aim of detecting disease at an early stage. In the Czech Republic, five cancer screening programmes are currently fully covered by public health insurance. These include screening for breast cancer, colorectal cancer and cervical cancer, early detection of lung and prostate cancer is also being piloted. The aim of this communication is to present nationwide programmes and the results of the evaluation of key performance indicators. MATERIAL AND METHODS:Based on the data from the National Health Information System, screening programmes are regularly monitored and evaluated. The basic indicators are epidemiological characteristics, such as incidence and mortality, but also indicators of the quality of the screening programme, such as coverage of the target population or the proportion of people with abnormal screening test results. RESULTS:Analytical outputs show that the incidence and mortality of colorectal and cervical cancer, where the goal is to detect precancerous lesions, are continuously decreasing. Breast cancer mortality is also declining, while incidence has been increasing over the long term, as the role of screening here is to detect cancer at an early stage. Coverage of the target population for breast and cervical cancer screening reaches up to 60%, while for colorectal cancer screening it is above 30%. As part of early detection of lung cancer, nearly 20,000 current or former smokers were examined over 3.5 years, and in more than 3% of cases, a positive finding was detected radiologically during the first screening episode, requiring further investigation. Approximately 250,000 men participated in early detection of prostate cancer over 1.5 years, and just under 9% were found to have elevated prostatic specific angigen levels. CONCLUSION:Screening programmes are available to the target population and fully covered by public health insurance. However, continuous monitoring and evaluation are essential, as are following international recommendations, developing the digitalization of healthcare, and providing ongoing education to both the lay and professional public. Available data demonstrate the effectiveness and positive population impact of screening programs.
Cancer risk is predominantly shaped by environmental exposures interacting with genetic susceptibility, yet modifiable non-genetic determinants remain insufficiently characterised. The human exposome framework promotes a comprehensive, life-course approach to studying chemical, biological, and physical exposures alongside socioeconomic and psychosocial factors, but it is underutilised in cancer research. Systematically mapping biomarkers of exposure to each hallmark of cancer could provide a powerful strategy to identify modifiable risk factors with translational relevance. Czechia, with its pronounced geographic variation in cancer incidence and strong research infrastructure, provides an ideal setting to pioneer such "functional exposomics" approaches. Integrating these methods into cancer research could help identify actionable environmental drivers and generate mechanistic insights to advance precision cancer prevention.
Early detection of cancer is one of the key factors influencing patient prognosis and overall cancer-related mortality. However, current population--based screening programs are limited to only a few selected diagnoses, and many highly lethal malignancies still lack an effective option for early detection. Multicancer early detection (MCED) tests represent a new group of blood-based screening methods aimed at identifying the presence of early-stage cancer across multiple primary sites through a single peripheral blood sample. They mainly rely on the analysis of circulating tumor DNA, including its methylation and fragmentation characteristics, or on combinations with protein markers or the detection of circulating tumor cells. These tests offer high specificity and are able to estimate the most likely site of origin of the tumor, which is crucial for guiding subsequent diagnostic workup. At present, the largest body of evidence is available for methylation-based and multiomic platforms. Prospective studies conducted so far in asymptomatic individuals suggest that MCED tests may enable the detection of cancers at clinically relevant stages, with a relatively low false-positive rate and an acceptable burden of follow-up investigations. At the same time, important limitations remain particularly lower sensitivity in the earliest stages of disease, the absence of standardized diagnostic algorithms following a positive result, and the lack of evidence for an effect on cancer-specific mortality and the incidence of advanced-stage disease. MCED tests therefore cannot yet be considered a replacement for established organ-specific screening programs. However, they appear to be a promising complement to current screening strategies, particularly for the detection of cancers for which no established screening exists. Their future clinical role will depend on the results of large prospective and randomized studies demonstrating their true benefit for both the population and healthcare systems. In addition to strong evidence of clinical benefit, widespread implementation into clinical practice will also require standardization of downstream diagnostic pathways and careful health-economic evaluation.
BACKGROUND:Microbiome analysis in cancer research has experienced a surge in interest comparable to the introduction of microarrays for tumor gene expression profiling 25 years ago. Associative studies investigating the composition of the microbiome in stool, tumor tissue swabs and tumor biopsies of oncology patients have been conducted across most cancer types, and their number continues to grow. Screening approaches based on non-invasive or minimally invasive sampling, including the analysis of stool, saliva, urine, and buccal and rectal swabs, are from a clinical perspective among the most promising, owing in part to simpler logistics and the possibility of repeated sampling. These types of specimens are commonly used in microbiome studies, making the microbiome an attractive target for both screening and diagnostic applications. AIM:This review aims to summarize current knowledge regarding the potential of the microbiome in the early detection of cancer, emphasizing its clinical applicability and limitations in the context of population-based prevention.
BACKGROUND:In the context of oncological diseases of (not only) the gastrointestinal tract and the oral cavity, the role of microorganisms is being increasingly discussed and investigated. A growing body of evidence supports the significance of specific microbial strains and their products both in the etiopathogenesis of certain cancers and in their prevention and therapy. AIM:This review summarizes recent findings on the targeted modulation of the human microbiota using probiotics (including Bifidobacteria, Lactobacilli, etc.), their products (postbiotics, e. g. butyrate), and formulations combining probiotics with prebiotics (synbiotics), in the context of cancer prevention and progression, adverse effects of anticancer therapy, and associated complications related to the disease and surgical treatment. The results of clinical studies demonstrate the benefits of these preparations, particularly in preventing and alleviating gastrointestinal symptoms and postoperative infectious complications, as well as inflammatory mucosal damage (including oral mucositis) in oncology patients, with multi-strain probiotic formulations demonstrating greater efficacy. Research is even underway in animal models to explore the use of probiotics in immunotherapy. Despite the promising results obtained from modulating the human microbiota to improve the quality of life of cancer patients, as well as for cancer prevention and potentially even therapy, broader clinical implementation is limited by interindividual variability of the microbiome, safety concerns in immunocompromised patients, and the insufficiently documented quality of some available products. Nevertheless, given the undeniable mechanistic and translational potential of probiotic, postbiotic, and synbiotic supplementation, continued clinical research in this field is highly warranted.
BACKGROUND:Endocrine-disrupting chemicals (EDCs) constitute a heterogeneous group of substances capable of interfering with hormonal regulation and thereby influencing the risk of initiation and progression of hormone-sensitive cancers. Their mechanisms of action include interactions with hormone receptors, modulation of hormone synthesis and metabolism, epigenetic alterations, and activation of specific signalling pathways. In recent years, the adverse outcome pathway (AOP) framework has gained prominence, as it enables linking molecular initiating events affected by EDCs to clinical outcomes, including carcinogenesis. An important role play thyroid hormones, which regulate cell proliferation, differentiation, and metabolism across tissues, and their deregulation by EDCs at multiple levels may influence the development of various cancer types. OBJECTIVE:The aim of this article is to summarise current knowledge on the main mechanisms of endocrine disruption that can influence cancer initiation and progression, and to highlight the relevance of the AOP framework for predicting risks associated with EDC exposure. The objective also includes drawing attention to the major groups of EDCs whose exposure has been associated with an increased risk of hormone-sensitive cancers, as well as their sources. CONCLUSION:Endocrine-disrupting chemicals to which people are commonly exposed may represent an important factor affecting hormonal balance and the potential development of cancer. Understanding their molecular mechanisms of action is essential for risk assessment and the formulation of preventive strategies. The AOP framework offers a promising tool for linking mechanistic data with clinical consequences and for predicting the carcinogenic potential of these substances.
AIM:The aim of this review is to summarize current evidence on the relationship between mental health, stress, sleep, and cancer prevention, and to propose a clinically applicable framework for integrating these topics into preventive practice without attributing a direct causal role in cancer development. MATERIAL AND METHODS:This narrative review is based on epidemiological, clinical, and meta-analytic studies examining mental health, sleep disturbances, and their associations with cancer risk, health-related behavior, and prevention. Relevant psycho-oncological and preventive care recommendations are also considered. RESULTS:Available evidence does not support mental disorders or sleep disturbances as direct causes of cancer. Their clinical relevance lies primarily in indirect pathways, particularly through health-related behavior, adherence to preventive recommendations, and the capacity to cope with long-term burden. Sleep disturbances additionally represent a modifiable risk factor for the development of several mental disorders, which may further influence preventive behavior. Psycho-oncological screening and a stepped--care approach to mental health support enable early identification of barriers to prevention with minimal burden on clinical practice. CONCLUSION:Mental health and sleep should be conceptualised as regulatory conditions of cancer prevention rather than causal factors. Translating scientific evidence into clear and clinically meaningful language, and incorporating it sensitively into physician-patient communication, is essential for their effective use in preventive care.
BACKGROUND:Microplastics and nanoplastics are ubiquitous environmental contaminants, and human exposure via ingestion and inhalation is increasingly recognized. Numerous studies report microplastics in human tissues and biological fluids, yet the biological relevance and robustness of these findings remain uncertain. This critical work evaluates current evidence on microplastics in the human body, focusing on exposure pathways, particle size relevance, and analytical limitations. Mechanistic data indicate that translocation across intestinal and pulmonary barriers is likely restricted to small microplastics (< 10 µm) and nanoplastics, raising questions about reports of larger particles in human tissues. Key challenges include secondary contamination, size-dependent detection limits, and methodological artifacts associated with common analytical techniques. Experimental evidence for biological effects, including inflammation, microbiome disruption, and cancer-related pathways, is discussed in the context of physiological relevance. AIM:Overall, our work highlights the need for standardized analytical methods, rigorous quality control, and mechanistic studies using realistic exposure scenarios to support sound microplastics related human health research.
BACKGROUND:Polygenic risk score (PRS) has the ability to stratify inherited susceptibility to cancer and, as a complement to monogenic testing, can identify individuals at increased genetic risk even when no pathogenic variant is detected in high- or moderate-penetrance genes. It reflects the combined additive effects of a large number of low-penetrance variants across the genome, and represents a continuum of genetic susceptibility with an approximately normal distribution. Clinically relevant differences are typically observed in individuals in the highest and lowest percentiles of the PRS distribution, while relative risk gradients depend on the cancer type, the specific PRS model, and the reference population used. PRS is not a single test but rather a family of statistical models that differ in their design, predictive performance, and transferability across populations, underscoring the need for external validation and population-specific calibration of absolute risk. Broader implementation is thus still held back by differences between individual PRS models, limited transferability, and the lack of harmonized guidance on indication, reporting, and clinical decision-making. Consequently, clinical use in the European Union remains largely confined to pilot studies and local projects. Within these initiatives, PRS is most commonly applied in two main ways - either as a triage tool for intensified diagnostics or screening in higher-risk groups, or as a component of multifactorial absolute-risk models (e. g. BOADICEA/CanRisk) that integrate PRS with other risk factors such as pathogenic variants in moderate-penetrance genes (e. g. ATM or CHEK2), family history, or lifestyle factors. By refining absolute-risk estimates, PRS may shift individuals across clinical decision thresholds for more intensive surveillance and preventive strategies. AIM:This review summarizes the principles of PRS, the main sources of variability between models, and its potential applications in risk stratification and personalized cancer screening. It also addresses limitations in transferability, the need for calibration, and the currently limited evidence for improvements in hard clinical outcomes.
BACKGROUND:Histiocytic diseases are significantly rarer than diseases derived from lymphocytic, plasmacytic, or myeloid lineages, and thus are encountered infrequently in hematology and oncology clinics. The most common form is Langerhans cell histiocytosis, which in adults has an incidence of 1-2 cases per 1 million; the others are considerably rarer, with their occurrence reported only by the number of described cases rather than through incidence or prevalence. Their rarity leads to delays in establishing an accurate diagnosis. OBJECTIVE:The group of histiocytic diseases includes seven clinical units: Langerhans cell histiocytosis, indeterminate dendritic cell histiocytosis, diseases from the juvenile xanthogranuloma group, Erdheim-Chester disease, Rosai-Dorfman disease, ALK-positive histiocytosis, and histiocytic sarcoma. Each of the described diseases has specific manifestations that distinguish it from the manifestations of other malignant blood disorders. The aim of this article is to remind the reader of these manifestations through images and text, thereby contributing to the timely recognition of these rare diseases. CONCLUSION:Treatment procedures are rapidly evolving, but the clinical presentations of these diseases remain unchanged. The disease profiles presented in this publication should aid in their early diagnosis and consequently in timely treatment.
BACKGROUND:Patients with advanced or recurrent endometrial cancer who progress after platinum-based chemotherapy face a poor prognosis, and treatment options have historically been limited. The introduction of immunotherapy, alone or in combination with targeted agents, has substantially expanded therapeutic options in subsequent treatment lines. This study evaluated the efficacy and clinical benefit of second- and subsequent-lines of systemic therapy in a real-life cohort of patients with advanced or recurrent endometrial cancer. METHODS:This retrospective, single-center analysis included patients treated at University Hospital Brno who were considered for second-line systemic therapy after failure of platinum-based chemotherapy between 2013 and 2024. Clinicopathological and molecular characteristics, systemic treatment modalities, best overall response, time to progression, and disease-specific survival were assessed. RESULTS:A total of 43 patients were identified; second-line treatment was initiated in 41 patients (95.3%). Of these, 26 (63.4%) received second-line chemotherapy, 14 (34.1%) received pembrolizumab alone or in combination with lenvatinib, and one patient (2.4%) received hormonal therapy. The median disease-specific survival for the entire cohort was 13.4 months (95% confidence interval 8.5-27.2 months). Among patients with re-administration of platinum-based chemotherapy, the median disease-specific survival was 27.2 months. Patients receiving pembrolizumab ± lenvatinib had a median survival of 23.4 months, whereas those treated with non-platinum chemotherapy had a median survival of 6.7 months. Two patients without active second-line treatment had a median disease-specific survival of 2.7 months. Nearly half of the patients treated with pembrolizumab ± lenvatinib experienced a prolonged time to progression compared with those receiving primary platinum-based chemotherapy. CONCLUSIONS:In patients with advanced or recurrent endometrial cancer after platinum failure, active systemic therapy may prolong survival and improve disease control. The greatest clinical benefit was observed with pembrolizumab alone or in combination with lenvatinib. An individualized, sequential approach to palliative systemic therapy is crucial to maximize clinical benefits.
BACKGROUND:Erdheim-Chester disease (ECD) is a rare disorder characterized by infiltrates of foamy histiocytes (histiocytes with abundant lipid inclusions - foamy cells) and inflammatory stroma, which induce a systemic inflammatory response. The disease typically infiltrates the bones causing osteosclerotic and mixed lesions with the characteristic "hot knees" pattern - increased uptake of radiopharmaceuticals in the epiphyses of bones near the knee joint. OBSERVATION:The patient had histologically confirmed ECD with negative test results for mutations in the BRAF gene and MEK pathway, but with aberrant cyclin D1 expression. The disease manifested with retrobulbar infiltrates, pericardial effusion, infiltration of the pancreas, retroperitoneum, and nerve roots. Secretion from the pericardial drain decreased after administration of high doses of methylprednisolone, followed by regular applications of anakinra. Extent of the disease was assessed by MRI of the head, PET/CT with the radiopharmaceuticals fluorodeoxyglucose (FDG) and sodium fluoride (NaF), and skeletal scintigraphy. FDG accumulated significantly in pathological infiltrates visible on low-dose CT. A pathological lesion with increased FDG accumulation was also present in the pituitary gland. FDG also showed increased accumulation in the bones, but the typical "hot knees" pattern was not present. This pattern, however, was visible on skeletal scintigraphy, and osteosclerotic lesions were most precisely detected using NaF-PET/CT. Treatment with interferon-alpha was unsuccessful. For second-line treatment, cladribine was used - in the first two cycles as monotherapy, and in the third and fourth cycles in combination with a low dose of cyclophosphamide. After the fourth cycle, symptoms of the disease regressed, and FDG-PET/CT showed disappearance or a significant reduction of pathological FDG accumulation in the disease lesions. Cladribine will be administered for a maximum of six cycles. CONCLUSION:FDG-PET/CT is currently the most appropriate examination for determining the extent of the disease as well as for assessing treatment response. However, the extent of osteosclerotic lesions, including the characteristic "hot knees" pattern, is more accurately visualized using NaF-PET/CT. Cladribine is an effective drug for both Langerhans cell histiocytosis and ECD. The therapeutic effect of cladribine, as well as its side effects, can be enhanced by adding cyclophosphamide. The inflammatory reaction induced by ECD was suppressed with anakinra.
