Hepatic myelopathy (HM) is a rare neurological complication in the end stage of many liver diseases and is characterized by bilateral spastic paraparesis without sensory and sphincter dysfunction. It occurs owing to metabolic disorders and central nervous system dysfunction associated with cirrhosis. Without timely and effective clinical intervention, the prognosis of these patients is devastating. Although liver transplantation (LT) is an effective treatment for HM, the prognosis of these patients remains unsatisfactory. Early recognition and diagnosis of this disease are essential for improving patient prognosis. Here, we report a case of hepatitis B virus-associated decompensated cirrhosis with HM. The patient recovered well after LT. We also summarize the clinical characteristics and post-transplant outcomes of 25 patients with HM treated by LT through 2023, including this case.

Medicinal plants have been recognized as a promising alternative treatment against some types of cancer, being rich sources of effective biochemical agents. The aim of this study, therefore, was to gather, through a systematic literature review, articles related to plants from the Brazilian Cerrado biome that have an action on different tumor cells.

Different keywords were used in the search mechanisms of Pubmed, Scielo, Science Direct, Scopus, and Lilacs databases. Of the studies found, titles that did not reflect the purpose of this review, those that did not provide access to the full text, and those that were published before 2005 were excluded. Articles referring to the activity of Cerrado plants in tumor cells published in the last sixteen years were selected, totaling thirty-nine articles. Registration number of this review: #CRD42020205579.

The extracts from the studied plants demonstrated significant antiproliferative effects against several tumor cell lines. 39 species of plants were identified belonging to the families: Combretaceae, Annonaceae, Celastraceae, Verbenaceae, Solanaceae, Myrtaceae, Rubiaceae, Bignoniaceae, Erythroxylaceae, Sapotaceae, Asteraceae, Elaeocarpaceae, Apocynaceae, Anacardiaceae, Calophyllaceae, Lythraceae, Mimosaceae, and Morseraceae. The extracts were obtained from different parts of the plants and different fractions were used.

It can be concluded that the Cerrado contains a wide variety of plants with antitumor actions, and further studies are needed to discover other species with anticancer potential, in addition to in vivo studies.

The World Health Organization Reporting System for Lung Cytopathology is the first international system that was developed to standardize the reporting of lung cytopathology specimens across all settings of cytopathology practice. The system is composed of five diagnostic categories, which apply to all lung cytopathology specimen types. Each category contains cytomorphologic criteria, an estimated risk of malignancy, and clinical management recommendations. International uniformity in the reporting of lung cytopathology will refine the communication between cytopathologists and clinicians and ultimately improve patient care. Furthermore, standardizing the cytomorphologic criteria for each lesion will improve reproducibility among cytopathologists and highlight areas in lung cytopathology that require further research. The system also provides best practice recommendations for the selection of ancillary tests to aid in the diagnosis of each lesion, or group of lesions, keeping in mind that resources will vary across different practice settings. The goal of this review is to summarize the cytomorphologic criteria, potential diagnostic pitfalls, ancillary testing, estimated risk of malignancy, and clinical management recommendations for each diagnostic category.

Clinical unmet need in managing nonalcoholic fatty liver disease (NAFLD), a common liver disorder affecting 25–30% of American adults is to develop noninvasive and robust biomarkers.

We re-measured liver AC by placing a region of interest (ROI, 3 cm tall and 3 cm wide) at 4.5 cm, 6 cm, and 7.5 cm from the skin and a large ROI (6.0 cm tall and 7.3 cm wide) on pre-recorded ATI images from 117 participants screened for NAFLD. The difference in AC value at variable ROI depths was tested using one-way ANOVA (analysis of variance). Diagnostic performances of AC at variable depths in determining hepatic steatosis were examined by area under receiver operating characteristic curve (AUC) using MRI-proton density fat fraction (MRI-PDFF) as reference and were compared using paired-sample Z-test.

Based on MRI-PDFF, 117 livers were divided to 27 normal livers (MRI-PDFF < 5%) or 90 steatotic livers (MRI-PDFF ≥ 5%). Differences in AUC and AC value at variable depths and size were statistically significant (p < 0.01). The best performance for determining hepatic steatosis was the AC measured at 6 cm from the skin (AUC = 0.92). Sources of errors in performing ATI included reverberation, blank color region, and acoustic shadowing within the measurement ROI.

ROI depth significantly influences liver AC estimation. The best ROI depth to measure liver AC in patients with BMI ≥ 30 may be at a depth of 6 cm from the skin. Technical considerations should be taken in performing liver ATI.

Hepatitis B virus (HBV) reactivation is commonly observed in individuals with chronic HBV infection undergoing antineoplastic drug therapy. Paclitaxel (PTX) treatment has been identified as a potential trigger for HBV reactivation. This study aimed to uncover the mechanisms of PTX-induced HBV reactivation in vitro and in vivo, which may inform new strategies for HBV antiviral treatment.

The impact of PTX on HBV replication was assessed through various methods including enzyme-linked immunosorbent assay, dual-luciferase reporter assay, quantitative real-time PCR, chromatin immunoprecipitation, and immunohistochemical staining. Transcriptome sequencing and 16S rRNA sequencing were employed to assess alterations in the transcriptome and microbial diversity in PTX-treated HBV transgenic mice.

PTX enhanced the levels of HBV 3.5-kb mRNA, HBV DNA, HBeAg, and HBsAg both in vitro and in vivo. PTX also promoted the activity of the HBV core promoter and transcription factor AP-1. Inhibition of AP-1 gene expression markedly suppressed PTX-induced HBV reactivation. Transcriptome sequencing revealed that PTX activated the immune-related signaling networks such as IL-17, NF-κB, and MAPK signaling pathways, with the pivotal common key molecule being AP-1. The 16S rRNA sequencing revealed that PTX induced dysbiosis of gut microbiota.

PTX-induced HBV reactivation was likely a synergistic outcome of immune suppression and direct stimulation of HBV replication through the enhancement of HBV core promoter activity mediated by the transcription factor AP-1. These findings propose a novel molecular mechanism, underscoring the critical role of AP-1 in PTX-induced HBV reactivation.

This review summarizes the current investigations that confirm the significance of liver fibrosis (LF) as an independent cardiovascular risk factor in non-alcoholic fatty liver disease (NAFLD). PubMed, Google Scholar, Web of Science platform, Reference Citation Analysis, and Cochrane Systematic Reviews were searched for articles published between 2008 and 2023. Relevant articles were identified using the following keywords: “cardiovascular diseases”, “cardiovascular risk factors”, “non-alcoholic fatty liver disease”, “nonalcoholic steatohepatitis”, and “liver fibrosis”. The reference lists of the identified articles were also searched for other relevant publications. The investigations that described LF as a cardiovascular risk factor in NAFLD met the inclusion criteria. NAFLD occupies a leading position among liver diseases worldwide. Cardiovascular disorders are the most significant cause of unfavorable outcomes in NAFLD patients. Currently, the relationship between them is well established. The pathophysiological mechanisms predisposing to the development of cardiovascular disorders in NAFLD include atherogenic dyslipidemia, impaired glucose metabolism and liver insulin resistance, low-grade systemic inflammation, endothelial dysfunction, cardiovascular remodeling, as well as gut dysbiosis, which are influenced by numerous genetic and epigenetic factors. Identification of cardiovascular risk factors in NAFLD is an important public health issue. At present, there is evidence that the presence of advanced LF may be a strong independent predictor and risk factor for cardiovascular disorders in NAFLD. It is obvious that early diagnosis of LF will allow to stratify NAFLD patients by cardiovascular risk groups and thereby determine the most optimal therapeutic interventions.

Hepatic ischemia-reperfusion injury (HIRI) is a prevalent complication of liver transplantation, partial hepatectomy, and severe infection, necessitating the development of more effective clinical strategies. Receptor activity–modifying protein 1 (RAMP1), a member of the G protein–coupled receptor adapter family, has been implicated in numerous physiological and pathological processes. The study aimed to investigate the pathogenesis of RAMP1 in HIRI.

We established a 70% liver ischemia-reperfusion model in RAMP1 knockout (KO) and wild-type mice. Liver and blood samples were collected after 0, 6, and 24 h of hypoxia/reperfusion. Liver histological and serological analyses were performed to evaluate liver damage. We also conducted in-vitro and in-vivo experiments to explore the molecular mechanism underlying RAMP1 function.

Liver injury was exacerbated in RAMP1-KO mice compared with the sham group, as evidenced by increased cell death and elevated serum transaminase and inflammation levels. HIRI was promoted in RAMP1-KO mice via the induction of hepatocyte apoptosis and inhibition of proliferation. The absence of RAMP1 led to increased activation of the extracellular signal–regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway and yes-associated protein (YAP) phosphorylation, ultimately promoting apoptosis. SCH772984, an ERK/MAPK phosphorylation inhibitor, and PY-60, a YAP phosphorylation inhibitor, reduced apoptosis in in-vitro and in-vivo experiments.

Our findings suggest that RAMP1 protects against HIRI by inhibiting ERK and YAP phosphorylation signal transduction, highlighting its potential as a therapeutic target for HIRI and providing a new avenue for intervention.

The presence of multinucleated giant cells in fine needle aspiration (FNA) specimens of neuroblastic tumors is not uncommon, but they are often not well-illustrated in the literature. The authors present a case of a 3-year-old boy with a large abdominal mass that was found to have striking multinucleated giant cells on FNA. The FNA specimen showed a cellular smear with a predominance of small, round cells with scant cytoplasm and hyperchromatic nuclei. There were also numerous multinucleated giant cells, some of which had up to 10 to 20 nuclei. The giant cells contained abundant cytoplasm and prominent nucleoli. The patient was subsequently diagnosed with ganglioneuroblastoma. The authors discuss the differential diagnosis of multinucleated giant cells in FNA specimens and argue that these cells can be a helpful diagnostic clue in the diagnosis of ganglioneuroblastoma. The importance of recognizing multinucleated giant cells in FNA specimens of other soft tissue tumors is also discussed.

Hepatocellular carcinoma (HCC) is a common cancer, and the body’s immune responses greatly affect its progression and the prognosis of patients. Immunological suppression and the maintenance of self-tolerance in the tumor microenvironment are essential responses, and these form part of the theoretical foundations of immunotherapy. In this review, we first discuss the tumor microenvironment of HCC, describe immunosuppression in HCC, and review the major biomarkers used to track HCC progression and response to treatment. We then examine antibody-based therapies, with a focus on immune checkpoint inhibitors (ICIs), monoclonal antibodies that target key proteins in the immune response (programmed cell death protein 1, anti-cytotoxic T-lymphocyte associated protein 4, and programmed death-ligand 1) which have transformed the treatment of HCC and other cancers. ICIs may be used alone or in conjunction with various targeted therapies for patients with advanced HCC who are receiving first-line treatments or subsequent treatments. We also discuss the use of different cellular immunotherapies, including T cell receptor (TCR) T cell therapy and chimeric antigen receptor (CAR) T cell therapy. We then review the use of HCC vaccines, adjuvant immunotherapy, and oncolytic virotherapy, and describe the goals of future research in the development of treatments for HCC.

Disease progression of chronic hepatitis B virus (HBV) infection is driven by the interactions between viral replication and the host immune response against the infection. This study aimed to clarify the relationship between HBV replication and hepatic inflammation during disease progression.

Two cross-sectional, one validation cohort, and meta-analyses were used to explore the relationship between HBV replication and liver inflammation. Spearman analysis, multiple linear regression, and logistic regression were used to explore the relationship between variables.

In the cross-sectional cohorts A and B including 1,350 chronic hepatitis B patients, Spearman analysis revealed a negative relationship between HBV replication (such as HBV DNA) and liver inflammation (such as ALT) in HBeAg-positive patients with higher HBV DNA >2×106 IU/mL (rho=−0.160 and −0.042) which turned to be positive in HBeAg-positive patients with HBV DNA ≤2×106 IU/mL (rho=0.278 and 0.260) and HBeAg-negative patients (rho=0.450 and 0.363). After adjustment for sex, age, and anti-HBe, results from logistic regression and multiple linear regression showed the opposite relationship still existed in HBeAg-positive patients with different DNA levels; the opposite relationship in HBeAg-positive patients with different DNA levels was validated in a third cohort; the opposite relationship in patients with different HBeAg status was partially confirmed by meta-analysis (overall R: −0.004 vs 0.481).

These results suggested a negative relationship between viral replication and liver inflammation in HBeAg-positive patients with high HBV DNA, which changed to a positive relationship for those HBeAg-positive patients with DNA less than 2×106 IU/mL and HBeAg-negative patients.

The overwhelming majority of genes in the human genome encode RNA molecules that are not translated into proteins. These RNA molecules are named non-coding RNAs (ncRNAs). ncRNAs play a crucial role in the regulation of gene expression and abnormalities in ncRNAs can cause disease progression, including atherosclerosis. ncRNAs regulate different stages of atherosclerosis progression, such as foam cell formation and lipid metabolism. Diverse types of ncRNAs have been studied, but the best known and widely used are small non-coding (sncRNAs), specifically microRNAs and small interfering RNAs, which are ∼22 nucleotides long. The majority of drugs based on ncRNAs are composed of sncRNAs. There is strong evidence that besides sncRNAs, other types of ncRNAs, such as long ncRNAs and circular RNAs, take part in the regulation of gene expression. This review summarized recent advances in ncRNAs and atherosclerosis.

Hepatocyte nuclear factor 1β (HNF1β) is essential for biliary development, while its genetic defect triggers the dysplasia of interlobular bile ducts, leading to life-threatening hepatitis and cholestasis. To date, this disorder has mainly been documented in neonates. Here, we report a case of cholestasis in an adult patient caused by a de novo HNF1β mutation. A liver biopsy revealed remarkable shrinkage of the portal area accompanied by a decrease or absence of interlobular bile ducts, veins, and arteries in the portal area. Our case showed that an HNF1β defect could induce late-onset cholestasis with paucity of the portal area in adulthood.

Genetic polymorphisms of CYP2D6 and CYP2C19 affect both the effectiveness and the occurrence of side effects of many antidepressants. By drug-drug-gene interactions (also referred to as phenoconversion), the phenotype of the patient can be changed. Both pharmacogenetic testing, drug-drug, and drug-drug-gene interaction checks are essential to individualize the dose of the antidepressant or start an alternative drug in accordance with the pharmacogenetic guidelines. The aim of this study was to analyze the frequency of divergent phenotypes (i.e. divergent from the common phenotypes considered normal), of phenoconversion (a genotype–phenotype mismatch), and of actionable genotypes (genotypes where a prescribing change may be indicated) in psychiatric inpatients with a depressive disorder.

Genotyping of CYP2D6 and CYP2C19 was performed in 104 patients 18 years of age or older who received inpatient treatment in a German psychiatric university hospital for a depressive disorder. Representation of the frequencies of divergent phenotypes, of phenoconversion, and of actionable genotypes were analyzed.

A divergent phenotype in one or both CYP enzymes was seen in 83.5% of the patients. The rate of CYP2D6 poor metabolizers increased by 142.4% (from 5.9% to 14.3%, p = 0.013) at admission and by 183.1% (from 5.9% to 16.7%, p = 0.004) at discharge because of phenoconversion. At discharge, 22% of the patients (n = 104) received an antidepressant with a dosing recommendation based on their CYP2D6 phenotype and 15.4% on their CYP2C19 phenotype. When considering phenoconversion, the rate increased by 17.4 to 26.0% (p = 0.221) for patients with the CYP2D6 genotype.

The clinical relevance of the results of the study is that phenotype conversion is common in patients treated for depression with medication. The discrepancy between the clinically observed phenotype and the phenotype expected based on the patient genotype underscores the need for greater consideration of both genetic and nongenetic factors.

Targeted therapy and immunotherapy have emerged as treatment options for hepatocellular carcinoma (HCC) in recent years. The significance of serine and glycine metabolism in various cancers is widely acknowledged. This study aims to investigate their correlation with the prognosis and tumor immune microenvironment (TIME) of HCC.

Based on the public database, different subtypes were identified by cluster analysis, and the prognostic model was constructed through regression analysis. The gene expression omnibus (GEO) data set was used as the validation set to verify the performance of the model. The survival curve evaluated prognostic ability. CIBERSORT was used to evaluate the level of immune cell infiltration, and maftools analyzed the mutations. DsigDB screened small molecule compounds related to prognostic genes.

HCC was found to have two distinct subtypes. Subsequently, we constructed a risk score prognostic model through regression analysis based on serine and glycine metabolism-related genes (SGMGs). A nomogram was constructed based on risk scores and other clinical factors. HCC patients with a higher risk score showed a poor prognosis, and there were significant differences in immune cell infiltration between the high- and low-risk groups. In addition, three potential drugs associated with prognostic genes, streptozocin, norfloxacin, and hydrocotarnine, were identified.

This study investigated the expression patterns of SGMGs and their relationship with tumor characteristics, resulting in the development of a novel model for predicting the prognosis of HCC patients. The study provides a reference for clinical prognosis prediction and treatment of HCC patients.

Breast cancer is the most prevalent malignancy and the leading cause of cancer-related death in women. Breast cancer is still an extremely difficult cancer to treat due to its significant metastasis. Mis-regulation of Notch signaling components such as Notch receptors/ligands and their interaction in breast cancer sparks tumor initiation, maintenance, and progression through induction of abnormal tumorigenesis while modulating vascular integrity, drug resistance, invasion, and migration. Numerous studies have shown that non-coding RNAs can regulate Notch signaling and accordingly impact breast cancer pathobiology. MiRNAs could regulate Notch signaling components directly or indirectly via sponging or suppressing other genes involved in the pathway. Further, lncRNAs interact with miRNAs and mRNAs, and lncRNA-miRNA-mRNA interaction networks function as substantial mediators in various pathways, including the Notch signaling pathway. Also, by targeting and sponging other genes, circRNAs could induce tumorigenic properties via the Notch signaling pathway. Due to the intricacy of human physiology, it is challenging for standard drugs to be effective, and cancer cells can develop resistance to treatment and have a significant self-renewal capacity. Moreover, because non-specific Notch signaling intervention targets both tumor cells and immune cells, it may have the reverse effect of regulating the formation of tumors. Thus, an in-depth understanding of the mechanisms could be useful in diagnosis, prognosis, and the development of novel medications that specifically target Notch signaling, improving the efficacy of cancer immunotherapy in the treatment of breast cancer. This review will discuss and clarify the mechanisms by which miRNAs, lncRNAs, and circRNAs affect the Notch signaling pathway leading to BC development.

Gastric cancer (GC) is a prevalent gastrointestinal malignancy, yet its early detection remains hindered due to the lack of available genetic markers. This study aimed to identify alternative genetic markers for the early prognosis and prevention of GC.

This objective was achieved through the analysis of differentially expressed genes (DEGs) from three datasets obtained from the Gene Expression Omnibus (GEO). By doing so, our goal was to identify hub genes associated with gastric adenocarcinoma that could serve as potential biomarkers for the early detection and management of GC. Three GEO datasets (GSE172032, GSE179581, and GSE181492), consisting of 10 normal and 10 GC samples were analyzed using the Galaxy web server. The visualizations of DEGs, including heatmaps, volcano plots, and MD plots, were generated via the same tool. ShinyGO performed Gene Ontology and KEGG enrichment analysis, while NetworkAnalyst identified a protein-protein interaction (PPI) network and screened 10 potential hub genes. Kaplan Meier plotter was used to analyze overall survival analysis for key hub genes, and NetworkAnalyst was used to assess protein-drug interactions for the top 10 hub genes.

A total of 1,079 common DEGs emerged across datasets, concentrating on significant GC-related pathways. Ten hub genes (H2BC21, H3C12, H2BC17, H3C2, H3C10, ERBB4, H2AC8, H3C8, H2BC14, and MAPT) were found to be linked to GC via PPI analysis. Survival analysis revealed that higher expression levels of ERBB4 and MAPT were associated with poor overall survival in GC patients. Furthermore, protein-drug interaction analysis revealed that the protein product of the MAPT gene exhibited a robust connection with drug compounds, specifically docetaxel and paclitaxel. These findings suggested that these drugs have the potential to inhibit the function of MAPT.

In summary, our findings provide putative candidate biomarkers, provide insights into GC treatment strategies, and highlight avenues for further research, contributing to a better understanding of the pathogenesis of GC.

Acetaminophen (APAP)-induced liver injury (AILI) has an increasing incidence worldwide. However, the mechanisms contributing to such liver injury are largely unknown and no targeted therapy is currently available. The study aimed to investigate the effect of BTF3L4 overexpression on apoptosis and inflammation regulation in vitro and in vivo.

We performed a proteomic analysis of the AILI model and found basic transcription factor 3 like 4 (BTF3L4) was the only outlier transcription factor overexpressed in the AILI model in mice. BTF3L4 overexpression increased the degree of liver injury in the AILI model.

BTF3L4 exerts its pathogenic effect by inducing an inflammatory response and damaging mitochondrial function. Increased BTF3L4 expression increases the degree of apoptosis, reactive oxygen species generation, and oxidative stress, which induces cell death and liver injury. The damage of mitochondrial function by BTF3L4 triggers a cascade of events, including reactive oxygen species accumulation and oxidative stress. According to the available AILI data, BTF3L4 expression is positively associated with inflammation and may be a potential biomarker of AILI.

Our results suggest that BTF3L4 is a pathogenic factor in AILI and may be a potential diagnostic maker for AILI.

Gallstone (GS) disease is common and arises from a combination of genetic and environmental factors. Although genetic abnormalities specifically leading to cholesterol GSs are rare, there are clinically significant gene variants associated with cholesterol GSs. In contrast, most bilirubin GSs can be attributed to genetic defects. The pathogenesis of cholesterol and bilirubin GSs differs greatly. Cholesterol GSs are notably influenced by genetic variants within the ABC protein superfamily, including ABCG8, ABCG5, ABCB4, and ABCB11, as well as genes from the apolipoprotein family such as ApoB100 and ApoE (especially the E3/E3 and E3/E4 variants), and members of the MUC family. Conversely, bilirubin GSs are associated with genetic variants in highly expressed hepatic genes, notably UGT1A1, ABCC2 (MRP2), ABCC3 (MRP3), CFTR, and MUC, alongside genetic defects linked to hemolytic anemias and conditions impacting erythropoiesis. While genetic cases constitute a small portion of GS disease, recognizing genetic predisposition is essential for proper diagnosis, treatment, and genetic counseling.

The correlation between gut, secreted metabolites, and hepatic diseases has strengthened over the last decade. Interactions of intestinal permeability, gut microbes, and derived metabolites influence the development and progression of nonalcoholic fatty liver disease (NAFLD), a prevalent disease that affects more than 30% of the global population. NAFLD is now called metabolic dysfunction-associated steatotic liver disease (MASLD) to better reflect the disease process. Here, we describe mechanisms of NAFLD development, the role of gut bacteria, gut metabolites, interventions for diagnosis, and the prognosis of NAFLD. We discuss new paradigms that challenge the conventional, addressing disease etiology and translational approaches in a new dimension. Previous studies shed light on intricate relationships of the gut microbiome with the liver, or the gut-liver axis. Bidirectional communication between the gut and the liver involves exchange of metabolites, immune signaling, and inflammatory responses that has potential for novel NAFLD/nonalcoholic steatohepatitis (NASH) treatments. In this review, we propose exploring functional metagenomics to develop NAFLD diagnostic methods and risk assessment. The prospects of genetic engineering, fecal transplants, and specialized diet as targets of novel therapeutic regimes to combat NAFLD/NASH are discussed. Changes in lifestyle and diet in the population, combined with genetic predisposition, have led to an increasing number of cases of NAFLD. The microbiome responds to diet, exercise, and the environment, and can modulate NAFLD in cases with surgical impediments. It is thus vital to explore its emerging roles in human healthcare and not only liver disease.

Cancer is a significant global health issue and a primary cause of death. Extensive research has led to the development of various anticancer medications, driven by an improved knowledge and comprehension of the molecular pathways involved in cancer growth. However, there is a need for new approaches to enhance the effectiveness of existing cancer therapies. Dietary phytochemicals have gained increasing attention due to their potential role in tumor prevention. These bioactive compounds derived from plants exhibit a wide range of beneficial effects on human health, including their ability to inhibit carcinogenesis and promote anticancer activities. Examples of dietary phytochemicals with promising properties include vitamin D, vitamin E, lycopene, fisetin, genistein, epigallocatechin gallate, crocetin, curcumin, cyanidins, and gingerol. These compounds often exert their effects by regulating interconnected molecular pathways associated with cancer development and progression. Some of these pathways include the apoptosis pathway, cyclooxygenase-2 pathway, ATP-dependent chromatin remodeling pathway, DNA methylation-epigenetic pathway, Hedgehog signaling pathway, signal transducer and activator of transcription protein-3 pathway, tumor angiogenesis inhibition pathway, and Wnt pathway. This comprehensive review aims to summarize the current knowledge on the role of dietary phytochemicals in tumor prevention, highlighting their mechanisms of action and potential therapeutic applications.