biomarkers

The diagnosis of ulcerative colitis (UC) today is limited to a small number of biomarkers. Trimethylamine-N-oxide (TMAO) is the product of reactions resulting from the degradation of dietary-free choline, phosphatidylcholine, and carnitine metabolism by the intestinal microbiota. Earlier studies showed his involvement in the pathogenesis of UC. To study the association of TMAO with clinical, laboratory, and endoscopic indicators of UC activity.

an observational cross-sectional comparative study was conducted based on the NCJSC “KMU” clinic, Karaganda, Kazakhstan. High-performance liquid chromatography measured TMAO concentration in 63 patients with UC (age Me 37 (30-52) and 38 healthy individuals (age Me 38 (28.5-49.5).

Median TMAO level in patients with UC-0.286 μmol/l was significantly lower than in the control group Me 0.646 μmol/l (p<0.0001). TMAO had significant differences in groups with clinically active and inactive colitis (P=0.003). TMAO correlated with disease activity by Montreal scale (r=-0.389, P=0.002) and severity of attack by Truelove-Witts (r=-0.301, P=0.027 respectively), patient’s age (r=0.377, P=0.003), stool frequency (r=-0.427, P=0.001); laboratory parameters: WBC (r=-0.31, P=0.042), blood albumin (r=0.379, P=0.002) and fecal calprotectin (r=-0.314, P=0.022). TMAO did not differ between groups divided by the extent of the pathological process and endoscopic activity.

in patients with UC, TMAO levels decrease compared with healthy individuals and differences in groups depend on the disease activity. These results give reason to consider changes in TMAO levels as a potential marker of UC and the severity of its course.

 The host defense process against invading bacteria leads to the destruction of the periodontium. Lamin A is an important protein for protecting DNA and preventing premature cell aging. This study investigated the expression of the Lamin A gene in periodontitis patients.

 Using an analytical cross-sectional design, Lamin A gene expression was evaluated in 23 periodontitis patients and 24 healthy individuals referred to the Periodontology Department of Mashhad Dental School and Hekmat Clinic, Mashhad, Iran. Gingival samples were collected, followed by RNA extraction, cDNA synthesis, and real-time PCR. Statistical analyses were conducted using SPSS.

 While the age distribution did not show significant differences between the groups, gender distribution was statistically different. Therefore, the study focuses on comparing Lamin A gene expression levels between the patient and healthy groups, separated by gender. Considering the analysis of 47 gingival tissue samples, the Lamin A gene expression level was higher in healthy participants, with the difference being statistically significant only in female participants (198.45±54.00 in healthy females vs. 143.52±29.29 in periodontitis females).

 These findings suggest that the expression of the Lamin A gene was higher in healthy individuals than in periodontitis patients. More studies are needed to draw more accurate conclusions. If confirmed in larger studies, this protein group might serve as potential biomarkers, enhancing periodontitis assessment strategies.
Keywords:

Colorectal cancer (CRC) holds the position of being the third most prevalent cancer and the second primary cause of cancer-related fatalities on a global scale. Approximately 65% of CRC patients survive for 5 years following diagnosis. Metastasis and recurrence frequently occur in half of CRC patients diagnosed at the late stage. This study used bioinformatics analysis to identify key signaling pathways, hub genes, transcription factors, and protein kinases involved in transforming primary CRC with liver metastasis potential. Prognostic markers in CRC were also identified. 

Experimental approach:

The GSE81582 dataset was re-analyzed to identify differentially expressed genes (DEGs) in early CRC compared to non-tumoral tissues. A protein interaction network (PIN) was constructed, revealing significant modules and hub genes. Prognostic markers, transcription factors, and protein kinases were determined. Boxplot and gene set enrichment analyses were performed. Findings/

This study identified 1113 DEGs in primary CRC compared to healthy controls. PIN analysis revealed 75 hub genes and 8 significant clusters associated with early CRC. The down-regulation of SUCLG2 and KPNA2 correlated with poor prognosis. SIN3A and CDK6 played crucial roles in early CRC transformation, affecting rRNA processing pathways.

Conclusion and implications: 

This study demonstrated several pathways, biological processes, and genes mediating the malignant transformation of healthy colorectal tissues to primary CRC and may help the prognosis and treatment of patients with early CRC.

This research’s comprehensive review and meta-analysis seek to offer additional non-invasive techniques for diagnosing and monitoring liver fibrosis, thereby serving as a dependable resource for clinical practice and scientific investigation.

To find pertinent research on the use of serum YKL-40 levels in liver fibrosis patients, databases including PubMed, Web of Science, WILEY ONLINE LIBRARY, Scopus, Embase, Cochrane Library, Science Direct, CNKI, Wanfang Data, VIP Information, and the China Biology Medicine Library System were searched. The search was conducted up to May 2024.

In studies comparing serum YKL-40 levels in patients with hepatic fibrosis and controls, the overall combined difference was 1.37 (0.66, 2.08), with the Chinese subgroup showing high heterogeneity, while the Egyptian study did not show heterogeneity. A total of 17 studies, including 2554 patients, were included. The combined sensitivity for diagnosing advanced fibrosis and severe fibrosis was 0.80 and 0.78 respectively, with specificities of 0.88 and 0.82. The AUC for advanced fibrosis and severe fibrosis were 0.91 and 0.87 respectively.

Serum YKL-40 shows potential value in diagnosis of liver fibrosis, but further clinical research is needed to confirm and improve its utility.

Colorectal cancer (CRC) is one of the leading causes of death worldwide and is increasingly recognized as a heterogeneous disease at the molecular level. The autophagy-related 5 ( ATG5 ) and light chain 3 ( LC3B ) genes are involved in the autophagy pathway and play crucial roles in physiological processes, including adaptation to starvation, prevention of neurodegeneration, expression of intracellular antigens, and tumor suppression.

This study aimed to elucidate the epigenetic alterations in the ATG5 and LC3B genes and analyze the polymorphism of ATG16L1 in CRC.

This case-control study included 320 blood samples divided into case and control groups, comprising 160 CRC samples and 160 healthy samples. Restriction fragment length polymorphism (RFLP) was used to genotype the ATG16L1 (Thr300Ala) polymorphism, while methylation-specific PCR (MS-PCR) was employed to assess promoter methylation of the ATG5 and LC3B genes. Logistic regression was used to compare methylation patterns and genotypes between case and control groups. Additionally, the chi-square test was applied to compare demographic variables between groups.

The data analysis revealed a significant difference in the methylation patterns of ATG5 and LC3B between the case and control groups. The promoter methylation status of the LC3B gene candidate region exhibited a lower methylation pattern in the case group (37.3%) compared to the control group (69.4%) (P < 0.001). Conversely, the ATG5 gene promoter showed higher methylation levels in the case group (80.8%) than in the control group (43.8%) (P < 0.001).

This study analyzed methylation changes in the ATG5 and LC3B genes in CRC patients. The findings suggest that alterations in the promoter methylation patterns of ATG5 and LC3B play significant roles in the pathogenesis of CRC. Additionally, the mutant genotype of ATG16L1 rs2241880 may increase susceptibility to CRC.

Researchers have successfully developed and validated diverse loading strategies, utilizing both endogenous and exogenous approaches, in laboratory and animal models, showcasing their effectiveness in advancing molecular biology research. Extracellular vesicles have advantages over synthetic carriers in disease management and therapeutics. However, their clinical application is hindered by challenges such as limited specificity, low production yield, storage stability, and targeting capability. Addressing these challenges and exploring exosome engineering techniques is crucial. Cell-derived exosomes can serve as carriers for therapeutic molecules, enabling targeted drug delivery. Understanding exosome formation and developing efficient engineering methods are essential for advancing clinical therapeutic strategies. Exosomes offer a unique approach to targeted drug delivery through intercellular communication. These natural liposomes carry endogenous biomolecules, ensuring biocompatibility and allowing for cargo loading. Genetic or chemical modifications can improve targeting and drug loading capabilities. Importantly, exosomes have weak interactions with serum proteins, extending the lifespan of the cargo. By combining the capabilities of artificial nanocarriers and intercellular signaling, exosomes provide new and reliable strategies for drug administration and medical interventions. This review examines diverse exosome types, preparation methodologies, cargo encapsulation, and their efficacy in delivering therapeutic agents across different diseases. It also highlights global companies involved in the development and testing of exosome-based therapies.

 Breast cancer (BC) can be categorized into 4 groups based on molecular and pathological evidence: Luminal A, Luminal B, HER2+ tumors, and triple-negative breast cancer (TNBC). TNBC has a poorer survival rate and a higher chance of recurrence and metastasis compared to other BC types, primarily due to its challenging treatment course. Claudin 4 (CLDN4), a transmembrane protein in tight junctions between cells, has been linked to poor prognosis and faster disease progression in these malignancies.

Patients previously diagnosed with TNBC and tested for CLDN4 overexpression were contacted for follow-up and to determine disease outcomes. The current health status, cause, and time of death (if applicable) were recorded. Patient files were accessed to obtain information on age, tumor size and grading, lymph node involvement, metastasis, Ki67, and CLDN4 expression.

Patients with high CLDN expression showed a significantly lower mortality rate. However, after controlling for other covariates, the hazard ratio (HR) was 0.48 (95%CI= [0.13 – 1.27]) in the crude model for survival, 0.54 (95%CI = [0.2 – 1.43]) when adjusted for age at diagnosis, and 0.58 (95%CI = [0.18-1.82]) when adjusted for other covariates. CLDN4 was also not correlated with tumor metastasis (HR=0.64, p=0.203, in the crude model; HR=0.52, p=0.409, when adjusted for other covariates). Patients in the CLDN4 high group had a significantly higher number of tumors >2cm.

Although previous studies have shown that CLDN4 overexpression worsens TNBC prognosis and increases metastasis or recurrence, the current study found no such association.

Recent evidence has shown that peripheral blood mononuclear cells (PBMCs) can reflect the epigenetic profile of tissues they interact with, such as malignant cells. The hypermethylation of MLH1 promoter is a well-defined epigenetic alteration in the development of colorectal cancer (CRC). This is the first study aimed to assess the diagnostic and prognostic values of the methylation level of MLH1 promoter in PBMCs of patients with CRC. In this case-control study, the methylation level at the promoter region of MLH1 was quantitatively analyzed in 60 CRC patients and 60 non-cancerous study participants via methylation-quantification of endonuclease-resistant DNA (MethyQESD). The receiver operating characteristic (ROC) curves were constructed and the areas under the curve were calculated to determine the diagnostic significance of MLH1 gene methylation. Our data showed a significant increase in methylation of MLH1 in CRC patients compared with healthy participants (P < 0.001). Moreover, the specificity of MLH1 hypermethylation for precise diagnosis of healthy participants was 75% and its sensitivity for CRC diagnosis was 76.7%. With ROC curve analyses, we found that MLH1 promoter methylation holds a likelihood of 76.8% for distinguishing between CRC patients and healthy individuals (P > 0.001). Besides, MLH1 methylation levels was significantly increased in CRC patients with higher tumor stages, suggesting a probable correlation between an increased percentage of methylation and tumor progression (P < 0.001). However, no statistically significant association was found between methylation status of MLH1 and microsatellite instability (P > 0.05). Our results propose that MLH1 methylation status in PBMCs can be used as a promising diagnostic and prognostic biomarker and reliable factor for CRC screening.

Red blood cell Distribution Width (RDW) can help diagnose blood diseases and predict mortality in heart disease. Fatigue is one of the common symptoms of Acute Myocardial Infarction (AMI) and can affect the quality of life of patients. This study aimed to investigate the link between RDW at admission and fatigue severity 2 weeks after AMI.

This cross‑sectional study examined 250 consecutive patients with AMI during 2023–2024. The patients were assessed for RDW and other laboratory and demographic variables within 24 h of admission. The Fatigue Severity Scale (FSS), which is a 9‑item and 7‑point scale, was completed for patients. A score >36 was considered as Post‑AMI Fatigue (PAF) and lower as non‑PAF. Data analysis was performed by SPSS version 22 and R version 4.2.2 software.

Our findings indicated that 71.20% of patients experienced fatigue after AMI. There were no significant differences between age, gender, laboratory parameters, past medical history, underlying diseases, and blood pressure of patients with and without fatigue (p > 0.05). RDW distribution for non‑PAF and PAF was 13.30% [12.50, 14.60%] and 13.30% [12.80, 14.00%], respectively, (p = 0.726). Multivariable regression results based on three models did not show any significant findings.

The present study is the first study, designed to determine the predictive value of RDW on post‑AMI fatigue, as far as we searched the recent literature. We did not find any significant relation between RDW and PAF. Therefore, it cannot be used to predict fatigue in patients with AMI until definitive results are found.

Welding is a process to connect different parts using various techniques. In industrial settings, shielded metal arc welding (SMAW), gas metal arc welding (GMAW), and tungsten inert gas welding (TIG) are the most common types of electric arc welding. In all these procedures, welders are exposed to a range of hazards such as gases and fumes that may affect their pulmonary function and oxidative stress status. This case-control study was conducted to investigate lipid peroxidation, oxidative stress, and pulmonary function status in industrial welders.

Case participants worked in one of three types of welding (SMAW, GMAW, TIG) (52 men), and control participants (40 men) were not exposed to welding hazards. Blood biomarkers MDA and TAC were evaluated to determine antioxidant levels, and FVC, FEV1, and FEV1/FVC indices were considered for pulmonary function.

The results showed that there was a significant difference in the levels of MDA, FVC, and FEV1 between the welders and the control group, but no significant difference was observed in the levels of TAC. It seems that among welder groups, the mean levels of MDA, FVC, and FEV1 in SMAW welders were significantly different compared to the other groups. Finally, MDA had a significant relationship with all pulmonary indices, and FVC had a significant relationship with all biomarkers of oxidative stress and other pulmonary functions.

The findings show that occupational exposure to welding hazards in different types of welding may affect oxidative stress and pulmonary function indices.

This systematic review and meta-analysis summarized the studies that evaluated the effects of acceptance and commitment therapy on biological measures in Iranians with type 2 diabetes. In addition, the study determined the combined effect size of the varying effect sizes observed in various studies.

A systematic search of Iranian scientific databases, including insane.ir, Magiran, SID, Noormags, and ISC, from 2013 to 2023, retrieved randomized controlled trials that evaluated the effects of acceptance and commitment therapy on biological measures in type 2 diabetes. The study was conducted based on the main PRISMA reporting guideline (the PRISMA 2020 statement), and a meta-analysis report was generated by reviewing the studies that met the inclusion criteria.

Among the 26 studies, 10 were deemed suitable for inclusion based on the PRISMA statement, while the remaining 16 were excluded. The effect size of acceptance and commitment therapy on the biological markers in type 2 diabetes was 0.767, indicating a significant effect. The average effect sizes for fasting blood glucose (FBS), 2-hour postprandial glucose (2HPP), and glycosylated hemoglobin (HbA1c) were 0.798, 0.586, and 0.711, respectively. These effect sizes suggest a significant effect for FBS, a relatively strong impact for 2HPP, and a strong effect for HbA1c.

Acceptance and commitment therapy significantly improve the biological measures of patients with type 2 diabetes. Furthermore, its impact on FBS and HbA1c indices exceeds that of HPP2.

Epilepsy is a prevalent disease worldwide which affects 1% of the global population, making it the fourth most common disease. The primary category of epilepsy, psychogenic nonepileptic seizures (PNES), can lead to significant time and financial burdens if not promptly diagnosed. Diagnosing epileptic seizures (ES) can be complex, with video electroencephalography (VEEG) monitoring, history taking, and interviews being the most effective methods. However, VEEG is costly and not always accessible.This study aimed to develop a cost-effective diagnostic approach using transcranial magnetic stimulation (TMS)-derived indicators. The motor threshold (MT), a key brain and spinal cord excitability indicator, differentiated ES from PNES. The study compared 24 patients with ES, 24 patients with PNES, and 24 healthy individuals in the control group, all aged between 31-57 years. The mean MT for individuals with ES and those with PNES was the same (73.5%), and there was no significant difference in the mean MT between the two groups of patients and individuals without any medical conditions (P > 0.05). The findings indicated that VEEG remained the preferred method for diagnosing various forms of epilepsy, particularly PNES. The MT derived from TMS and the general assessment of motor cortex excitability may not be a suitable diagnostic criterion for distinguishing ES from PNES.

Timely treatment actions are critical for the early detection of sepsis in patients at high risk of acute kidney injury (AKI). This study aimed to investigate inflammatory biomarkers as potential predictors of AKI in patients with sepsis.

This prospective observational cohort study included 300 patients who received treatment in the Intensive Care Unit (ICU) of hospitals located in Padang, Indonesia. We obtained blood samples to evaluate inflammatory biomarkers, such as interleukin-6 (IL-6), tumor necrosis factor-a (TNF-a), and procalcitonin (PCT). AKI development was predicted using multivariate logistic regression analysis to identify independent inflammatory biomarkers.

IL-6, TNF-α, and PCT levels were markedly elevated in patients who developed AKI compared with those who did not (p < 0.001). The multivariable logistic regression analysis showed that IL-6 (OR = 1.82; 95% CI = 1.25-2.66; p = 0.002) and PCT (OR = 2.45; 95% CI = 1.58-3.80; p < 0.001) can both predict the development of AKI in patients with sepsis. The area under the curve (AUC) for IL-6 was 0.70, whereas the AUC for PCT was 0.81. These findings demonstrate that IL-6 and PCT exhibit strong predictive abilities for the onset of AKI in patients with sepsis. The ideal threshold values for IL-6 and PCT were 12.91 pg/mL and 1.79 ng/mL, respectively.

IL-6 and PCT can serve as inflammatory biomarkers for predicting the occurrence of AKI in patients with sepsis.

The literature on the potential protective role of serum bilirubin levels in the development of Acute Exacerbation of Chronic Obstructive Pulmonary Disease (AECOPD) has produced conflicting findings. This study aimed to investigate the potential relationship between serum total and direct bilirubin levels and the risk of acute exacerbation in COPD.  Over a period of 18 months, a total of 99 patients were recruited from two major hospitals in Mashhad, Iran, comprising 49 individuals with stable COPD and 50 with AECOPD. After obtaining informed consent and conducting a comprehensive medical history and physical examination, both groups underwent an assessment of various laboratory indices, such as total and direct bilirubin levels. Appropriate statistical analysis was applied to assess the potential associations between bilirubin concentrations and the risk of AECOPD.  The study population had a mean age of 64.97±10.12 years, and there was no significant difference in gender distribution (p=0.546). The majority of subjects (55.6%) were male. The serum levels of AST and ALT were significantly higher in the AECOPD group (p<0.001). Additionally, although there were no significant differences in total bilirubin levels between the two groups (p=0.323), there was a significantly higher level of direct bilirubin in the AECOP group (p<0.001).  Serum direct bilirubin levels were higher in COPD patients with acute exacerbation. It may be an independent biomarker for screening the COPD patients with and without acute exacerbation. Further studies are required to validate the findings.

Peri-implantitis is implant-associated inflammation that leads to irreversible loss of surrounding bone. Early diagnosis increases the success of peri-implantitis treatment. Despite various studies associated with this most common complication, early detection of the onset of peri-implantitis remains a major challenge. Molecular biomarkers are applicable detectors for the early detection of numerous diseases and monitoring their development. The present study aimed to predict interactome networks of up/down regulated proteins and analyze drug-gene interaction in peri-implantitis to identify the diagnostic and druggable genes.

In this in silico study, a suitable gene expression profile related to peri-implantitis was retrieved from Gene Expression Omnibus. Screening differentially expressed genes (DEGs) was carried out based on the cut-off criteria |log2 (fold change)|>2 and P < 0.05. Interactome networks were constructed and analyzed by the STRING database (Version: 12.0) and the Cytoscape software (version: 3.9.1). Finally, to investigate drug-gene interaction, detected hub genes were analyzed by DGIdb (version: 5.0.6).

A total of 216 genes were identified as DEGs (129 down-regulated and 87 up-regulated genes) in peri-implantitis. Regarding Cytoscape analysis, FCGR3B, CSF3R, AQP9, TREM1, and P2RY13 were the top 5 hub nodes of up-regulated DEGs, and CXCL10, OASL, IFIT1, RSAD2, and ISG15 were the top 5 hub nodes of down-regulated DEGs. Among these key nods, AQP9, CSF3R, CXCL10, IFIT1, ISG15, OASL, and, FCGR3B were therapeutic targets and had approved drugs.

In this research, seven genes have been identified as druggable genes in peri-implantitis which can be used to treat and diagnose this disease. However, these results and identified genes need to be validated by clinical or experimental methods. Key Words: Biomarkers, gene expression, peri-implantiti

Breast cancer is the most common malignancy among women and a leading cause of cancer-related mortality. Early detection is crucial for improving treatment outcomes. This study investigates the roles of lysophosphatidic acid (LPA) and autotaxin (ATX) in the early diagnosis of breast cancer among Iraqi women. A case-control study was conducted involving 75 women diagnosed with breast cancer and 75 healthy controls. Blood samples were collected, and biochemical parameters, including LPA and ATX levels, were measured using the ELISA technique. Statistical analyses were performed with SPSS version 24, and receiver operating characteristic (ROC) analysis was used to evaluate diagnostic capabilities. The majority of breast cancer patients were aged 50-59 years (33.3%). Histologically, invasive ductal carcinoma was the most prevalent subtype (82.6%). Biochemical analysis revealed significant differences in alanine aminotransferase, total serum bilirubin, and alkaline phosphatase levels between patients and controls. LPA levels were significantly elevated in the patient group (868.48±142.11 pg/ml) compared to controls (212.01±54.94 pg/ml), while ATX levels were also higher (2252.20±399.46 pg/ml vs. 951.40±209.21 pg/ml). ROC analysis indicated that both LPA and ATX exhibited high diagnostic sensitivity (98%) and specificity (100%). In Iraqi women, elevated serum levels of LPA and ATX may serve as potential diagnostic biomarkers for breast cancer, highlighting their role in disease progression. Further studies are warranted to explore their clinical applications in breast cancer diagnosis and management.

Mitochondrial metabolism disruption increases neuron excitability and reduces migraine attack threshold. This study investigates whether serum fibroblast growth factor-21 (FGF-21) levels in chronic migraine relate to headache severity and response to sodium valproate treatment. This pilot study involved 30 patients with chronic migraine treated with sodium valproate. Serum FGF-21 levels were assessed at baseline and after 12 weeks of treatment. Pain severity and disability were evaluated using visual analogue scale (VAS) and Migraine Disability Assessment (MIDAS). Paired t-test was used for the quantitative variables. The qualitative variables were evaluated using Pearson’s chi-square test and Fisher’s exact test. Moreover, correlation coefficients were calculated. A P < 0.05 was considered statistically significant. Mean age of the patients was 42.9 ± 11.3 years. There was a significant reduction in headache severity between baseline and the end of the study regarding VAS scores (8.50 ± 1.50 vs. 5.30 ± 2.20, P < 0.001). The same reduction was observed in MIDAS during the study (61.20 ± 33.20 vs. 20.31 ± 17.07, P < 0.001). However, there was no significant changes in serum levels of FGF-21 over three months (299.53 ± 479.80 vs. 491.33 ± 456.64, P = 0.810), nor any relationship between these levels and headache severity scores (MIDAS: P = 0.658, VAS: P = 0.708). The results of this study did not show a significant correlation between FGF-21 serum levels and changes in VAS and MIDAS throughout the study. Further research on various mitochondrial pathways can provide valuable insights into the migraine pathophysiology and help identify more effective biomarkers for monitoring therapeutic regimens.

Endometriosis (EM) is a condition that causes infertility with decreasing uterine receptivity. It is reported that it affects about 20-25% of all infertile women. Some genetic markers play a crucial role in pathogenesis and infertility.

This study investigates the role of miR-200a and miR-223-3p in embryo implantation and their association with EM-related infertility.

In this case-control study, 36 women who referred to the Center for Research on Reproductive Health and Infertility of Babol University of Medical Sciences and Fatemeh Al-Zahra Infertility Specialized Treatment Center in Babol, Iran between June 2022 and July 2023 were evaluated. Participants were divided into 2 EM and control groups (n = 18/each). Endometrial samples were collected from participants between 17th and 24th days of their menstrual cycle. Histopathological examination (hematoxylin and eosin and periodic acid schiff) was performed to confirm the secretory stage, and miR-200a and miR-223-3p expressions were analyzed by quantitative reverse transcriptase-polymerase chain reaction.

Histological analysis confirmed that both groups were in the secretory stage. Additionally, miRNA expression results showed a significant decrease in the miR-200a and miR-223-3p expression levels in EM group compared to control group. The expression level of miR-223-3p and miR-200a in the eutopic endometrial tissue of women with EM was notably lower than those in the control group.

Our results suggest that miR-200a and miR-223-3p are involved in the EM pathogenesis, while other genes and signaling pathways are probably involved in the implantation failure.

Context: 

Colorectal cancer (CRC) is one of the most common causes of cancer-related deaths worldwide, particularly in developed countries. Despite advances in detection and treatment, CRC remains difficult to diagnose in its early stages, complicating patient outcomes. Recently, long non-coding RNAs (lncRNAs) have emerged as significant regulators in cancer biology, offering new opportunities for cancer diagnostics.

Evidence Acquisition: 

This review highlights the molecular mechanisms through which LncRNA ROR influences CRC development, its diagnostic potential as a biomarker, and the future challenges of integrating LncRNA ROR into clinical practice.

Future research must focus on large-scale validation studies and explore the therapeutic implications of targeting LncRNA ROR.

Overall, this review positions LncRNA ROR as a promising biomarker with potential applications in both CRC diagnosis and treatment.