Background: Mongolia has the highest incidence of liver cancer worldwide, largely driven by a high prevalence of hepatitis virus infections. Mutations in oncogenes and tumor suppressor genes provide valuable insights into the molecular mechanisms of hepatocellular carcinoma (HCC). Aims: This study aimed to investigate the prevalence of mutations in key oncogenes and tumor suppressor genes in Mongolian HCC patients and to explore their molecular mechanisms, particularly in relation to hepatitis virus infections. Methods and Results: We analyzed 55 tumor tissue samples from Mongolian HCC patients (2019–2021), identifying mutations in TP53 , CTNNB1 , AXIN1 , KRAS , and JAK1 through sequencing. Western blotting was used to assess β‐catenin and p53 protein levels. Our findings showed p53 overexpression in tumors with TP53 mutations (F270I and S362S), while mutations such as R213* and a short‐sequence deletion upstream of intron 7 produced premature stop codons, resulting in truncated p53 and loss of tumor suppressor function. β‐catenin accumulation was observed in tumors with CTNNB1 mutations (D32N/Y, S33C/Y, S34V, S37P, T41A, and S45P). CCND1 expression, a key target of the Wnt/β‐catenin pathway, was significantly upregulated in tumors harboring CTNNB1 and AXIN1 mutations ( p = 0.02213). Statistical analysis revealed a positive correlation between β‐catenin and CCND1 expression levels ( r = 0.42703). Hepatitis virus infections were significantly associated with these mutations ( p < 0.01), suggesting a link between viral infection and genetic alterations in HCC development. Compared to TCGA data, our cohort displayed a significantly higher mutation frequency ( p < 0.001 and p < 0.05), indicating potential regional genetic and environmental influences. Conclusion: This study provides insights into the molecular mechanisms of HCC in Mongolia, highlighting distinct mutational patterns in TP53 , CTNNB1 , AXIN1 , and KRAS . The association between hepatitis virus infections and these mutations underscores their potential oncogenic impact and may inform future therapeutic strategies for HCC in this population.

Post-translational modification (PTM) is a vital biological process significantly impacting protein structure and function. It involves adding functional groups to the main and side chains during and after protein synthesis, thereby modifying their structure and function. PTMs are essential in shaping proteins into their final, functional, and three-dimensional forms. While numerous PTMs are still under active investigation and exploration. Herewith, we briefly overview some of the most prevalent PTMs, elucidate their associated functions, and establish connections between PTMs and a diverse range of diseases. Notably, we elucidate the profound influence of PTMs on neurodegenerative diseases and cancer, and provide a deep understanding of their many effects. Lastly, it considers a concise overview of PTM computational methods and databases, shedding light on the cutting-edge techniques and resources used to analyze and explore post-translational modifications. Трансляцийн дараах өөрчлөлтийн молекул механизм ба түүний зарим өвчлөлд үзүүлэх нөлөө Хураангуй. Трансляцийн дараах өөрчлөлт (ТДӨ) нь уургийн нийлэгжлийн үед, эсвэл нийлэгжлийн дараа уургийн гол болон хажуугийн гинжинд функциональ бүлэг нэмэх замаар уургийн бүтэц болон үйл ажиллагаанд нөлөөлдөг биологийн чухал үйл ажиллагааны нэг юм. Маш олон тооны ТДӨ-үүд судлагдсаар байгаа бөгөөд энэхүү тойм өгүүлэлд бид хамгийн түгээмэл арван ТДӨ-үүд болон тэдгээрийн үйл ажиллагааны талаар авч үзэв. Үүнээс гадна ТДӨ нь төрөл бүрийн өвчин, эмгэгтэй холбоотой байдгаас түгээмэл тохиолддог тархи, мэдрэлийн эмгэгүүд болон хавдрын биологийн үйл ажиллагаанд ТДӨ хэрхэн нөлөөлж байгаа талаар, түүнчлэн ТДӨ-ийн судалгааны аргууд болон мэдээллийн сангийн тухай тоймлон танилцуулав.Түлхүүр үгс: уургийн өөрчлөлт, уураг-уургийн харилцан үйлчлэл, ТДӨ-ийн мэдээллийн сан

Background/Objectives: Advanced maternal age (≥35 years) significantly increases the risk of fetal chromosomal abnormalities, particularly trisomies 21, 18, and 13. Non-invasive prenatal testing (NIPT) based on cell-free fetal DNA (cffDNA) in maternal plasma has substantially improved the accuracy and safety of prenatal screening. Methods: We previously developed and clinically validated a multiplex droplet digital PCR (ddPCR)-based NIPT assay for detecting fetal trisomies 21, 18, and 13 in Mongolia. The assay targeted specific loci on chromosomes 21, 18, and 13, using chromosome 1 as an internal reference. A Z-score threshold >3 indicated high risk, and all positive results were confirmed by invasive karyotyping. Results: In this study we collected 74 pregnant women of advanced maternal age and samples were successfully analyzed, with high technical performance (mean >100,000 accepted droplets per reaction and clear signal separation). Ten high-risk pregnancy cases were identified (8 trisomy 21 and 2 trisomy 18), all of which showed complete concordance with confirmatory karyotyping. Complete concordance with available reference standard results were observed in this limited cohort. No trisomy 13 cases were detected. Conclusions: This ddPCR-based NIPT assay exhibited excellent diagnostic accuracy and reproducibility in a Mongolian cohort of advanced maternal age pregnancies. Its technical simplicity, relatively low cost, and minimal infrastructure requirements make it a promising tool for implementation in resource-limited settings. However, the small sample size limits generalizability, and larger multicenter studies are needed to confirm clinical utility across broader populations, including low-risk pregnancies.

Background/Objectives: Advanced maternal age (≥35 years) significantly increases the risk of fetal chromosomal abnormalities, particularly trisomies 21, 18, and 13. Non-invasive prenatal testing (NIPT) based on cell-free fetal DNA (cffDNA) in maternal plasma has substantially improved the accuracy and safety of prenatal screening. Methods: We previously developed and clinically validated a multiplex droplet digital PCR (ddPCR)-based NIPT assay for detecting fetal trisomies 21, 18, and 13 in Mongolia. The assay targeted specific loci on chromosomes 21, 18, and 13, using chromosome 1 as an internal reference. A Z-score threshold > 3 indicated high risk, and all positive results were confirmed by invasive karyotyping. Results: In this study, we collected 74 pregnant women of advanced maternal age and samples were successfully analyzed, with high technical performance (mean > 100,000 accepted droplets per reaction and clear signal separation). Ten high-risk pregnancy cases were identified (eight trisomy 21 and two trisomy 18), all of which showed complete concordance with confirmatory karyotyping. Complete concordance with available reference standard results were observed in this limited cohort. No trisomy 13 cases were detected. Conclusions: This ddPCR-based NIPT assay exhibited excellent diagnostic accuracy and reproducibility in a Mongolian cohort of advanced-maternal-age pregnancies. Its technical simplicity, relatively low cost, and minimal infrastructure requirements make it a promising tool for implementation in resource-limited settings. However, the small sample size limits generalizability, and larger multicenter studies are needed to confirm clinical utility across broader populations, including low-risk pregnancies.

Mongolia has the highest liver cancer incidence in the world, primarily attributed to hepatitis virus infections and the prevalence of liver diseases. The predominant focus in existing studies involved the detection of virus infections, and immunization against HBV, with HBsAg serving as a primary marker. In this study, blood donation samples were evaluated, which were positive for HBV and negative for HCV, HAV, HIV, and syphilis by ELISA test at the National Center for Transfusion Medicine (NCTM) of Mongolia. Furthermore, titer determination was performed by reverse passive hemagglutination (PHA) assay, and the antigen serotype was identified on an isolated HBsAg. Our result showed that, among 83 HBV-positive blood plasmas, 10 exhibited a high HBsAg titer, and the serotypes ayr and ayw were identified. The samples were categorized into groups A and B, and to analyze HBsAg reliability, the prototype models were assembled using HBsAg isolated from the high antigen yield group (A). As a result, the prototype models were stable in 3 months, but the sensitivity and specificity of the antigen were weaker compared to its standard. Хепатитийн B вирус (HBV)-ийн халдвартай хүний цуснаас HBsAg ялган, серотипийг тодорхойлсон дүн Хураангуй. Монгол улсын хүн амын дундах хепатитийн вирусийн халдвар болон вирусийн шалтгаант элэгний өвчлөлийн тохиолдол дэлхийд тэргүүлэх байранд байдаг. Олон улсад хепатитийн B вирус (HBV)-ийн оношилгоо болон дархлаажуулалтын судалгаанд гадаргуугийн эсрэгтөрөгч (HBsAg)-ийг өргөнөөр ашигладаг. Бид манай Цус сэлбэлт судлалын үндэсний төв (ЦССҮТ)-д цуглуулсан HBV-ийн халдвартай 83 донорын цусны ийлдэс дэх HBsAg-ийн илэрцийг тогтоон, эсрэгтөрөгчийн илэрц өндөр 10 дээжийг А болон Б бүлэгт ангилан HBsAg-ийг ялгаж, тус бүрд ayr болон ayw серотипүүдийг тодорхойлсон. Улмаар эсрэгтөрөгчийн агууламж өндөр А бүлгээс ялган авсан бөмбөлөг ба утаслаг эсрэгтөрөгчийг ашиглан прототип загварыг гарган авч шинж чанарыг тодорхойлоход тэдгээрийн тогтвортой байдал сайн хэдий ч мэдрэг болон өвөрмөц чанар нь стандарт эсрэгтөрөгчтэй харьцуулахад сул болохыг тогтоов. Энэ нь бидний судалгаагаар ayr болон ayw серотип бүхий эсрэгтөрөгч илэрсэнтэй хамааралтай байх боломжтой. Түлхүүр үгс: серотип, эсрэгбиеийн таньц, прототип загвар

The expression of p53 and beta-catenin proteins in hepatocellular carcinoma (HCC) samples with mutations in the tumor suppressor TP53 gene, which has a high frequency of mutations in liver cancer, and the CTNNB1 gene, which plays an important role in the Wnt signaling pathway, were identified. As a result, the beta-catenin protein was increased in 83.33% of liver tumor samples with CTNNB1 gene mutation, and p53 protein expression was increased in 50% of samples with TP53 gene mutation. According to this, it may be that liver tumors were caused by changes in p53 and beta-catenin protein expression. Элэгний хорт хавдрын эсийн p53, бета-катенин уургийн экспресс Элэгний хорт хавдрын мутацийн өндөр давтамжтай тохиолддог хавдар дарангуйлагч ТР53 ген болон Wnt дохиоллын замд чухал үүрэгтэй оролцдог CTNNB1 генийн мутаци илэрсэн элэгний хавдрын дээжүүдэд уургийн (p53, бета катенин) нийлэгжлийг вестерн блотын аргаар судлав. Судалгааны дүнд CTNNB1 генийн мутацитай элэгний хавдрын дээжүүдийн 83.33%-д бета-катенин уураг, ТР53 генийн мутацитай дээжүүдийн 50%-д р53 уургийн нийлэгжил тус тус нэмэгдсэн байв. Үүнээс үзэхэд p53 болон бета-катенин уургийн нийлэгжлийн өөрчлөлтөөр элэгний хавдар үүссэн байх магадлалтай. Түлхүүр үгс: мутаци, хавдар, вестерн блот