Background: Cervical cancer is a common disease among women. Treatment for cervical cancer includes surgery, radiation therapy, chemotherapy, or a combination of chemotherapy and radiation therapy. Cisplatin is the first-line chemotherapy drug for cervical cancer. Research has shown that about 20% of cervical cancer patients become resistant to chemotherapy, which results in decreased results, tumor recurrence, and poor prognosis. Therefore, researching new drugs, improving the sensitivity of cervical cancer cells to cisplatin, and improving the effectiveness of cervical cancer treatment is the basis of this research. Aim: To investigate the inhibitory effect of curcumin on cisplatin-resistant cervical cancer Hela/DDP and SiHa/DDP cell lines. Materials and Methods: The study utilized cisplatin-resistant cervical squamous carcinoma (SiHa/DDP) and adenocarcinoma (Hela/DDP) cell lines. The cells in the experimental group were treated with 8.5 μM of curcumin, while the control group received only the culture medium. A colony formation assay was conducted to assess cell proliferation, with colonies stained using crystal violet; the number of colonies was then counted and compared between the two groups. Results : 1. In the Hela/DDP cell line, the control group formed an average of 507.7±15.70 colonies, whereas the experimental group, treated with curcumin, formed 112.3±16.17 colonies. The difference between the groups was statistically significant (p < 0.0001). 2. In the SiHa/DDP cell line, the control group had an average of 450.3±17.95 colonies, while the experimental group treated with curcumin had 198.3±13.05 colonies. This difference was also statistically significant (p < 0.0001). Conclusions 1. Curcumin significantly reduces the proliferation of cisplatin-resistant cervical squamous cell carcinoma (Hela/DDP) cells. 2. Curcumin significantly reduces the proliferation of cisplatin-resistant cervical adenocarcinoma (SiHa/DDP) cells.

Background: Lung cancer remains the leading cause of cancer-related mortality worldwide, accounting for approximately 1.8 million deaths annually and representing 18% of all cancer deaths¹. According to the GLOBOCAN 2024 report, 2.4 million new cases were registered globally, ranking second after breast cancer². Non-small cell lung cancer (NSCLC) constitutes 85% of lung cancer cases, with adenocarcinoma being the most common subtype³. The objective of this study is to map the prevalence of HER2 activation and mutations in EGFR, EML4-ALK, ROS1, BRAF, and KRAS genes among lung cancer patients in Mongolia, and to evaluate their correlations with clinical and morphological parameters (age, sex, smoking status, stage, and morphology). Aim: To determine the distribution pattern of HER2 activation and EGFR, EML-ALK, ROS1, BRAF, KRAS gene mutations among patients with lung cancer in Mongolia, and to evaluate their associations with clinical and morphological characteristics. Materials and Methods: A retrospective study was conducted using archived materials from lung cancer patients at the Clinical Pathology, Molecular Genetics, and Pathology Laboratories of the National Cancer Center of Mongolia, covering the period from 2019 to June 2025. DNA Extraction from Tumor Tissue: Formalin-fixed paraffin-embedded (FFPE) tissue blocks from patients diagnosed with lung cancer, stored in the pathology department archives, were selected for the study. Sections of 5–10 μm thickness were cut, mounted on glass slides, stained with hematoxylin and eosin (H&E), and reviewed by a pathologist. Areas containing ≥20–30% tumor cells were identified and macro-dissected for analysis. Real-Time PCR Assay for Detection of EGFR/BRAF/KRAS/EML4-ALK/ROS1 Mutations: EGFR mutation detection was performed using the PANAMutyper™ EGFR Mutation Detection Kit (Panagene, Daejeon, South Korea) according to the manufacturer’s instructions. PCR reactions were carried out on a compatible instrument (Roche LightCycler 480, Germany) as recommended by the manufacturer. Statistical analysis was performed using Prisma-10 software. Results: A total of 282 lung cancer cases were included in the study. EGFR mutations were detected in 44% of cases and were absent in 56%. No significant age-related differences were observed (p=0.2636); however, EGFR mutations were significantly more frequent in females (36.6% vs. 19.6%, p=0.0019). No statistically significant differences were found across disease stage, T, N, or M classifications (p>0.05). No association was identified between smoking status and EGFR mutations (p=0.4178). Morphologically, EGFR mutations were significantly more prevalent in adenocarcinoma (54.83%) compared to squamous cell carcinoma (SCC) (31.8%; p=0.002). Of the 282 cases, adenocarcinoma accounted for 155 (54.9%) and SCC for 116 (41.1%). Overall, EGFR mutations were positive in 43.97% of cases, with a higher prevalence in adenocarcinoma (24.82%) than in SCC (13.1%). By exon: - Exon 18 mutations were detected in 6% of cases, predominantly in adenocarcinoma (6%, 4.25%). - Exon 19 mutations occurred in 8.15% and are associated with sensitivity to targeted therapy. - Exon 20 mutations were found in 3.19%, with the T790M resistance variant in 1.77%. - Exon 21 mutations were observed in 9.57%, more common in adenocarcinoma (9.57%) than in SCC (3.19%). Survival analysis stratified by stage at diagnosis showed significantly longer median survival in early-stage patients (18.6 months). Kaplan-Meier curve comparison, log-rank test, and hazard ratio calculations confirmed statistically significant differences (p < 0.05), indicating that disease stage is a key prognostic factor. Conclusion The study findings reveal a high prevalence of EGFR mutations among Mongolian patients with lung adenocarcinoma, underscoring the need for widespread implementation of targeted therapy (EGFR-TKIs). In contrast, mutation rates were lower in SCC and other morphological subtypes, highlighting the importance of investigating alternative molecular markers in these subgroups.

Background: Globally, gastric cancer accounts for 1,089,000 new cases and 769,000 deaths annually, ranking fifth in overall cancer incidence and third in cancer-related mortality. The aim to determine HER2 expression in patients with gastric cancer and to evaluate its correlation with clinical and immunological biomarkers, as well as the need for further laboratory diagnostics. Aim: To determine HER2 expression in patients with gastric cancer and to evaluate its association with clinical and immunological biomarkers, as well as the potential need for further laboratory diagnostics. Materials and Methods: A retrospective study was conducted using archived materials from patients with gastric cancer at the Clinical Pathology, Molecular Genetics, and Pathology Laboratories of the National Cancer Center of Mongolia, covering the period from 2019 to June 2025. HER2 protein expression in tumor tissue was assessed using immunohistochemistry (IHC), and chromogenic in situ hybridization (CISH-HER2) was employed to confirm gene amplification. Statistical analysis was performed using the Prisma-10 software. Results: In our study, among 210 cases of gastric cancer evaluated by IHC for HER2, 46 (21.9%) were HER2-positive and 164 (78.1%) were HER2-negative. When comparing patients with gastric cancer stratified into HER2 1+ (negative) and HER2 3+ (positive) groups, no statistically significant differences (p < 0.05) were observed in age, sex, tumor location (surgically resected tissue), morphology, or disease stage. However, a higher proportion of males was noted in the HER2 3+ group (80.9%), though this did not reach statistical significance (p = 0.0879). Significant associations were found with tumor markers. Elevated serum CA-72-4 (>5 ng/mL) was more frequent in the HER2 3+ group (58.8%; p = 0.0069). In contrast, elevated CA-19-9 (>35 U/mL) was more common in the HER2 1+ group (93.5%; p = 0.0117), and elevated CEA (>6.9 U/mL) was also predominant in the HER2 1+ group (90.6%; p = 0.002). These findings suggest that HER2 3+ status predominates in cases with elevated CA-72-4, which may influence diagnostic strategies and HER2-targeted therapies (e.g., trastuzumab). Conversely, elevated CA-19-9 and CEA were more associated with HER2 1+ status, indicating a need for further detailed investigation of these markers in relation to HER2 expression. In patients evaluated by CISH for HER2 expression, stratification into HER2-positive and HER2-negative groups revealed no statistically significant differences (p < 0.05) in age, sex, tumor location, morphology, stage, or serum tumor markers (CA-72-4, CA-19-9, CEA). This suggests that HER2 status (positive/negative) may be independent of these variables. Although HER2 positivity was higher in poorly differentiated tumors (48% vs. 30.6% negative; p=0.1414) and in stage IV disease (50% vs. 39.3% negative; p=0.2607), these differences were not statistically significant. Elevated serum markers (CA-72-4, CA-19-9, CEA) were observed but showed no significant correlation with HER2 status. Conclusion Determining the molecular profile of gastric cancer patients can significantly contribute to refining clinical diagnosis, developing treatment strategies, enhancing therapeutic outcomes, and improving patients’ quality of life.