Objective: This study aimed to evaluate the relationship between tumor protein (P53), glutathione peroxidase (GPx), Super oxide dismutase (SOD), cancer antigen (CA15-3) in breast cancer, as well as the impact of variables such as age, location, duration of Illness, and kind of therapy. Methodology: This case-control study carried out between November 2024 to April 2025, at Sadr Teaching Hospital, Oncology Department and Al-Zubair General Hospital, Basrah, Iraq. A total of 178 participants were chosen as a sample; we chose 89 breast cancer patients as cases and 89 healthy individuals as controls. We measured the levels of P53, GPx, SOD, CA15-3. Results: The study revealed significant differences in P53 levels between patients and healthy controls (P<0.001), associated with age, geographic location, and treatment type, while GPx levels were decreased in patients. No significant differences were observed in SOD or CA15-3 levels. Factors such as geographic location, treatment type, and disease duration had no significant impact on the measured concentrations. Additionally, positive correlations were found between P53 and GPx1, as well as between GPx1 and SOD. Conclusion: Age is a major risk factor for breast cancer. The decreased levels of P53 and GPx1 indicate the role of oxidative stress, highlighting the need to investigate biomarkers and genetic factors to improve disease understanding and management. No significant differences were observed in the other variables.

Background: Breast cancer is the most prevalent cancer globally and a major public health challenge in low and middle-income countries (LMIC) like Pakistan. Despite advances in treatment, poor adherence to chemotherapy remains a concern, affecting survival, recurrence and quality of life. Adherence is influenced by individual, social, cultural and systemic factors. Objective: This review uses the WHO-Multidimensional Adherence Model (WHO-MAM) to identify key factors influencing chemotherapy adherence among breast cancer patients in LMICs. It aims to highlight underexplored domains particularly behavioural and cultural influences and suggest directions for targeted interventions and policy development. Methods: This scoping review was conducted using literature published between 2019 and 2025, sourced from PubMed, Scopus and Google Scholar. A total of 51 full-text articles were reviewed, 20 articles were included based on relevance to chemotherapy adherence and applicability to LMIC settings. Key Findings: Chemotherapy adherence is influenced by socioeconomic barriers (e.g., financial constraints, low education), healthcare system limitations (e.g., poor provider communication, limited oncology access), and treatment-related challenges (e.g., side effects). Patient-related factors such as mental health, perceived stigma, and cultural beliefs are significant but underexplored, especially in South Asia. Conclusion: Improving chemotherapy adherence requires patient-centred, culturally informed strategies and health system reforms. Greater attention to behavioural and cultural factors is essential for designing interventions that are both practical and effective in LMIC settings.

Background: Epithelial ovarian carcinoma (EOC) remains one of the most fatal gynecologic cancers, often presenting at an advanced stage and prone to frequent recurrence despite aggressive treatment. Identifying reliable prognostic biomarkers is essential for improving patient stratification and optimizing adjuvant treatment strategies. This study investigated the expression patterns of programmed death-ligand 1 (PD-L1) and CD44, a recognized cancer stem cell (CSC) marker, and examined their relationships with clinicopathological features, recurrence risk, and survival outcomes in EOC. Methods: A retrospective study was performed involving 90 patients with histologically confirmed EOC managed at National Cancer Institute, Cairo University. Immunohistochemistry was utilized to assess PD-L1 and CD44 expression in tumor samples. The associations between biomarker expression, clinical and pathological variables, recurrence-free survival (RFS), and overall survival (OS) were analyzed using Kaplan–Meier survival curves, multivariate logistic regression, and Cox proportional hazards models. Results: PD-L1 was expressed in 42.2% of tumors and showed significant associations with advanced International Federation of Gynecology and Obstetrics (FIGO) stage (p=0.017), higher tumor grade (p=0.004), presence of distant metastasis (p=0.002), and increased recurrence rates (p<0.001). CD44 positivity was identified in 71.1% of cases, predominantly among serous carcinoma subtypes (p=0.010), and was likewise linked to a higher recurrence risk (p<0.001). Patients with PD-L1-positive tumors exhibited a notably shorter median RFS compared to PD-L1-negative patients (31.3 vs. 54.7 months, p<0.001), as did CD44-positive individuals relative to their CD44-negative counterparts (36.3 vs. 56.7 months, p<0.001). Neither biomarker, however, demonstrated a statistically significant effect on OS during a median follow-up of approximately five years. Notably, patients with concurrent PD-L1 and CD44 expression experienced the poorest RFS outcomes (mean 30.9 months), while those negative for both markers showed the most favorable prognosis (mean 56.6 months, p<0.001). Multivariate analysis confirmed PD-L1 (OR 4.86, p=0.003) and CD44 (OR 9.61, p=0.006) as independent predictors of recurrence. Conclusions: The expression of PD-L1 and CD44 in EOC is independently associated with an elevated risk of disease recurrence, and their co-expression identifies a particularly high-risk patient subset. Although neither marker significantly influenced overall survival within the study’s follow-up period, their combined assessment holds promise for enhancing prognostic models and guiding the selection of patients for intensified monitoring and clinical trials exploring immune checkpoint blockade and CSC-targeted therapies.

Background: Meningiomas exhibit variable biological behavior, with mitotic activity and brain invasion being critical histopathological markers of aggressiveness. While Vascular Endothelial Growth Factor (VEGF) is implicated in tumor progression, its precise role in driving these specific aggressive features in meningioma remains to be fully elucidated. This study investigated the association between immunohistochemical VEGF expression, mitotic activity, and brain invasion in meningioma. Methods: We conducted a retrospective, cross-sectional analysis of 73 surgically resected meningioma specimens. VEGF expression was semi-quantitatively scored via immunohistochemistry (negative, weak, moderate, strong) and correlated with mitotic counts (per 10 high-power fields, HPF) and the presence of brain invasion. Associations were assessed using the chi-square test. Results: High VEGF expression was significantly associated with a higher mitotic index (≥4 mitoses/10 HPF) (p=0.005); notably, 80% (8/10) of cases with high mitotic activity demonstrated moderate to strong VEGF expression. Furthermore, VEGF expression was significantly elevated in brain-invasive meningiomas compared to their non-invasive counterparts (p=0.007), with 75% (3/4) of invasive cases exhibiting strong VEGF expression. Conclusion: Elevated VEGF expression strongly and statistically significantly correlates with both increased mitotic activity and brain invasion in meningiomas. These findings underscore VEGF’s crucial role as a mediator of tumor proliferation and parenchymal infiltration, positioning it as a potential biomarker for aggressive meningioma and a promising target for future therapeutic interventions.

Background: Curcuma longa (turmeric), a traditional medicinal plant, has demonstrated significant antitumor properties in various cancer models. This study investigates the therapeutic efficacy of turmeric extract in the treatment of breast cancer in female rats, focusing on its mechanisms of action and molecular targets. Methods: Female Wistar rats were induced with mammary tumors using 7,12-dimethylbenz [a] anthracene (DMBA). The treated group received standardized doses of turmeric extract orally for six weeks. Tumor volume, histopathological changes, apoptosis markers (e.g., caspase-3), and oxidative stress biomarkers (e.g., MDA, SOD) were evaluated. Results: Rats treated with Curcuma longa showed a significant reduction in tumor size compared to the untreated group (p < 0.05). Histological analysis revealed increased apoptosis and reduced angiogenesis. Molecular assays indicated downregulation of NF-κB and upregulation of p53 expression. Conclusion: Turmeric demonstrated potent antitumor effects in breast cancer–induced rats through modulation of oxidative stress, inflammation, and apoptosis pathways. These findings support further investigation into Curcuma longa as a complementary therapeutic agent in breast cancer management.

Background: Ovarian and endometrial malignancies are complex diseases, since a defect in hormone balance can be the most important cause of tumor formation. Aim of study: Examine and identify the association between ER TA repeats with endometrial and ovarian cancers in Basrah women. Patients: Groups include 50 healthy controls and 50 cancer patients, divided into 20 endometrial cancer patients and 30 ovarian cancer patients. Results and Discussion: The result shows TA 11–12 repeats are the most common in endometrial cancer in 68% of cancer patients, followed by TA≥10 in 8% and 4% for both 13–14 repeats and ≤15, whereas TA repeats 11–12 and ≤15 repeats are the most common in ovarian cancer in 22% for each one, followed by ≥10 TA in 10% and 13–14 in 6%. The control groups have four groups of repeat numbers: 11–12 TA repeat in 68%, 13–14 in 20%, ≤15in 10%, and ≥10 in 2%. Simultaneously, a substantial association exists between the two types of cancers and the TA repeat length variation of the estrogen receptor type alpha. Conclusion: The length of the TA repeat in estrogen receptor alpha has a significant risk for ovarian and endometrial cancer.

Objectives: This study aims to evaluate and compare the efficacy of three methods for inducing prostate tumors in male Wistar rats: hormonal induction using testosterone propionate, chemical induction with cadmium chloride, and a combination of both agents. The research seeks to enhance understanding of the interactions between environmental and hormonal factors in prostate cancer development. Materials and Methods: Twenty-five male Wistar rats (180-220 grams) were randomly assigned to five groups: a control group (no induction), a low-dose cadmium chloride group (1 mg/kg), a high-dose cadmium chloride group (2 mg/kg), a testosterone propionate group (5 mg/kg), and a combination group (1 mg/kg cadmium chloride + 5 mg/kg testosterone). Each treatment was administered over four weeks, followed by a four-week observation period. Histopathological analyses were conducted on prostate tissues using Hematoxylin and Eosin (H&E) staining to assess tumor characteristics and progression. Results: Histopathological examination revealed that the control group exhibited normal prostate architecture. The low-dose cadmium chloride group showed mild hyperplasia, while the high-dose group displayed significant dysplastic changes. The testosterone propionate group demonstrated hyperplastic and pleomorphic epithelium, indicative of early tumorigenesis. The combination group exhibited the most aggressive tumors, characterized by severely dysplastic epithelium and stromal invasion. Survival rates were notably lower in the combination group, indicating increased health risks associated with dual exposure. Conclusions: The study concludes that the combination of cadmium chloride and testosterone propionate results in a more aggressive tumor phenotype compared to either agent alone, suggesting a synergistic effect in prostate carcinogenesis. These findings underscore the importance of using combined hormonal and chemical induction models to better replicate human prostate cancer for experimental research. Further studies are recommended to explore molecular mechanisms and optimize induction protocols for improved translational relevance in prostate cancer research.

Background: Volumetric arc therapy (VMAT) based stereotactic radiotherapy (SRT) or stereotactic body radiation therapy (SBRT) is a highly advanced radiation therapy technique that uses intensity-modulated radiation beams delivered in multiple arcs. After optimization, different segments of small sizes and shapes are created in an arc that will influence the indices like homogeneity index (HI), conformity index (CI), gradient index (GI), number of segments (NOS) which in turn will increase or decrease the total treatment time in terms of monitor units (MUs). The dose calculation algorithm faces difficulty in predicting the accurate dose for these small segments because of the lack of charged particle equilibrium (CPE) and requires precise modeling of lateral electron scatter. The segmentation parameter minimum segment width (MSW) can control the generation of these small-sized segments. It can also affect the quality and deliverability of a VMAT plan. Methods: This retrospective study includes 33 patients with lung, liver, and brain tumors (11 patients for each site) treated with the SRT/SBRT technique using a 6 MV flattening filter-free (FFF) beam. Four different plans with MSW 0.5 cm, 1 cm, 1.5 cm, and 2 cm were created by medical physicist using the Monaco treatment planning system (TPS) version 5.11.03. Results: A statistically significant reduction in MU (P= 0.01 for brain, P= 0.005 for lung) and NOS (P=0.034 for brain, P=0.011 for lung) was observed for brain and lung cases in plans with MSW 1 cm. For liver cases, along with MU and NOS (P= 0.029 & 0.013 respectively), the paired t-test shows a statistically significant difference (P= 0,046, 0.019 & 0.009) in the GI for intergroup comparison between two plans at different MSW. Improved GI in the case of plans with narrower segments (MSW 0.5 cm and 1 cm) corresponding to sharp dose fall-off compared to plans with broader segments (MSW 1.5 cm and 2 cm). There is no statistical difference in other parameters including global maximum dose and target coverage for plans at different MSW for all cases. Conclusion: VMAT plans for SRT/SBRT generated with an MSW of 1.0 cm demonstrated comparable dose distributions to plans with MSWs of 0.5 cm with fewer MUs for brain, liver, and lung cases treated with 6 MV FFF beams.

Background: Colorectal cancer (CRC) has a high mortality rate due to the development of liver metastases. Mutations in RAS and mismatch repair (MMR) genes are common in CRC, with Kirsten rat sarcoma viral oncogene (KRAS) mutations occurring in approximately 44% of cases and MSI in 15%. Both mutations are associated with poor prognosis. The study aims to identify MSI status and KRAS mutations in liver-metastatic CRC at a hospital in eastern Indonesia. Methods: In this cross-sectional study, 57 patients with liver-metastatic CRC were included. We evaluated KRAS mutations and microsatellite instability (MSI) status in patients’ DNA extracted from paraffin blocks. The procedures involved included specimen examination, DNA extraction, and genetic sequencing. The data were analyzed using SPSS version 25.0. Fisher’s exact test was utilized to evaluate the relationship between MSI status and KRAS mutations. A significance level of p<0.05 was considered statistically significant. Results: This study included patients aged 16–80 years with liver-metastatic colon cancer. Patients were primarily male with left-sided tumors of adenocarcinomatous histopathology and high histopathological grade. Of the 57 subjects, 31.6% had MSI-high (MSI-H) tumors and 21.1% expressed mutant KRAS. The majority of MSI-H tumors (82% of patients) expressed mutant KRAS, while most MSI-low (MSI-L) tumors (60% of patients) expressed wild-type KRAS. However, Fisher’s exact test indicated no significant relationship between MSI status and KRAS mutation status in liver-metastatic colon cancer (p = 0.489). Conclusions: This study found no significant relationship between MSI status and KRAS mutation status in patients with liver-metastatic colon cancer.

Introduction: Extracellular Matrix (ECM) is often abnormally produced, degraded, and remodelled, which creates a pro-tumorigenic environment in cancer and leads to tumor growth, angiogenesis, invasion and metastasis. This study aimed to investigate ECM genes by microarray-based transcriptome analysis and miRNA that target ECM genes in triple-negative breast cancer (TNBC). Materials and Methods: The current study evaluated 682 TME-related genes using Array Comparative Genomic Hybridization (aCGH) in 55 patients with TNBC. Results: 266 ECM genes were studied by transcriptome analysis, and it was observed that 132 ECM genes were up-regulated and 25 ECM genes were down-regulated in TNBC. Regarding upregulated genes, the majority of the genes were of Collagen family genes. Regarding downregulated genes, 14 genes were of Integrin family genes. PPI network analysis of upregulated genes using the STRING database, five hub genes identified were FN1, COL3A1, COL1A2, COL1A1, and COL6A2. Five of eight ranking methods identified FN1 and COL1A1 as the top most upregulated hub genes. The top 5 significant down-regulated hub genes were ITGB2, ITGAM, ITGAX, ITGB3, and ITGA4. Of 8 ranking methods, 7 ranking methods identified ITGB2, ITGAM and ITGAX as the most significant down-regulated hub genes. Further, target gene - miRNA regulatory networks using the miRTargetLink 2.0 tool. Conclusion: ECM genes FN1, COL1A1, ITGB2, ITGAM and ITGAX may be involved in disease progression in TNBC and, after validation, may be considered therapeutic targets for TNBC