The tumor suppressor p53 and the Wnt pathway effector β-catenin represent two of the most frequently dysregulated molecular components across human malignancies. Although gallbladder cancer (GBC) predominantly affects adults, the pattern and clinicopathological correlates of p53 and β-catenin dysregulation in GBC may illuminate how these pathways behave in different biological contexts, including developmental and pediatric oncological settings, where analogous pathway alterations drive distinct tumor types.

To characterize p53 and β-catenin expression patterns in gallbladder carcinoma by immunohistochemistry, correlate findings with clinicopathological parameters, and discuss in a qualified, hypothesis-generating framework the parallels and divergences between these pathway alterations and those reported in pediatric malignancies.

A cross-sectional study analyzed 61 neoplastic and 49 non-neoplastic gallbladder lesions (2017-2021) using standardized immunohistochemistry for p53 (clone DO-7; Dako/Agilent, 1:100) and β-catenin (clone E247; Abcam, 1:200). Expression patterns were correlated with clinicopathological parameters using chi-square and Fisher's exact tests. Findings were discussed in the context of published pediatric cancer literature, with explicit acknowledgment of inter-study methodological heterogeneity.

p53 overexpression (defined as >20% nuclear positivity) occurred in 78.2% of GBC cases versus 11.1% of benign lesions, correlating significantly with tumor grade and stage (p<0.05). Aberrant β-catenin expression (cytoplasmic/nuclear) was observed in 81.8% of malignant cases, with nuclear localization in 36.3%, correlating with poor differentiation. These patterns qualitatively parallel though are not directly quantitatively comparable to those reported in pediatric hepatoblastoma, Wilms' tumor, and pediatric sarcomas.

p53 and β-catenin dysregulation in GBC exhibits qualitative parallels to patterns reported in pediatric cancers, suggesting shared oncogenic pathway biology. These observations are hypothesis-generating and warrant validation through functional studies in appropriate preclinical models before therapeutic implications can be drawn.

The limited specificity of prostate-specific antigen (PSA) increases the risk of unnecessary biopsies and overtreatment. This study aimed to evaluate the diagnostic and prognostic value of serum S100A4, along with CA-9, CA-12, Annexin A1/A2, and Galectin-3, in prostate cancer.

This prospective case-control study, conducted between July 2024 and September 2025, included 80 patients with histopathologically confirmed prostate cancer and 40 age-matched healthy controls. Patients were stratified into low-risk (ISUP grades 1-2) and high-risk (ISUP ≥3) groups. Serum biomarker levels were measured using ELISA. Diagnostic and prognostic performance was assessed by receiver operating characteristic (ROC) analysis, with cut-off values determined using the Youden index. Logistic regression analyses were performed to identify independent biomarkers.

Serum CA-12 and CA-9 levels were significantly higher in prostate cancer patients than in controls (p = 0.004 and p = 0.032, respectively). Although S100A4 levels were lower in prostate cancer patients compared with controls, they were significantly higher in high-risk patients within the cancer cohort (p = 0.002). Logistic regression identified S100A4 (p = 0.032) and CA-12 (p = 0.004) as independent predictors of prostate cancer diagnosis. ROC analysis demonstrated excellent diagnostic accuracy for CA-12 (>52.9 ng/mL; AUC = 0.99) and S100A4 (<9.96 ng/mL; AUC = 0.98). For prognostic stratification, S100A4 (>8.27 ng/mL; AUC = 0.97) and CA-12 (>72.8 ng/mL; AUC = 0.91) effectively distinguished high-risk from low-risk disease.

S100A4 and CA-12 exhibit strong diagnostic and prognostic performance in prostate cancer. When used alongside PSA, S100A4 and CA-12 may improve risk stratification in patients with suspected prostate cancer and help reduce unnecessary prostate biopsies.

Urothelial carcinoma (UC) of the bladder remains a significant clinical challenge due to its high rates of recurrence and progression. Reliable biomarkers to predict tumor behaviour are still needed. GATA3 and HER2 have gained attention in this context, but their combined prognostic value has not been fully established. This study aims to evaluate the immunohistochemical expression of GATA3 and HER2 in bladder UC and to examine their association with key pathological parameters and patient outcomes.

One hundred archival UC specimens (2018-2022) were reviewed. Immunohistochemical staining for GATA3 and HER2 was performed and scored using a semi-quantitative H-score. Clinicopathological data and 3-year follow-up information were analysed to assess correlations with recurrence, progression, and survival.

GATA3 expression was detected in 80% of tumors, while HER2 was positive in 25%. Both markers were significantly associated with low-grade histology and non-muscle-invasive disease. Tumors co-expressing GATA3 and HER2 showed the most favorable outcomes, including lower recurrence and improved 3-year disease-free survival. In multivariate analysis, GATA3 retained independent prognostic significance (HR 0.45, p=0.006). HER2 demonstrated a favorable trend that did not reach statistical significance after adjustment for grade and stage (HR 0.60, p=0.12), suggesting its prognostic signal is partially mediated by tumor differentiation.

In multivariate analysis, GATA3 retained independent prognostic significance (HR 0.45, 95% CI 0.25-0.80, p=0.006), while HER2 did not (HR 0.60, 95% CI 0.35-1.03, p=0.12). However, combined GATA3/HER2 positivity identified a luminal subgroup with significantly better outcomes, supporting the utility of this marker panel for prognostic stratification in early-stage bladder UC.

Breast cancer (BC) is the most common cancer among women globally, with Iranian women showing an earlier onset compared to those in Western countries. Genetic variations in the PI3K/AKT/mTOR signaling pathway have been implicated in cancer susceptibility, but limited studies exist on the association of these polymorphisms with BC risk in the Iranian population. This study aimed to investigate the associations of specific polymorphisms in the AKT1, PIK3CA, and mTOR genes with BC susceptibility in an Iranian population.

A case-control study was conducted with 222 confirmed BC patients and 230 cancer-free controls. Genotyping of AKT1 rs1130214 and rs1130233, PIK3CA rs6443624, and mTOR rs1883965 polymorphisms was performed using PCR-RFLP methods. Statistical analysis was carried out using logistic regression to evaluate the associations between genotypes and BC risk.

The AKT1 rs1130214 polymorphism was associated with a significantly reduced BC risk (codominant model: OR=0.44, 95% CI=0.30-0.65, p<0.001; allelic model: OR=0.52, 95% CI=0.38-0.72, p<0.001). Conversely, AKT1 rs1130233, PIK3CA rs6443624, and mTOR rs1883965 polymorphisms were linked to an increased BC risk in various inheritance models. For instance, the mTOR rs1883965 G>A variant showed a significantly higher risk (dominant model: OR=2.75, 95% CI=1.84-4.12, p<0.001).

This study indicates that polymorphisms in AKT1, PIK3CA, and mTOR genes are associated with altered BC risk among Iranian women. These findings propose that genetic variants in the PI3K/AKT/mTOR pathway could serve as potential biomarkers for BC susceptibility. Further research with larger cohorts and diverse populations is necessary to confirm these associations.

Breast cancer (BC) remains the most common malignancy in women worldwide, highlighting the need for reliable non-invasive biomarkers for early detection. miR-141-3p, a member of the miR-200 family, has shown context-dependent roles in tumorigenesis, but its diagnostic specificity and clinical relevance in the plasma of patients with BC remain incompletely understood. Therefore, this study aimed to assess the diagnostic potential and functional role of miR-141-3p in BC.

Plasma miR-141-3p levels were quantified in breast cancer patients and healthy controls using RT-qPCR. Diagnostic capacity was evaluated via receiver‑operating characteristic (ROC) analysis. Associations between circulating miR-141-3p expression and BC risk were assessed using odds ratios (ORs). In vitro functional assays in MCF‑7 cells (miR‑141‑3p overexpression) examined effects on proliferation, migration, and regulation of target genes.

Circulating miR-141-3p was significantly upregulated in BC patients. ROC analysis yielded an AUC of 0.877 (95% CI: 0.782-0.971), demonstrating good diagnostic performance. No statistically significant stage-dependent difference was observed, suggesting that circulating miR-141-3p dysregulation may not simply reflect tumour burden. In vitro, miR‑141‑3p overexpression suppressed MCF‑7 cell proliferation and migration and reduced expression of EMT‑associated markers. Furthermore, strong inverse correlations were observed between miR‑141‑3p levels and its predicted oncogenic targets.

Circulating miR‑141‑3p shows promise as a non‑invasive biomarker for BC detection and risk discrimination, although its specificity as a stand-alone marker may be limited. Its in vitro effects on proliferation, migration, and EMT markers indicate potential functional relevance. Further validation in larger cohorts and through in vivo studies is warranted.

Colorectal cancer (CRC) is the second-leading cause of cancer-related mortality globally, with a rising incidence in Bangladesh. This study aims to identify pathogenic KRAS and BRAF mutations contributing to anti-EGFR resistance in CRC patients.

Two sets of primers were used: one was adopted from a published paper, and another was designed using Primer3Plus. They were optimized for specific PCR amplicons of 173 bp and 230 bp from exon 2 of KRAS and exon 15 of BRAF, respectively. Targeted Sanger sequencing was performed to analyze mutations in these amplicons in 46 CRC patient samples.

KRAS mutations were detected in 5 samples (10.87%), comprising two G12D, one G12V, and two G13D variants. Notably, no BRAF V600E mutation was identified. These results stand in sharp contrast to global data, where KRAS mutations at these loci occur in approximately 40% of cases and BRAF V600E mutations in about 10%. Such mutations are clinically significant because they confer resistance to anti-EGFR therapy, underscoring the distinct molecular profile observed in this cohort.

The lower prevalence of KRAS and BRAF mutations indicates the potential effectiveness of anti-EGFR therapies in Bangladeshi CRC patients than other populations.

High-grade serous ovarian carcinoma (HGSOC) is the most aggressive subtype of epithelial ovarian cancer and is frequently associated with BRCA1 dysfunction. This study aimed to evaluate the clinicopathological correlation of BRCA1 expression and mutation status assessed by immunohistochemistry (IHC) and next-generation sequencing (NGS) with the Whole Exome Sequencing (WES) approach.

A retrospective observational study was conducted on thirty-six formalin-fixed paraffin-embedded HGSOC samples. BRCA1 expression was evaluated by IHC using a 10% nuclear staining cutoff. BRCA1 mutation profiling was performed using NGS with a whole-exome sequencing (WES) approach. Clinicopathological variables were analyzed using Fisher's exact test.

Abnormal BRCA1 expression was observed in 11.1% of cases, while BRCA1 mutations were detected in 27.8%. Most mutations were somatic (70%) and predominantly loss-of-function variants (90%). A significant association was found between abnormal BRCA1 expression and younger age (p = 0.023), whereas no association was observed with other clinicopathological parameters.

BRCA1 expression loss in HGSOC is associated with younger patient age. The discordance between IHC and mutation status highlights the complementary role of protein expression and molecular testing. A combined IHC-NGS approach may improve the identification of BRCA1 deficiency and support therapeutic decision-making, particularly in the context of targeted therapy.

To assess the clinical impact of maintenance capecitabine following first-line modified FOLFIRINOX in patients with metastatic pancreatic cancer (mPC), focusing on progression-free survival (PFS), overall survival (OS), quality of life (QoL), and the toxicity profile.

This phase II prospective trial, 60 patients with histologically confirmed stage IV pancreatic adenocarcinoma (ECOG PS ≤1, normal organ function, and measurable metastatic disease) who were enrolled after completing modified FOLFIRINOX. Participants were randomized into two groups: Arm A received maintenance capecitabine, and Arm B underwent observation only.

Baseline patient and disease characteristics were comparable between both groups. The pancreatic head was the predominant tumor site (73.3% in Arm A vs. 86.7% in Arm B). After six months of maintenance therapy, stable disease was reported in 33.3% of Arm A and 0% of Arm B. Toxicity levels were not significantly different. Patients in Arm B demonstrated earlier deterioration in QoL, with median time to decline of 3.2 months compared with 6.9 months in Arm A. Median PFS and OS favored the capecitabine arm (6.13 vs. 3.57 months and 14.20 vs. 10.97 months, respectively). Multivariate Cox regression confirmed treatment arm as the most independent prognostic factor influencing both PFS and OS.

Maintenance capecitabine after first-line modified FOLFIRINOX in mPC was well tolerated and may enhance PFS and OS while maintaining an acceptable quality of life.

Nasopharyngeal cancer (NPC) is highly prevalent in Asia; however, no established screening program exists to identify high-risk individuals. This study evaluated the potential utility of real-time PCR cycle threshold (Ct) values of Epstein-Barr virus (EBV) DNA detection in nasopharyngeal swabs (NS) as a practical non-invasive screening approach.

Nasopharyngeal cytobrush (CB) and swab (NS) samples were collected from 98 patients with NPC, and NS samples were collected from 174 non-NPC individuals. Real-time PCR targeted the EBNA1 gene, with a Ct cutoff < 35 defined as positive. Beta-globin amplification served as an internal control to verify sample adequacy.

In NPC patients, 79% and 81% were EBNA1 positive in CB and NS specimens, respectively. In non-NPC individuals, 10.3% were EBNA1 positive. Median Ct values were 24.4 in NPC patients and 34.4 in non-NPC individuals (p<0.001). Using a Ct cutoff of <35, the diagnostic performance of detecting EBNA1 in NS specimens showed 81% sensitivity, 90% specificity, and 90% accuracy.

A real-time PCR Ct cutoff of< 35 for EBNA1 detection provides a practical and effective non-invasive screening tool for NPC in endemic populations. Further validation in prospective cohorts is required.

Head and neck cancer (HNC) is a growing global health concern, with rising incidence in India. Patients undergoing HNC surgery experience postoperative challenges due to altered airway anatomy and complex reconstruction. Enhanced Recovery After Surgery (ERAS) protocols recommend early mobilization (EM) to improve postoperative outcomes; however, its implementation remains inconsistent.  Evidence regarding EM practices in this population is limited. This study aimed to evaluate EM practices and their barriers in post HNC surgery patients in a tertiary care setting.

A prospective observational study was conducted among adults undergoing HNC surgery. Patients with neurological deficits or preoperative non-ambulatory status were excluded. Mobilization was assessed daily until postoperative day (POD) 5 using the ICU Mobility Scale (IMS). Barriers to EM were documented using a validated checklist and categorized into three domains. Logistic regression analyses were performed to identify factors associated with non-ambulatory status (IMS<5). Adjusted odds ratios (aORs) with 95% confidence intervals (CIs) were reported. A p<0.05 was considered statistically significant.

Among the 69 patients included, 69.6% patients received in-bed exercises, while 27.5% had not been mobilized on POD 1. On POD 3, 23.1% were ambulated with assistance. More than 75% of the patients were ambulated and shifted to the wards by POD 5. Major functional and clinical barrier domains included nasotracheal intubation (75.4%), respiratory distress (53.6%) and free flap reconstruction (28.9%). The system-provider domain included low prioritization of EM (46.4%) and communication gaps among healthcare professionals (7.26%). This domain was independently associated with non-ambulatory status (aOR 0.402, 95% CI 0.172-0.817, p=0.020).

EM practices showed a consistent but gradual improvement over the five postoperative days. Though patient related barriers were common, the overall mobility outcomes were mainly determined by the system-provider domain of barriers. Addressing barriers to EM is crucial for enhancing its practice and ensuring adherence to EM protocols.