Pembrolizumab, an immune checkpoint inhibitor targeting the programmed cell death 1 (PD-1) protein, is widely used for renal cell carcinoma but rarely causes central nervous system adverse events such as myelitis. A 58-year-old woman with stage IV renal clear cell carcinoma developed radiating hip pain, paresthesia, hypoesthesia (T10 and below), constipation, urinary retention, and sudden right-eye blurred vision one month after her sixth cycle of pembrolizumab and lenvatinib. Neurologic examination revealed asymmetrical inferior paraparesis, upper motor neuron signs, and right eye papilledema. MRI demonstrated patchy hyperintensity on C2-C6 and T2-T5, supportive of myelitis. Intravenous methylprednisolone was initiated, leading to pain relief and motor improvement. This is the first reported case of pembrolizumab-induced myelitis in Indonesia, emphasizing the importance of early recognition and corticosteroid therapy for optimal recovery.

Triple negative breast carcinoma (TNBC) is a rapid progressive tumor and has a poor overall survival. Therefore, it is crucial to find out effective molecular targets and develop optimal therapeutic strategies for TNBC. In this study, immunohistochemical staining was used to detect expressions of programmed death-ligand 1 (PD-L1) and phosphatase and tensin homolog (PTEN) in 136 breast carcinomas including 50 TNBC. The effect of PTEN on regulation of PD-L1 expression was assessed in vitro in the PTEN knockdown TNBC cells. We found that PD-L1(SP142) positive rate in TNBC (48.0%) was significantly higher than non-TNBC (23.3%). PTEN negative rate was 42% in TNBC. The inverse correlation between PTEN and PD-L1(SP142) expression in TNBC was statistically significant (P<0.05). After PTEN knockdown, PD-L1 expression in TNBC cells increased significantly, and the expression level of AKT increased simultaneously. PTEN knockdown promoted cell proliferation, viability and G1/S switch of TNBC cells. These results suggested that PTEN may involve in regulation of PD-L1 expression, because PTEN loss can upregulate PD-L1 expression in TNBC. Antitumor immunity of PD-L1 could be enhanced in TNBC when targeting PTEN at the same time.

Introduction: Colorectal cancer during pregnancy is a complex and rare condition often presenting with benign gastrointestinal symptoms that overlap with normal pregnancy related changes, leading to delayed or misdiagnosis. Further, hepatic metastases may complicate recognition, especially when initially interpreted as benign lesions such as hemangiomas. So, early identification and management are crucial and remain challenging for optimizing maternal and fetal outcomes. Clinical Description: A case of 39-year-old gravida 5 para 4 at 24 weeks+1 day with chronic hypothyroidism, longstanding anemia and a one year history of epigastric + right upper quadrant pain with suspected hemorrhage from a known liver hemangioma. Further imaging suggested a malignant hepatic lesion where colonoscopy and biopsy confirmed stage IV metastatic colon adenocarcinoma with liver and adrenal metastases. Her condition deteriorated and delivered a stillborn infant at 26 weeks of 780 grams following placental abruption. She continued to decline despite supportive care and died. Conclusion: This case illustrates the diagnostic challenges of colorectal cancer in pregnancy where nonspecific symptoms and inaccurate imaging results contributed to delayed diagnosis. The aggressive nature of the disease emphasizes the importance of prompt diagnosis and integrated care approach to improve both maternal and fetal outcome.

Background: Hepatocellular carcinoma (HCC) faces significant challenges in early diagnosis and prognostic assessment, necessitating novel molecular biomarkers. The role of GCN1 in tumorigenesis remains unclear, warranting systematic investigation of its clinical value. Methods: Utilizing multi-omics data from 164 HCC patients in the TCGA database, we comprehensively evaluated the diagnostic and prognostic value of GCN1 through differential expression analysis, Cox proportional hazards regression, and gene set enrichment analysis (GSEA). Results: GCN1 expression was significantly upregulated in tumor tissues (P<0.001), with ROC analysis demonstrating an AUC of 0.921 (95% CI: 0.893-0.950) for discriminating tumor from normal tissue. Clinical correlation analysis revealed that high GCN1 expression significantly associated with advanced T stage (OR=1.941, P=0.002) and AFP levels >400 ng/ml (OR=3.697, P<0.001). Multivariate survival analysis confirmed its independent prognostic value (HR=1.454, P=0.038). Functional analysis indicated GCN1 promotes tumor progression by regulating cell cycle (NES=2.385) and axon guidance (NES=2.307) pathways. Conclusion: This study first elucidates the dual clinical value of GCN1 in HCC, providing a theoretical foundation for developing novel diagnostic biomarkers and prognostic evaluation systems. Future research should validate its molecular mechanisms and explore potential targeted therapies.