Author

M. Sonbol

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Review Open access 2026

Biomarker-Driven Precision Oncology in Advanced Gastroesophageal Adenocarcinoma: Current Standards and Future Directions

: Advanced gastroesophageal adenocarcinomas (GEA) have undergone a major therapeutic shift from empiric chemotherapy toward biomarker-driven precision oncology. Routine incorporation of immunohistochemistry (IHC), in situ hybridization, next-generation sequencing (NGS), and liquid biopsy have enabled identification of actionable subgroups that now guide first-line and subsequent treatment selection. Four biomarkers have established clinical utility in current practice: mismatch repair deficiency (dMMR)/microsatellite instability-high (MSI-H) status, human epidermal growth factor receptor 2 (HER2) amplification or overexpression, programmed death ligand 1 (PD-L1) expression, and claudin 18.2 (CLDN18.2). MSI-H/dMMR represents the strongest predictor of durable benefit from immune checkpoint inhibition across treatment lines. HER2-positive disease has evolved beyond trastuzumab-based therapy with the emergence of antibody–drug conjugates and bispecific antibodies that are redefining outcomes. PD-L1 combined positive score (CPS) remains most impactful in selecting patients for first-line chemo-immunotherapy, while its predictive role beyond first line is less consistent. Most recently, CLDN18.2 targeting has expanded therapeutic options in HER2-negative disease, with zolbetuximab establishing a new first-line standard and multiple antibody drug conjugate strategies emerging. This review aims to summarize the current evidence supporting biomarker-driven treatment strategies in advanced GEA, highlight practical biomarker testing considerations, and discuss ongoing challenges and future directions in precision oncology.

Fares Jamal, Abdullah Alsulaiman, Oudai Sahwan et al. · Oncology Research · 0 citations

Open access Sep 2026

Colon cancer in a patient with a mosaic monoallelic germline pathogenic NF1 gene variant

Pathogenic variants in the tumor suppressor gene NF1 cause neurofibromatosis type 1 (NF1), one of the most common hereditary cancer predisposition syndromes. Pathogenic NF1 variants have been associated with an increased risk of several cancers; however, the relationship between NF1 variation and colon cancer remains underreported. We report a 41-year-old woman with a mosaic monoallelic germline pathogenic NF1 variant, NM_000267.3:c.1756_1759del (p.Thr586Valfs*18), previously detected on germline multigene panel testing in saliva at a variant allele frequency of approximately 35%. She later presented with fatigue, dyspnea on exertion, and iron-deficiency anemia. Computed tomography, colonoscopy, biopsy, mismatch repair immunohistochemistry, surgical pathology, and tumor next-generation sequencing led to the diagnosis of right-sided colon adenocarcinoma that was mismatch repair deficient (dMMR) and microsatellite instability-high (MSI-H). She underwent right hemicolectomy, recovered postoperatively, and entered standard surveillance; at the time of manuscript development, she was also receiving systemic therapy. This case highlights the co-occurrence of an NF1 variant and dMMR colorectal cancer and underscores the need for further studies to determine whether this represents a coincidental finding or a biologically meaningful association.

Feras Alsabagh, Karam M. Chaaban, M. Girardo et al. · Exploration of Neuroscience · 0 citations