Tuberculosis Research and Epidemiology (2)Colorectal Cancer Treatments and Studies (1)Nonmelanoma Skin Cancer Studies (1)Mycobacterium research and diagnosis (1)Infectious Diseases and Tuberculosis (1)
Cetuximab, a monoclonal antibody targeting the epidermal growth factor receptor (EGFR), is associated with various adverse reactions, among which skin-related adverse events (AEs) are common. This case report details a patient who developed severe skin AEs after cetuximab administration and outlines a reproducible management protocol. The patient, a 44-year-old man with KRAS wild-type metastatic rectal cancer, was undergoing cetuximab-based chemotherapy. Approximately 10 days after initiating a cetuximab monotherapy cycle following prior combination regimens, he developed severe Grade 3-4 acneiform rash and erythema multiforme-like lesions with ulceration, exudation, crusting, scaling, and hyperpigmentation on the face and anterior chest. Evaluation included physical examination, dermatology consultation, skin biopsy for histopathology and direct immunofluorescence, and laboratory tests (including serum IgE, eosinophil count, C-reactive protein, HLA-A*31:01 genotyping, viral serologies, and bacterial cultures). Management involved permanent discontinuation of cetuximab, high-dose intravenous methylprednisolone (1.5 mg∙kg∙day), cyclosporine (3 mg∙kg∙day), supportive wound care in a burn unit, and topical ocular/oral care. Symptoms improved significantly within 72 h, with a 90% reduction in lesion severity by day 14. Therapy was successfully transitioned to bevacizumab plus FOLFOX after dermatologic recovery, with no rash recurrence during follow-up. This case highlights the importance of early recognition, multidisciplinary management, and protocol-driven intervention for severe cetuximab-induced skin toxicity to ensure patient safety and treatment continuity.
Early diagnosis is paramount for enhancing survival rates and prognosis in the context of malignant diseases. Hepatocellular carcinoma (HCC), the second leading cause of cancer-related deaths worldwide, poses significant challenges for its early detection. In this study, we present an innovative approach which contributed to the early diagnosis of HCC. By lanthanide encoding signal amplification to map glycan-linkages at the single-cell level, the minute quantities of "soft" glycan-linkages on single cell surface were converted into "hard" elemental tags through the use of an MS2 signal amplifier. Harnessing the power of lanthanides encoded within MS2, we achieve nearly three orders of magnitude signal amplification. These encoded tags are subsequently quantified using single-cell inductively coupled plasma mass spectrometry (SC-ICP-MS). Linear discriminant analysis (LDA) identifies seven specific glycan-linkages (α-2,3-Sia, α-Gal, α-1,2-Fuc, α-1,6-Fuc, α-2,6-Sia, α-GalNAc, and Gal-β-1,3-GalNAc) as biomarkers. Our methodology is initially validated at the cellular level with 100% accuracy in discriminating between hepatic carcinoma HepG2 cells and their normal HL7702 cells. We apply this approach to quantify and classify glycan-linkages on the surfaces of 55 clinical surgical HCC specimens. Leveraging these seven glycan-linkages as biomarkers, we achieve precise differentiation between 8 normal hepatic specimens, 40 early HCC specimens, and 7 colorectal metastasis HCC specimens. This pioneering work represents the first instance of employing single-cell glycan-linkages as biomarkers promising for the early diagnosis of HCC with a remarkable 100% predictive accuracy rate, which holds immense potential for enhancing the feasibility and precision of HCC diagnosis in clinical practice.