Comparative analysis of basal cell and squamous cell carcinoma: clinical, histopathological, and therapeutic perspectives

Аннотация

Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) represent the two most prevalent forms of non-melanoma skin cancer. Although both arise from keratinocytes, they differ in etiology, clinical behavior, histopathology, and management strategies. This thesis explores the pathogenesis, risk factors, clinical presentations, diagnostic techniques, and current treatment modalities for BCC and SCC, highlighting their differences and implications for patient prognosis. Particular emphasis is placed on recent advances in targeted therapies and immunomodulatory treatment. 1. Introduction. Non-melanoma skin cancers (NMSCs) account for the majority of malignancies diagnosed globally, with BCC and SCC comprising approximately 80% and 20% of cases respectively. These tumors are predominantly caused by ultraviolet (UV) radiation-induced DNA damage, with additional contributions from immunosuppression, chronic wounds, and genetic predispositions. Understanding their distinct biological behavior is critical for optimizing management and reducing recurrence or metastasis. 2. Etiology and Risk Factors 2.1 Basal Cell Carcinoma (BCC): - UV-B radiation as primary mutagenic factor (notably p53 mutations) - Association with PTCH1 gene mutations (Hedgehog signaling pathway dysregulation) - Common in fair-skinned individuals (Fitzpatrick skin types I-II) - Ionizing radiation, arsenic exposure, immunosuppression (e.g., organ transplant recipients) 2.2 Squamous Cell Carcinoma (SCC): - Cumulative UV exposure and actinic keratosis as precursor lesions - HPV infection (notably HPV-16, -18) in anogenital and periungual regions - Chronic inflammatory skin disorders (e.g., hidradenitis suppurativa) - Smoking, immunosuppression, and genetic syndromes (e.g., xeroderma pigmentosum) 3. Clinical Features and Diagnostic Approach 3.1 BCC: - Presents as pearly, translucent papules with telangiectasias - Slow-growing, locally invasive, rarely metastatic - Common subtypes: nodular, superficial, morpheaform (sclerosing), pigmented 3.2 SCC: - Appears as hyperkeratotic, erythematous plaques or nodules, often ulcerated - Higher metastatic potential than BCC, especially in immunosuppressed patients or tumors of the lip and ear - Frequently arises from actinic keratoses or areas of chronic injury 3.3 Diagnosis: - Clinical evaluation followed by dermoscopy 105 - Biopsy (shave, punch, or excisional) - Histopathology: BCC (basaloid cells with peripheral palisading, mucinous stroma); SCC (keratin pearls, intercellular bridges, atypical squamous proliferation) - Imaging and sentinel node biopsy in advanced SCC cases 4. Management Strategies 4.1 Surgical Treatment: - Standard excision with histological margin assessment - Mohs micrographic surgery (particularly for BCC in cosmetically sensitive or recurrent cases) - Curettage and electrodesiccation (superficial lesions) 4.2 Non-surgical Treatments: - Topical therapies (imiquimod, 5-fluorouracil) for superficial BCC and SCC in situ - Photodynamic therapy (PDT) - Cryotherapy 4.3 Advanced and Metastatic Disease: - Radiation therapy for non-surgical candidates - Hedgehog pathway inhibitors (e.g., vismodegib, sonidegib) for advanced BCC - Systemic chemotherapy and immune checkpoint inhibitors (e.g., cemiplimab) for advanced SCC 5. Prognosis and Follow-Up - BCC: Excellent prognosis, low recurrence with appropriate excision, negligible metastasis risk - SCC: Variable prognosis based on size, depth, differentiation, and perineural invasion; metastatic risk up to 5% - Regular dermatologic follow-up essential due to risk of recurrence or new primary lesions 6. Recent Advances and Future Directions - Role of artificial intelligence in early detection - Biomarker development for treatment response prediction - Novel immunotherapeutic combinations - Genetic profiling to guide personalized therapy