Squamous cell carcinoma

Squamous cell carcinoma (SCC) arises from keratinocytes of the epidermis and its adnexa (follicular infundibulum, sebaceous ducts, terminal sweat ducts), favoring exposed sites such as scalp, face, neck and dorsal hands. It may ulcerate early, often arising on chronic ulcers, chronic sinus openings or chronic nonhealing scars. Clinically it may be cauliflower-like with raised irregular edges and uneven base, bleeding easily, often malodorous from infection. Local invasion and regional nodal metastasis occur; lower-extremity lesions often accompany osteomyelitis or periostitis.

Common Symptoms

Scales; papule; epidermal keratosis; chronic ulcer; squamous epithelium; crescent-shaped lytic bone defect; crusting

Causes

In 1948 Blum showed the carcinogenic rays are the 290-320 nm portion of sunlight. UV damages cellular DNA and impairs repair, causing skin cancer. Melanin protects against UV, explaining why fair-skinned people are prone, and sunbathing habits raise risk. Ozone depletion increases UV exposure and skin cancer. Chemicals such as arsenic and asphalt also cause cutaneous SCC; workers exposed to asphalt have ~12 times higher SCC rates. Polycyclic aromatic hydrocarbons, coal tar, creosote, paraffin, anthracene, tobacco tar and chromates are carcinogenic, especially for SCC. Human papillomavirus types 16, 18, 30 and 33; immunosuppression and organ transplantation are important triggers. Genetics also matters; in China Sun et al. (1956) reported 191 skin cancers with SCC accounting for 78.5%, whereas Bosenberg (1953) in Germany found SCC only 15%. Since Percivall Pott first described scrotal SCC in chimney sweeps (1775), many triggers have been identified: chronic UV exposure is primary, followed by radiation injury, thermal injury and carcinogenic chemicals. 1. Precancerous dermatoses: actinic keratosis, leukoplakia, arsenical keratosis, X-ray/radium dermatitis, epidermodysplasia verruciformis, chronic ulcers/sinuses, chronic osteomyelitis, chronic lupus erythematosus, lupus vulgaris and lichen sclerosus may induce or complicate SCC. 2. Excess radiation: chronic dermatitis plus excess radiation can cause malignant transformation; poorly protected radiology workers are at risk. 3. Scars: traumatic scars, especially burn scars, favor SCC. 4. Secondary chronic skin disease: lupus vulgaris, LE, leukoplakia, chronic ulcers/sinuses, burn scars, radiodermatitis, chronic granuloma, epidermodysplasia verruciformis, chronic osteomyelitis, lichen sclerosus can induce or complicate SCC. Pathology shows three cancer cell types: (1) differentiated prickle cells: larger, polygonal/short-spindle, abundant eosinophilic cytoplasm with intercellular bridges; nuclei vary, with multinucleate giant nuclei and mitoses. (2) keratinocytes: singly or in clusters with horn pearls (onion-like concentric keratin layers), large hyperchromatic nuclei, eosinophilic cytoplasm — the hallmark of SCC. (3) undifferentiated/low-differentiation spindle cells: smaller, scant cytoplasm, dark nuclei, no reticulin. SCC is usually well differentiated (~75% high grade). Broders grading: grade I undifferentiated cells <25% with many horn pearls; grade II <50%; grade III <75% with dyskeratotic cells and atypical mitoses; grade IV >75% undifferentiated, no keratin, no intercellular bridges. Most SCC are grade I-II by Broders.

Treatment

Surgery; drug therapy; supportive care

Prevention

SCC is highly malignant with poor prognosis. Prevention targets known triggers: remove causative factors, avoid excess sun/UV/X-ray and frequent contact with arsenic/asphalt chemicals; actively treat chronic ulcers or leukoplakia with regular follow-up.

Recommended Department

It is recommended to visit the oncological surgery department; before the visit you may first book an appointment and connect with experts through this platform.

Warm reminder: The above information is provided for health education reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek care at a regular hospital in time.