In New Zealand, basal Cell Carcinoma is managed by oncologists. Basal cell carcinoma is the most common cancer diagnosed in humans, with an estimated 4.3 million cases treated annually in the United States — more than all other cancers combined (Rogers 2015 incidence study). It arises from basal keratinocytes of the epidermis or hair follicles after years of cumulative ultraviolet damage, and concentrates on sun-exposed skin: the face, ears, scalp, and dorsa of the hands.
Basal cell carcinoma (ICD-10: C44) is a low-grade malignancy arising from basal keratinocytes in the interfollicular epidermis and pilosebaceous units. It is the most common form of non-melanoma skin cancer (NMSC) and the most frequently diagnosed cancer in fair-skinned populations worldwide. The dominant molecular driver is constitutive activation of the Hedgehog signaling pathway, most often through inactivating mutations in the PTCH1 tumor suppressor gene (90%) or activating mutations in SMO (10%). Cumulative ultraviolet exposure produces characteristic UV-signature mutations (C-to-T transitions at dipyrimidine sites).
The key symptoms of Basal Cell Carcinoma are: A pearly, translucent, dome-shaped papule with visible fine surface blood vessels (telangiectasias) and rolled borders, most often on the face, scalp, or ears, slowly enlarging over months to years., A non-healing sore that bleeds easily with minor trauma, scabs over, partially heals, and then breaks down again — a sore that has not fully healed in 4-6 weeks needs evaluation., A flat, scaly, slightly erythematous patch on the trunk or extremities that resembles eczema or psoriasis but does not respond to topical steroids or moisturizers., A white, scar-like flat plaque with indistinct borders that subtly thickens or develops fine telangiectasias — typical of morpheaform BCC, the most diagnostically challenging variant., A pigmented papule that mimics melanoma — often blue, gray, or brown, sometimes with multiple colors — diagnosed by biopsy showing basaloid features with melanin., Recurrent ulceration with rolled, raised, pearly edges and a central crater (rodent ulcer) in long-neglected disease, often eroding through cartilage of the nose or ear., Itching, tenderness, or mild burning at the lesion site, although most BCCs are asymptomatic and noticed incidentally..
Diagnosis of basal cell carcinoma begins with clinical inspection of any persistent skin lesion using dermatoscopy. Classic dermatoscopic features include arborizing telangiectasias, blue-gray globules, leaf-like areas, spoke-wheel patterns, and ulceration — these reach over 95% diagnostic accuracy in trained hands. Skin biopsy confirms the diagnosis histologically and is performed for any clinically suspicious lesion, even when dermatoscopy is highly suggestive. Punch biopsy (3-4 mm) is preferred for nodular and morpheaform variants because it provides full-thickness tissue including the deep dermis where infiltrative behavior is identified; shave biopsy is acceptable for clearly superficial lesions but may miss infiltrative deep components. Histology demonstrates basaloid cell nests with peripheral palisading, mucinous stroma, and retraction artifact. Subtype identification (nodular, superficial, morpheaform, basosquamous) drives treatment choice and risk stratification per NCCN guidelines. For tumors above 2 cm, on high-risk anatomic sites (central face, eyelids, ears, scalp), or with aggressive histology, imaging with MRI evaluates depth, perineural invasion, and bone involvement. CT is reserved for confirmed bone destruction or deep extension. Sentinel lymph node biopsy is not standard for BCC because regional spread is exceedingly rare. Differential diagnosis includes intradermal nevus, sebaceous hyperplasia, fibrous papule, melanoma (for pigmented variants), squamous cell carcinoma, and chronic eczema or psoriasis (for superficial BCC). The decisive test is always histopathology.
Basal cell carcinoma carries an excellent prognosis when treated early. Five-year cure rates exceed 95% for primary low-risk lesions managed with standard excision and reach 99% with Mohs micrographic surgery. Locally advanced disease and metastatic BCC are rare (under 0.1% lifetime risk) but carry 5-year survival of 30-40% even with systemic therapy. The dominant long-term issue is not mortality but recurrence and second-primary BCC: 35-50% of patients develop a new NMSC within 5 years of a first BCC. Anatomic site, histologic subtype, and previous treatment failure are the main recurrence predictors — morpheaform and basosquamous variants on the central face have the highest recurrence risk. Survival from a single BCC is essentially equivalent to age-matched controls. The decisive prognostic factor is patient adherence to lifelong dermatologic surveillance, photoprotection, and early treatment of new lesions. Cosmetic and functional outcomes depend on tumor size and location; Mohs surgery and reconstructive techniques preserve form and function in the vast majority of facial cases.
Any persistent, non-healing, or pearly skin lesion warrants dermatologist evaluation. Mohs micrographic surgeons should manage high-risk BCC on the face, head, and neck, recurrent disease, lesions over 2 cm, and tumors with aggressive histology. Medical oncologists and head-and-neck surgeons coordinate care for locally advanced or metastatic disease.
Find specialists →Wound healing after Mohs or excisional surgery takes 2-4 weeks for primary closure and 4-8 weeks for skin grafts or local flaps. Sutures are removed at 5-7 days on the face and 10-14 days on the trunk. Scar maturation continues for 6-12 months. Topical treatments (imiquimod, 5-fluorouracil) produce intense inflammation lasting 2-6 weeks. Hedgehog inhibitor responses in advanced disease appear over 1-3 months and may continue for 6-12 months. Full return to daily activities is usually within 1-2 weeks after outpatient surgical treatment.
Regular exercise (150 minutes weekly of moderate activity) supports general health and is encouraged. Outdoor exercise should pair with strict photoprotection — long sleeves, wide-brimmed hat, sunscreen, and timing outside peak UV hours. Indoor activity (swimming pools with sun protection, gyms) avoids UV entirely.
Look for board certification in dermatology and, for high-risk facial BCC, fellowship training in Mohs micrographic surgery (American College of Mohs Surgery certification). For advanced disease, seek multidisciplinary cancer centers offering Hedgehog pathway inhibitors and immunotherapy clinical trials. Continuity of care matters: post-treatment surveillance is lifelong because of recurrence and second-primary risk.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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