Melonoma medicine

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Melanoma (Malignant Melanoma)

Overview

Melanoma is the most lethal cutaneous malignancy, responsible for more than 77% of skin cancer deaths. It arises from melanocytes — pigment-producing cells found predominantly in skin, but also in the eyes, ears, GI tract, leptomeninges, and oral/genital mucous membranes. Almost half arise from preexisting nevi; the remainder develop on previously normal-appearing skin.

— Textbook of Family Medicine 9e

Risk Factors

Fair complexion, light eyes, red or blond hair
Inability to tan; predisposition to burn; heavy freckling
Excessive childhood sun exposure; >3 blistering childhood sunburns
Large number of common or dysplastic nevi
Giant congenital nevi
Family or personal history of melanoma
Immunosuppression
PUVA, tanning lamps, xeroderma pigmentosum
BRAF gene mutations — frequent in melanomas on non-chronically sun-exposed skin in Caucasians
KIT gene mutations / cyclin D1 amplification — associated with acral and mucosal lentiginous subtypes

— Andrews' Diseases of the Skin

Clinical Recognition — ABCDE Criteria

Letter	Feature
A	Asymmetry
B	Border irregularity
C	Color variegation
D	Diameter >6 mm
E	Evolving (change over time)

A changing or newly acquired nevus in a person over 20 is the most common warning sign. Bleeding, itching, ulceration, or pain in a pigmented lesion are less common but also warrant evaluation.

Subtypes

Subtype	Frequency	Notes
Superficial spreading	60–70%	Most common; occurs on trunk or legs
Nodular	15–30%	Often solid black; thickness predicts poor prognosis
Lentigo maligna	5–15%	Face in elderly; prolonged radial growth phase
Acral lentiginous	5–10%	Great toe, thumb; most common in African Americans

— Textbook of Family Medicine 9e

Diagnosis & Biopsy

Excisional biopsy with 1–2 mm of surrounding normal skin is optimal
"Scoop shave" biopsies are acceptable if specimen depth >1–2 mm
Breslow depth (tumor thickness in mm) is the single most important prognostic indicator
Staging also considers: ulceration (histologic), lymph node involvement, and metastasis site
Thin tumors (Breslow <1 mm) carry >90% 10-year survival

Staging — Breslow Depth Summary

Breslow Depth	Surgical Margin
<1 mm	1 cm margin
1–2 mm	1–2 cm margin
>2 mm	2 cm margin

Sentinel lymph node biopsy (SLNB) is performed for lesions >1 mm, or <1 mm with ulceration or increased mitotic rate.

Treatment Algorithm

Melanoma treatment flowchart based on tumor thickness and lymph node status

Goldman-Cecil Medicine — Treatment pathways for newly diagnosed melanoma

Key decision points:

≤1 mm, no ulceration, mitotic count <1/mm² → Wide local excision only; no further treatment
>1 mm, or <1 mm with ulceration/high mitotic rate → Wide excision + SLNB
- SLNB negative + tumor >4 mm or 2–4 mm with ulceration → Consider adjuvant therapy + surveillance
- SLNB positive → Monitor lymph node basin with serial ultrasound + adjuvant therapy recommended

Adjuvant & Systemic Therapies

Immunotherapy

Ipilimumab (anti-CTLA-4) — demonstrated improved survival in recalcitrant metastatic melanoma in phase III trials
PD-1 inhibitors (nivolumab, pembrolizumab) — checkpoint blockade; mainstay of advanced disease
High-dose interleukin-2 (IL-2) — older option; significant toxicity

Targeted Therapy

BRAF inhibitors (vemurafenib, dabrafenib) — for BRAF V600E-mutant melanoma (~50% of cases)
MEK inhibitors (trametinib, cobimetinib) — often combined with BRAF inhibitors to delay resistance
KIT inhibitors (imatinib) — for KIT-mutant acral/mucosal melanomas

Radiation

Adjuvant radiation considered for high-risk nodal disease or extensive regional involvement

Chemotherapy

Dacarbazine (DTIC) — historically first-line; largely replaced by immunotherapy and targeted agents
Temozolomide — oral alkylating agent with CNS penetration

Prognosis

Stage I (thin, localized): >90% 5-year survival
Stage III (nodal involvement): ~40–70% depending on burden
Stage IV (distant metastasis): historically <10% 5-year survival; significantly improved with modern immunotherapy/targeted therapy combinations

Special Populations

Pregnancy: Nevi often darken uniformly due to estrogen/progesterone receptor expression on melanocytes. Asymmetric or irregularly pigmented changes still warrant biopsy. Melanoma during pregnancy is associated with shorter disease-free intervals but no proven adverse effect on overall survival.
Children: Melanoma is rare; occurs equally from normal skin and preexisting nevi. Diagnosis is often delayed due to low clinical suspicion.
Darker skin types: Acral lentiginous is the predominant subtype; incidence of other subtypes is very low.

— Andrews' Diseases of the Skin; Textbook of Family Medicine 9e

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