Malignant melanoma is a cancer that starts in melanocytes, the cells that give your skin its color. It accounts for a small fraction of all skin cancers but causes the majority of skin cancer deaths because of its ability to spread to other organs. When caught early and still confined to the skin, the five-year survival rate is essentially 100%. Once it reaches distant organs, that drops to about 35%.
How Melanoma Develops
Melanocytes sit in the outer layer of your skin and produce pigment called melanin. When UV radiation or other factors damage the DNA inside these cells, they can begin growing out of control. The transformation from a normal melanocyte to a cancerous one isn’t a single event. It involves a buildup of genetic changes: proteins that normally keep cell division in check get switched off, while signals that promote growth get stuck in the “on” position.
About 38.5% of melanomas carry a mutation in a gene called BRAF, which drives the cell to multiply. Another 16% have mutations in a related growth gene called NRAS. These same mutations can appear in ordinary moles, but what separates a harmless mole from melanoma is the accumulation of additional chromosomal damage. A mole with one growth-promoting mutation typically stays stable. A melanoma has layer upon layer of genetic disruption that lets cells invade deeper tissue and eventually enter the bloodstream.
Between 8% and 12% of melanomas run in families, often linked to inherited changes in a gene that produces a key cell-growth brake called p16. For most people, though, susceptibility depends more on genes that control skin pigment and DNA repair ability.
Who Is Most at Risk
Fair skin is the single strongest demographic risk factor. People who always burn and never tan (Fitzpatrick skin type I) face the highest risk, followed by those who usually burn and tan minimally (type II). But melanoma occurs across all skin tones. Research shows a positive correlation between UV exposure and melanoma incidence in White, Hispanic, and Black populations alike.
The pattern of sun exposure matters as much as the total amount. Intermittent, intense sun exposure, the kind you get on a beach vacation or a weekend hike after months indoors, is a stronger risk factor for melanoma than steady, daily sun exposure. A history of sunburn, especially during childhood, significantly raises lifetime risk. About 80% of melanomas develop in parts of the world where light-skinned populations get this kind of intermittent intense exposure.
Other risk factors include having a large number of moles (50 or more), a personal or family history of melanoma, a weakened immune system, and certain genetic conditions that impair DNA repair.
The Four Main Subtypes
Not all melanomas look or behave the same way. There are four major subtypes, each with distinct characteristics.
Superficial Spreading Melanoma
This is the most common type, making up roughly 70% of all melanomas. It grows outward across the skin surface for months to years before pushing deeper. It typically appears as a flat or slightly raised brown patch with irregular borders and uneven color, including shades of black, blue, or pink. It can appear anywhere on the body but favors the trunk and head in men and the lower legs in women. Because of its long horizontal growth phase, there’s often a meaningful window to catch it early.
Nodular Melanoma
About 15% of melanomas are nodular, and they’re more dangerous because they grow downward into the skin almost immediately. They look like a raised dome or bump, usually dark brown to black, though about 5% have no pigment at all and can resemble a blood blister or flesh-colored bump. This subtype is most often found on the trunk.
Acral Lentiginous Melanoma
This subtype makes up about 8% of melanomas overall but is the most common form in people with darker skin. It accounts for up to 70% of melanomas in Black patients and 46% in Asian patients. It appears on the palms, soles of the feet, or under fingernails and toenails. Like nodular melanoma, it progresses aggressively from surface growth to deep invasion.
Lentigo Maligna Melanoma
The least common major subtype at about 5% of cases, this form develops on chronically sun-exposed skin, typically the face and arms of older adults. It can exist as a flat, slowly expanding brown patch for many years before becoming invasive. When it does turn invasive, a dark or raised blue-black nodule usually develops within the patch.
How to Spot It: The ABCDE Rule
Most melanomas are first noticed by the person who has them or by someone close to them. The National Cancer Institute uses a five-feature checklist to describe what early melanoma looks like:
- Asymmetry: one half of the mole doesn’t match the other.
- Border irregularity: the edges are ragged, notched, or blurred, and pigment may bleed into surrounding skin.
- Color variation: multiple shades of brown, black, and tan within one lesion, sometimes with areas of white, gray, red, pink, or blue.
- Diameter: most melanomas are larger than 6 millimeters across (about the size of a pencil eraser), though they can start smaller.
- Evolving: any change in size, shape, color, or texture over weeks to months.
The “E” may be the most important letter on that list. A mole that’s changing is worth getting checked, even if it doesn’t tick every other box. Nodular melanomas in particular can be symmetrical and uniformly colored, so change over time is sometimes the only early clue.
Diagnosis and Biopsy
If a suspicious spot is found, the next step is a biopsy. For suspected melanoma, an excisional biopsy is preferred when the size and location allow it. This means removing the entire lesion along with a small margin of normal skin so a pathologist can assess the full depth and architecture. When a lesion is too large or in a difficult location, a wedge or punch biopsy can be used to sample a representative section.
The pathologist measures how deep the melanoma extends into the skin, reported in millimeters as the Breslow depth. This measurement is the single most important factor in determining the stage and predicting outcomes. Thin melanomas (1 mm or less) that haven’t ulcerated carry an excellent prognosis. Thicker tumors, especially those deeper than 4 mm, have a much higher chance of having already spread.
Staging and What It Means
Melanoma staging combines three factors: how thick the tumor is and whether it’s ulcerated, whether cancer has reached nearby lymph nodes, and whether it has spread to distant organs. The stages range from 0 (melanoma confined to the outermost skin layer, called in situ) through IV (distant spread).
The thickness thresholds that define early stages are 1.0 mm, 2.0 mm, and 4.0 mm. Whether the surface of the melanoma has broken down (ulceration) also shifts the stage upward, because ulcerated melanomas behave more aggressively at every thickness level. Stage III means the cancer has reached regional lymph nodes, classified further by whether the spread is microscopic or visible and how many nodes are involved. Stage IV means the melanoma has traveled to distant sites like the lungs, liver, brain, or bone.
The survival numbers reflect how much stage matters. Seventy-seven percent of melanomas are caught while still localized, and those patients have a five-year relative survival rate of 100%. For the 10% diagnosed after regional lymph node spread, survival is about 76%. The 5% found at the distant stage face a 35% five-year survival rate, though this number has improved substantially in recent years thanks to new treatments.
Treatment Options
For early-stage melanoma, surgery is the primary treatment. The melanoma is cut out along with a margin of healthy skin. The width of that margin depends on the tumor’s thickness. For thin melanomas, this is often a straightforward office procedure with minimal scarring. For thicker tumors, a sentinel lymph node biopsy may be performed at the same time. This involves identifying the first lymph node that drains the area around the tumor and checking it for cancer cells to determine whether the melanoma has started to spread.
Advanced melanoma treatment has been transformed by two categories of drugs. The first is immunotherapy, specifically checkpoint inhibitors. Normally, cancer cells can flip an “off switch” on your immune cells by displaying certain proteins on their surface. These proteins bind to receptors on T cells (called PD-1 and CTLA-4) and essentially tell the immune system to stand down. Checkpoint inhibitors block that interaction, freeing T cells to recognize and attack the tumor. These drugs have turned some cases of metastatic melanoma, once considered rapidly fatal, into long-term survivable disease.
The second category is targeted therapy for patients whose tumors carry a BRAF mutation. These drugs directly block the overactive growth signal that the BRAF mutation creates. They’re often used in combination with drugs that block a related downstream signal, improving effectiveness and making it harder for the cancer to develop resistance. Targeted therapy tends to shrink tumors quickly, while immunotherapy can take longer to show results but sometimes produces more durable responses.
For melanoma that has spread to a small number of sites, radiation or surgery to remove individual metastases can also play a role, particularly for brain metastases.