Types of melanoma skin cancer – Canadian Cancer Society


Melanoma skin cancer can grow into and destroy nearby tissue. It can also spread (metastasize) to other parts of the body. Melanoma skin cancer is also called cutaneous melanoma and malignant melanoma of the skin.

There are 4 main types of melanoma skin cancer – superficial spreading, nodular, lentigo maligna and acral lentiginous.

Superficial spreading melanoma

Superficial spreading melanoma is the most common type of melanoma skin cancer. It makes up about 70% of all melanoma skin cancers.

Superficial spreading melanoma tends to grow outward (called radial growth) and spread across the surface of the skin. But it can also start to grow down into the skin (called vertical growth).

It is often flat and thin (less than 1 mm thick) with an uneven border. It varies in colour and may have different shades of red, blue, brown, black, grey and white.

Sometimes superficial spreading melanoma starts from a mole that is already on the skin.

Superficial spreading melanoma usually develops on the central part of the body (trunk), arms and legs. It tends to happen on the back in men and the legs in women.

Nodular melanoma

Nodular melanoma is the second most common type of melanoma skin cancer. It makes up about 15% to 20% of all melanoma skin cancers.

Nodular melanoma grows down into the skin. It grows and spreads more quickly than other types of melanoma skin cancer. It is a raised growth that sticks out from the skin (polypoid). The growth may be shaped a mushroom with a stem or stalk (pedunculated). It is usually black, but sometimes can be red, pink or the same colour as your skin.

Nodular melanoma usually develops on the face, chest or back. It can be found on areas of skin not exposed to the sun.

Lentigo maligna melanoma

Lentigo maligna melanoma most often develops in older people. It makes up about 10% to 15% of all melanoma skin cancers.

Lentigo maligna melanoma usually appears as a large, flat tan or brown patch with an uneven border. It tends to get darker as it grows and has many shades of brown or black.

It often starts from an in situ tumour called lentigo maligna, which is an early form of the growth only in the top or outer layer of the skin (epidermis).

Lentigo maligna melanoma usually grows outward across the surface of the skin for many years before it starts to grow down into the skin.

Lentigo maligna melanoma usually develops on areas of skin that are regularly exposed to the sun without protection, such as the face, ears and arms.

Acral lentiginous melanoma

Acral lentiginous melanoma is most common in people with dark skin, such as those from African, Asian and Hispanic ancestries. It is not related to being exposed to the sun. It makes up less than 5% of all melanoma skin cancers.

Acral lentiginous melanoma appears as a small, flat spot of discoloured skin that is often dark brown or black. It usually grows outward across the surface of the skin for a long time before it starts to grow down into the skin.

Acral lentiginous melanoma usually develops on the soles of the feet, on the palms of the hands or under the nails. It is often hard to diagnose acral lentiginous melanoma because it’s hard to see abnormal areas on the soles of the feet or under the nails.

Rare types of melanoma

Some rare types of melanoma do not start in the skin. The following types of melanoma are rare.

Mucosal lentiginous melanoma develops on the thin, moist lining of some organs or other parts of the body (mucosa or mucous membrane), such as the nasal passages, mouth, throat (pharynx), rectum, anal canal and vagina. It is not related to being exposed to the sun most melanoma skin cancers. It is usually diagnosed at a late stage and tends to grow and spread quickly.

Intraocular melanoma starts in the eye. It is the most common type of eye cancer. Find out more about eye cancer (intraocular melanoma).

Desmoplastic melanoma develops in the thick, inner layer of skin (dermis) or the layer of connective tissue that surrounds the mucosa (submucosa). It often appears as a lump that is the same colour as your skin. It tends to grow down into the skin. Desmoplastic melanoma often develops on the head, neck, upper back or areas of the body with a mucosa.


A non-cancerous (benign) growth on the skin that is usually tan, brown or flesh-coloured.

Moles are made up of a cluster of melanocytes (cells that make melanin, which gives skin, hair and eyes their colour). They may be raised or flat.

Also called nevus.


Melanoma: Practice Essentials, Overview, Indications and Guidelines


Medical therapy is used as adjuvant treatment in advanced stages of unresectable or metastatic melanoma and, most recently, for resected, advanced-stage disease.

 Approvals from the US Food and Drug Administration (FDA) include trametinib (Mekinist), dabrafenib (Tafinlar), ipilimumab (Yervoy), vemurafenib (Zelboraf), pembrolizumab (Keytruda), and nivolumab (Opdivo). Trametinib is a MEK inhibitor indicated for melanoma with BRAF V600E or V600K mutations.

Dabrafenib is a BRAF protein kinase inhibitor indicated for melanoma with BRAF V600E mutation. Ipilimumab is a targeted T-cell antibody that binds to CTLA-4. Vemurafenib is an inhibitor of some mutated forms of BRAF serine-threonine kinase, including BRAF V600E.

Pembrolizumab and nivolumab are monoclonal antibodies to programed cell death-1 (PD-1) protein. They block the interaction between PD-1 and its ligands (ie, PD-L1 and PD-L2). [16, 17]

The combination of binimetinib (Mektovi), a MEK inhibitor, plus encorafenib (Braftovi), a BRAF inhibitor, was approved by the FDA in June 2018 for patients with unresectable or metastatic melanoma with a BRAF V600E or V600K mutation.

Approval followed the success of the phase 3 COLUMBUS trial, in which, compared with treatment with vemurafenib alone, binimetinib/encorafenib therapy led to double the median progression-free survival time (7.3 mo vs 14.9 mo, respectively).


A study by Hecht et al indicated that patients with BRAF-mutated melanoma have better overall survival and experience less toxicity when vemurafenib treatment is interrupted during radiotherapy instead of administered concomitantly.

For patients who underwent interrupted treatment, median overall survival from the start of radiotherapy and from the beginning of vemurafenib treatment was 10.1 and 13.1 months, respectively, compared with 6.6 and 10.9 months, respectively, for the group that received concomitant therapy.

Moreover, there was a greater incidence of skin toxicity of grade 2 or higher ( Common Terminology Criteria for Adverse Events [CTCAE]) in the concomitant patients than in the interrupted group. [19]

In October 2015, the FDA approved talimogene laherparepvec (Imlygic), a genetically modified, live attenuated herpes simplex virus programmed to replicate within tumors and manufacture granulocyte-macrophage colony-stimulating factor (GM-CSF), an immunostimulatory protein.

The first oncolytic viral therapy approved by the FDA, talimogene laherparepvec is indicated for the local treatment of unresectable cutaneous, subcutaneous, and nodal lesions in cases of postsurgery melanoma recurrence.

It is administered by injection into lesions that are visible, palpable, or detectable by ultrasonographic guidance. [20]

Approval was results from OPTiM (OncoVEX [GM-CSF] Pivotal Trial in Melanoma), a randomized, controlled study conducted in 436 adults with unresectable regionally or distantly metastatic melanoma. In the trial, 295 patients were treated with talimogene laherparepvec, while 141 patients received with GM-CSF.

 Those who were treated with talimogene laherparepvec had a 16.3% durable response rate (the rate of complete response plus partial response beginning within the first 12 months and lasting continuously for ≥6 months), compared with 2.1% in patients given GM-CSF. A complete response was obtained in 32 patients (10.

8%) treated with talimogene laherparepvec, versus just one patient (0.7%) who received GM-CSF. [20, 21]

Adjuvant treatment for resected melanoma

In addition to its use against unresectable or metastatic melanoma, in December 2017 nivolumab received FDA approval as an adjuvant therapy for patients who have undergone complete resection of melanoma with lymph node involvement or metastatic disease.

Approval stemmed from the CheckMate-238 trial. In that study, investigators found that in completely resected patients with stage IIIB/C or IV melanoma, those treated with nivolumab had a higher 12-month recurrence-free survival rate than did patients treated with ipilimumab (70.

5% vs 60.8%, respectively). [22]

Pembrolizumab gained FDA approval in February 2019 for adjuvant treatment of resected, high-risk stage 3 melanoma. Approval was data from a phase 3, double-blind trial showing the rate of 1-year recurrence-free survival to be significantly greater with pembrolizumab than with placebo (75.4% vs 61%, respectively). [23]

Surgical therapy for melanoma is the predicted risk of local recurrence and metastatic disease and the potential morbidity of the operation. If the lesion has not spread beyond the primary site, it is potentially curable. Most of these lesions are thin (< 1 mm or CL I or II).

After making the diagnosis, widely excise the tumor or previous biopsy site. Use a 0.5- to 1-cm margin for melanomas in situ. No further therapy other than observation for nodal or recurrent disease is necessary.

For a T1 lesion, 1-cm excision margins are adequate, but lesions greater than 1 mm require 2-cm margins. Studies demonstrate no improvement in recurrence or survival rates with larger margins of resection.

Attempt primary closure and perform skin grafting or flap closure if necessary.

For lesions with a depth greater than 1 mm, many authorities recommend sentinel lymph node biopsy at the time of wide local excision (see Stage II below).

Perform a 2-cm surgical resection on stage II lesions. No recurrence or survival advantage is gained when 2-cm margins are compared with wider margins (4-6 cm), as has been confirmed in a 2011 European study. [24] Smaller resection decreases the need for skin grafting and inpatient hospital stay. [25]

Perform a complete therapeutic lymphadenectomy on patients with suspected lymph node metastases physical examination findings. This consists of excision of all lymph nodes in the affected regional lymph node basin.

Consider sentinel lymph node biopsy if no clinically positive nodes are present. With the use of blue dye, radioisotope, or both, injected at the site of the primary melanoma, the first-echelon node can be identified within the regional lymph node basin.

Send this sentinel node to the pathologist for analysis using routine stains, immunohistochemistry, and even polymerase chain reaction in some centers. If the sentinel node is positive, then regional lymph node metastases is probable; importantly, perform a complete lymph node dissection. The correlation is the thickness of the primary tumor.

If the sentinel lymph node is negative, the chance is 99% that all others are negative. This procedure is becoming the standard of care for tumors greater than 1 mm in depth.

Hyperthermic arterial limb perfusion with melphalan for extremity melanomas has been studied as an adjuvant therapy. One study found it to be beneficial in that it produced higher response rates and overall survival rates than those for surgery alone. Other studies do not demonstrate benefit.

Adjuvant chemotherapy and/or biological therapy are also undergoing clinical evaluation. One study demonstrated that high-dose interferon alfa-2b resulted in prolonged relapse-free survival and overall survival compared with no adjuvant therapy.

A follow-up study by the same group demonstrated preliminary results indicating high-dose interferon achieved a relapse-free survival benefit over no adjuvant treatment but not over low-dose interferon. Neither high- nor low-dose interferon had a significant overall survival advantage compared with observation alone.

High-dose interferon can be associated with significant toxic/adverse effects (ie, liver toxicity), and some patients require dose reduction because it may not be well tolerated.

Wide local excision of the primary tumor with 2-cm margins remains first-line therapy. [1] No survival advantage is demonstrated with wider resection margins. Skin grafting or other tissue-transfer techniques may be necessary to close the defect. Perform regional lymph node dissection because a stage III melanoma represents nodal disease.

If the nodal status is unknown, consider a sentinel lymph node biopsy to determine if the disease is stage I, II, or III. As in stage II disease, the treatment failure rate is higher with wide local excision alone in this group compared with stages 0 and I. Many clinical trials currently are exploring similar options as adjuvant therapy.

Advanced metastatic melanoma is usually refractory to standard therapy; thus, consider these patients for clinical trials. Some treatments have yielded various objective responses, although they are usually short-lived.

Dacarbazine (DTIC) and the nitrosoureas, carmustine (BCNU) and lomustine (CCNU), produced a 20% objective response rate. Response rates for interferon alfa and interleukin 2 range from 8-22% and 10-20%, respectively. Recently, 2 studies have shown promising results.

One study showed improved rates of overall and progression-free survival in patients with previously untreated metastatic melanoma with the BRAF V600E mutation who received vemurafenib versus standard dacarbazine.

[26] Another trial showed improved survival for metastatic melanoma patients treated with ipilimumab and dacarbazine versus placebo and dacarbazine. [27]

Another study looking at treatment of advanced extremity melanoma showed that hyperthermic isolated limb perfusion therapy is a more effective way of controlling this type of situation than isolated limb infusion therapy. [28] Currently, other studies in progress are comparing other cytotoxic and biologic drug regimens.

Surgical resection of isolated metastases in the gastrointestinal tract, the brain, the lungs, or bone may be performed for palliation, with occasional long survival. Metastatic lymph nodes also may be removed for palliation. Radiation may provide symptomatic relief for metastases to bone, the brain, or viscera.

In-transit metastases arise in the lymphatics or soft tissue between the primary lesion and the regional lymph node basin at a rate of 2-3%. In addition to wide surgical excision as for a primary lesion, isolated hyperthermic limb perfusion is probably the most effective treatment for extremity lesions.

Radiation and intralesional BCG vaccine injections have had varied success.

Surgical excision offers the most efficacious results in sites where it can be accomplished; however, melanoma is usually refractory to most standard systemic therapy.

Evaluate for metastases. Begin this evaluation with a detailed history and physical examination. The most common metastatic sites, in descending order, are the regional lymph nodes, skin and subcutaneous tissue (in-transit lesions), and lungs. Other possibilities include the brain, the liver, and bone.

In the absence of signs or symptoms of metastatic disease after performing the history and physical examination, obtain a chest radiograph. If abnormalities are observed, follow this with a chest CT scan.

Check serum alkaline phosphatase and lactate dehydrogenase levels. If these are abnormal or if the patient has a history of weight loss, anorexia, or abdominal pain, obtain a liver ultrasound, abdominal CT scan, or both.

Any abnormalities in the neurologic examination or a history of headaches, vertigo, numbness, or weakness warrant a head CT scan.

A bone scan also may be indicated for isolated bone pain or an elevated alkaline phosphatase level.

Use lymphoscintigraphy to identify the correct lymph node basin(s) that drain the site of the primary tumor. This is an essential aid in preoperative planning.

When performing the wide local excision, first consider the surgical margins. If primary closure is not feasible, skin grafting or tissue transfers may be needed.

The use of blue dye and radiotracer together provides excellent results and is sensitive in finding the sentinel lymph node.

Frozen section specimens have largely been abandoned because the process destroys the ability to analyze the node using immunohistochemistry.

Send the lesion and lymph node specimens to experienced pathologists for review. After the primary tumor is evaluated, the lymph node(s) should undergo hematoxylin and eosin staining. If findings are negative for melanoma, use immunohistochemical techniques.

Specific staining for S-100 protein and HMB-45 monoclonal antibody increases the detection of lymph node micrometastases. More elaborate techniques using reverse transcriptase polymerase chain reaction are still investigational.

They can detect the tyrosinase gene, which is specific for the melanocyte.

Close follow-up care is essential to monitor for new primary lesions, recurrence, or metastases. History and physical examination are the cornerstones, with further testing (eg, chest radiography, blood chemistries) if suggestive findings are encountered. Most practitioners observe patients every 3-6 months initially and then eventually decrease the frequency, although no consensus exists.

Physicians observe patients with thicker tumors more frequently than patients with thinner lesions. Follow-up care with a dermatologist is strongly recommended. Educate patients on self-examination for detection of new or recurrent lesions and for recognition of the signs and symptoms of metastatic disease because the risk of developing a second melanoma or having recurrence is well recognized.

For excellent patient education resources, visit eMedicineHealth's Cancer Center. Also, see eMedicineHealth's patient education articles Skin Cancer, Skin Biopsy, and Mole Removal.




Melanoma is a type of skin cancer that begins in pigment-producing cells called melanocytes. This cancer typically occurs in areas that are only occasionally sun-exposed; tumors are most commonly found on the back in men and on the legs in women.

Melanoma usually occurs on the skin (cutaneous melanoma), but in about 5 percent of cases it develops in melanocytes in other tissues, including the eyes (uveal melanoma) or mucous membranes that line the body's cavities, such as the moist lining of the mouth (mucosal melanoma).

Melanoma can develop at any age, but it most frequently occurs in people in their fifties to seventies and is becoming more common in teenagers and young adults.

Melanoma may develop from an existing mole or other normal skin growth that becomes cancerous (malignant); however, many melanomas are new growths. Melanomas often have ragged edges and an irregular shape. They can range from a few millimeters to several centimeters across. They can also be a variety of colors: brown, black, red, pink, blue, or white.

Most melanomas affect only the outermost layer of skin (the epidermis). If a melanoma becomes thicker and involves multiple layers of skin, it can spread to other parts of the body (metastasize).

A large number of moles or other pigmented skin growths on the body, generally more than 25, is associated with an increased risk of developing melanoma. Melanoma is also a common feature of genetic syndromes affecting the skin such as xeroderma pigmentosum.

Additionally, individuals who have previously had melanoma are nearly nine times more ly than the general population to develop melanoma again. It is estimated that about 90 percent of individuals with melanoma survive at least 5 years after being diagnosed.

In the United States, melanoma is the fifth most common cancer in men, affecting 30 in 100,000 men per year, and the sixth most common cancer in women, affecting 18 in 100,000 women per year. About 1 in 43 individuals in the United States will develop melanoma in their lifetime. Light-skinned people have a 20 times greater risk of developing melanoma than dark-skinned people.

Melanoma is caused by a combination of environmental and genetic factors. The greatest environmental risk factor for developing melanoma is exposure to ultraviolet (UV) radiation from the sun. The risk for melanoma is greatest in individuals who have brief but intense sun exposure rather than moderate, long-term exposure. UV radiation can also come from tanning beds (indoor tanning).

UV radiation damages DNA. Most of the time, this kind of DNA damage causes cells to self-destruct (undergo apoptosis) or permanently stop cell division (undergo senescence). However, melanocytes are more resistant than other kinds of cells to the effects of UV radiation.

Even if their DNA is damaged, melanocytes are unly to undergo apoptosis. As abnormal melanocytes continue to grow, they accumulate genetic mutations, particularly in genes that control cell growth and division (proliferation), senescence, and apoptosis.

Ultimately, the cells become able to proliferate without control or limit and can resist cell death, leading to the formation and growth of a melanoma.

Most cases of melanoma are sporadic, which means that the genetic changes are acquired during a person's lifetime and are present only in the melanocytes that give rise to the melanoma. These changes, which are called somatic mutations, are not inherited.

Studies suggest that in some cases somatic variations in multiple genes, each with a small effect, combine to increase the risk of developing the condition. Many of these gene variations are associated with a light complexion and increased freckling and moles.

However, it is unclear what contribution each of these genetic changes makes to disease risk. Other somatic gene mutations have large effects on melanoma risk and a mutation in one gene is enough to significantly increase the risk of developing cancer.

Somatic mutations in the BRAF and CDKN2A genes are some of the most common in sporadic melanoma.

In about 10 percent of cases, melanoma occurs in multiple members of the same family. Un sporadic melanoma, these familial cases are typically caused by inherited genetic changes that increase the risk of developing this type of cancer.

These genetic changes, which are classified as germline mutations, are present in essentially all of the body's cells. The primary genes involved in familial melanoma are CDKN2A and MC1R.

The CDKN2A gene plays a role in regulating cell senescence and the MC1R gene influences skin pigmentation. Shared nongenetic factors can also influence the development of melanoma in family members; for example, family members may live in the same sun-exposed environment.

In people with germline mutations, changes in other genes, together with environmental and lifestyle factors, also contribute to the possible development of melanoma.

Most cases of melanoma are sporadic, which means that they occur in people with no apparent history of the disorder in their family.

When the disorder is familial, it can be due to shared environmental factors or shared genetic factors or both.

The genetic factors are usually inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to increase the risk of developing melanoma.

When melanoma occurs as part of a genetic syndrome, the risk of melanoma follows the inheritance pattern of the syndrome.

  • cutaneous melanoma
  • malignant melanoma


Melanoma – American Osteopathic College of Dermatology (AOCD)


Melanoma is tumor of the skin that is cancerous (malignant). It grows from the melanocytes, the cells that color and tan the skin. Melanoma is also called cutaneous melanoma or malignant melanoma. The incidence of melanoma is increasing worldwide at a rate of about 5% per year.

It is a more serious problem than the more common skin cancers, basal cell cancer or squamous cell cancer. Un these cancers, melanoma often will spread (metastasize) to other parts of the body. 96,480 new cases of melanoma are expected to be diagnosed in the US in 2019, with 7000 resulting in death.

It is the 5th most common cancer in men and 6th most common in women. For people 25 to 29, it the #1 most diagnosed cancer in the United States.

Melanoma can spread by local extension (through lymphatics) and/or by hematogenous routes (through the bloodstream) to distant sites. The risk of relapse may decrease over time, but late relapses are not uncommon.

Melanoma can appear on the body as a new mole, or one that has changed in size, shape, feeling or color, or developed oozing or bleeding. Adult men most often get melanoma on the trunk, especially between the shoulder blades, or on the head or neck. Women most often get melanoma on the arms and legs. It can rarely form in children.

Most melanomas are dark, but some are not, and may be flesh colored or pink to red. If there is a serious question of skin cancer, the mole or pigmented area will be cut out (local excision). This is usually done in a doctor's office. It is important that this remove the entire mole if possible.

The lab will analyze the removed skin. If melanoma is found they will report how deep and aggressive it appears. Then a physical exam and lab tests will be done to look for signs that cancer cells have spread to other parts of the body. This is called staging. A doctor needs to know the stage of the disease to plan treatment.

In the earliest melanomas, the abnormal cells are found only in the outer layer of skin cells and do not invade the body. It is more advanced if the growth goes deeper than 4 millimeters (less than 1/6 of an inch) into the skin.

Most melanomas fall between these two extremes.

More serious still are melanomas that have spread to the body tissue below the skin, show additional tumor around original tumor (satellite tumors), or have spread to lymph nodes or other organs.

Surgery is the primary treatment of all stages of melanoma. A second procedure is normally done to ensure complete removal of the melanoma. Complete removal of all the melanoma before it has spread is the only sure cure for melanoma.

Usually, the biopsy site and a rim of apparently normal skin are removed. This is called a re-excision. The amount removed depends on how deep the melanoma has grown.

Skin may have to be taken from another area of the body and put (or “grafted”) where the cancer has been taken out.

Radiation therapy uses beams of energy to destroy cancer cells. It is usually done on the area where lymph nodes are removed in case any cancer cells remain.

Chemotherapy uses drugs to kill cancer cells. However, chemotherapy has not been shown to be very effective in treating melanoma. In the last 10 years, newer therapies have emerged which are finally decreasing the death rate of melanoma.

One of these therapies is immunotherapy which stimulates the body’s own immune system to fight cancer. Immunotherapy can be systemic or local. Systemic treatments travel through the bloodstream to reach all parts of the body, which is helpful if the melanoma has spread from its original location. Local treatments are injected directly into the melanoma lesions.

Another treatment is targeted therapy which is a medication that interferes directly with the function of abnormal molecules within tumor cells that regulate their growth. This slows down or stops the growth of melanoma cells without harming normal tissue.

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The medical information provided in this site is for educational purposes only and is the property of the American Osteopathic College of Dermatology. It is not intended nor implied to be a substitute for professional medical advice and shall not create a physician – patient relationship.

If you have a specific question or concern about a skin lesion or disease, please consult a dermatologist.

Any use, re-creation, dissemination, forwarding or copying of this information is strictly prohibited unless expressed written permission is given by the American Osteopathic College of Dermatology. 


What are the Signs & Symptoms of Melanoma?

Often, melanoma begins as a mole or a bump on the skin. It's important to know if a mole has changed in size, shape, or color.

Keep this ABCDE rule in mind when checking moles:

  • A for asymmetry: If you were to cut the mole down the middle, would the left and the right sides look different?
  • B for border: Are the edges blurry and undefined? Does it look it's spreading sideways?
  • C for color: Does the mole look darker or lighter than usual, or does it have an area of new color — perhaps black, blue, purple, red, or white?
  • D for diameter: Is the mole larger than the eraser on a pencil top?
  • E for evolving: Has there been any change in the size, shape, color, or elevation of the mole?

Melanoma most commonly develops on the trunk, head, and neck for guys, and the lower legs for girls.

What Causes Melanoma?

One of the most important contributors to melanoma is ultraviolet (UV) sun damage. Cells that have been damaged — particularly by short bouts of bad, blistering sunburns during childhood or regular tanning bed use as a teen or young adult — are more ly to become cancerous over time.

Sometimes melanoma begins in an area where there is no dark spot or bump.

Melanoma happens when melanocytes stop working normally. Because of a genetic change (mutation), they begin growing control, sticking together to form tumors, crowding out healthy cells, and damaging surrounding tissue.

Who Gets Melanoma?

Risk factors that can increase a person's chances of melanoma include:

  • a fair complexion (light skin that freckles or burns easily)
  • blue or green eyes
  • blond or red hair
  • having many moles (usually, more than 25)
  • UV exposure (from the sun or a tanning bed)
  • having a history of frequent or severe sunburns
  • having a relative with melanoma or a family history of oddly shaped moles
  • age (older people are at greater risk)
  • having had melanoma before

Though less ly, people can still get melanoma even if they're young, have no family history of cancer, or have dark skin.

How Is Melanoma Diagnosed?

The doctor will do a biopsy, removing all or part of the lesion (the affected area of skin) and look at its cells under a microscope. A biopsy shows if the cells are cancerous. It can also show how deep they are in the skin, which can help doctors predict the risk of the melanoma spreading.

How Is Melanoma Treated?

Melanoma treatment can include:

  • surgery to remove the cancerous lesion
  • chemotherapy: tumor-killing medicines are given by mouth, through an injection (a shot), or intravenously (into a vein)
  • targeted therapy: specific medicines that find and attack cancer cells without hurting normal cells
  • immunotherapy (biologic therapy): when doctors stimulate the body's own immune system to fight cancer cells

The treatment chosen depends on:

  • how big and how deep the lesion is
  • what part of the body it is on
  • whether the cancer has spread

Can Melanoma Be Cured?

Melanoma that's caught early, when it's still on the surface of the skin, can be cured.

Untreated melanoma can grow downward into the skin until it reaches the blood vessels and lymphatic system. This lets it travel to distant organs, the lungs or the brain. That's why early detection is so important.

Can Melanoma Be Prevented?

You can't control how fair your skin is or whether you have a relative with cancerous moles. But there are things you can do to lower your risk of developing melanoma. The most important is limiting your exposure to the sun.

Take these precautions:

  • Avoid the strongest sun of the day — between 10 a.m. and 4 p.m.
  • Use broad-spectrum sunscreen (SPF 30 or more) whenever you're in the sun.
  • Wear a wide-brimmed hat and cover up with long, loose cotton clothing if you burn easily.
  • Stay the tanning salon. Even one indoor tanning session increases your risk of getting melanoma.

Also, be sure to check your moles often (you may need to ask a friend to help with those hard-to-reach areas, your back and scalp). Keep dated records of each mole's location, size, shape, and color, and get anything suspicious checked out right away.

Not all skin cancer is melanoma, but every case of melanoma is serious. So now that you know more about it, take responsibility for protecting yourself and do what you can to lower your risk.

You can find more information online at:

  • Skin Cancer Foundation
  • American Cancer Society

Reviewed by: Andrew W. Walter, MD

Date reviewed: January 2019