Melanoma Maligna
Published on May 18, 2026
Risk Factors
Family history, fair skin/light eyes/red-blonde hair (Fitzpatrick type I), history of sunburn, numerous or dysplastic nevi, chronic sun exposure, tanning bed use, immunosuppression (post-transplant, hematologic disease), atypical nevus syndrome
Etiology
Malignant transformation of melanocytes originating from neural crest cells; can arise in skin as well as extracutaneous sites (GI tract, brain) where neural crest cells migrate
Presentation
Changing mole (color, size, shape), new pigmented lesion with irregular borders, bleeding/crusting/itching nodule; often found incidentally during routine skin examination
Classic Exam
ABCDE criteria: Asymmetry, Border irregularity, Color variation, Diameter >6 mm, Evolution; pigmented lesion with multiple colors (brown, black, blue-gray, red, white); satellite lesions or in-transit metastases; palpable regional lymphadenopathy
Diagnostics
Dermoscopy showing atypical pigment network, blue-white veil, irregular streaks, regression structures; histopathology with atypical melanocyte nests at dermo-epidermal junction, pagetoid spread, loss of maturation; IHC markers S100, Sox10, HMB-45, Melan-A; Breslow thickness and ulceration status for staging
Management
Wide local excision with margins based on Breslow thickness (in situ: 0.5-1 cm, up to 1 mm: 1 cm, 1-2 mm: 1-2 cm, >2 mm: 2 cm); SLNB for Breslow >=1 mm; adjuvant pembrolizumab 200 mg IV q3w or 400 mg IV q6w for stage III; systemic therapy with checkpoint inhibitors or BRAF/MEK inhibitors for advanced disease
Keywords
"Changing mole," "irregular borders with multiple colors," "Breslow thickness," "ABCDE criteria," "blue-white veil on dermoscopy," "sentinel lymph node biopsy," "BRAF V600 mutation"
01Pathophysiology
Melanoma maligna arises from the malignant transformation of melanocytes, which are pigment-producing cells derived from the neural crest. Because their embryologic origin is neural crest, melanocytes are not limited to skin. They migrate during development to the GI tract, meninges, and other mucosal surfaces, which explains why melanoma can occur in extracutaneous locations such as the oral cavity, nasal sinuses, anorectal region, and genitourinary tract.
The pathogenesis involves a combination of genetic susceptibility and UV-induced DNA damage. Intermittent intense sun exposure (the pattern that causes blistering sunburns) is more strongly associated with superficial spreading melanoma and nodular melanoma, while chronic cumulative sun exposure drives lentigo maligna melanoma. UV radiation induces mutations in key oncogenes, most notably BRAF (found in up to 56% of melanomas, particularly SSM and NM), NRAS, and c-KIT (more common in acral and mucosal subtypes). BRAF V600 mutations activate the MAPK signaling pathway, promoting uncontrolled cell proliferation and survival.
The number of melanocytic nevi (both common and dysplastic) shows a stronger correlation with melanoma risk than their size, reflecting overall melanocyte burden and genetic instability. Immunosuppressed patients (transplant recipients, hematologic malignancies) have a disproportionately elevated risk because intact immune surveillance is critical for eliminating transformed melanocytes.
Histologically, melanoma progresses through two phases. The radial growth phase represents horizontal spread within the epidermis and superficial dermis; the tumor is thin and carries a favorable prognosis. The vertical growth phase marks invasion into deeper dermis and subcutis, granting the tumor metastatic potential. This progression directly correlates with Breslow thickness, the single most important histologic prognostic factor.
02Classification and Clinical Manifestation
Subtypes of Cutaneous Melanoma
Superficial Spreading Melanoma (SSM)
Proportion
~70%
Typical Patient/Location
Lower extremities (women), upper back (men); intermittent sun-exposed areas
Clinical Features
Flat lesion with irregular borders, uneven pigmentation, multiple colors (brown, black, blue-gray, red, white); often arises from pre-existing nevus
Growth Pattern
Slow radial phase (months to years); often mistaken for atypical nevus or seborrheic keratosis
Key Genetic Feature
High BRAF mutation rate (up to 56%)
Nodular Melanoma (NM)
Proportion
15-30%
Typical Patient/Location
Trunk
Clinical Features
Elevated, dome-shaped nodule; blue-black or blue-red, homogeneous color; 5% are amelanotic
Growth Pattern
Rapid vertical growth (weeks to months); lacks a clear radial phase
Key Genetic Feature
High BRAF mutation rate
Lentigo Maligna Melanoma (LMM)
Proportion
10-15%
Typical Patient/Location
Chronically sun-damaged skin of face (cheeks, nose), neck, scalp, ears; elderly patients
Clinical Features
Flat, slowly enlarging brown macule with irregular color variation (brown and tan shades); begins as lentigo maligna (melanoma in situ) before becoming invasive
Growth Pattern
Very prolonged radial phase
Key Genetic Feature
c-KIT aberrations (28%) more common than BRAF (6%); rarely associated with nevi
Acral Lentiginous Melanoma (ALM)
Proportion
2-8% of melanoma in light-skinned; 29-72% in dark-skinned populations
Typical Patient/Location
Palms, soles, subungual areas; mean age ~65 years
Clinical Features
Brown-to-black patch with irregular borders on acral skin; subungual variant presents as longitudinal melanonychia (brown-black nail streak) at great toe or thumb
Growth Pattern
Variable
Key Genetic Feature
BRAF (21%), c-KIT (13%), c-KIT copy number changes up to 36%
Desmoplastic Melanoma (DM)
Proportion
Uncommon
Typical Patient/Location
Head and neck in patients aged 60-70; chronically sun-exposed skin
Clinical Features
Firm, sclerotic, or indurated lesion; ~50% amelanotic; ~50% associated with lentigo maligna
Growth Pattern
Tends toward perineural invasion; high local recurrence but low nodal metastasis
Key Genetic Feature
NF1 mutations (>90%); lacks BRAF/NRAS mutations; high UV-mutation burden
Mucosal Melanoma
Proportion
1.3%
Typical Patient/Location
Conjunctiva, nasal/sinus cavity, oral cavity, genital/anorectal, urethral mucosa
Clinical Features
Pigmented patches or bleeding masses on mucosal surfaces; often detected late
Growth Pattern
Variable
Key Genetic Feature
NRAS/KRAS mutations (5-30%); activates MAPK pathway
Subtype | Proportion | Typical Patient/Location | Clinical Features | Growth Pattern | Key Genetic Feature |
|---|---|---|---|---|---|
Superficial Spreading Melanoma (SSM) | ~70% | Lower extremities (women), upper back (men); intermittent sun-exposed areas | Flat lesion with irregular borders, uneven pigmentation, multiple colors (brown, black, blue-gray, red, white); often arises from pre-existing nevus | Slow radial phase (months to years); often mistaken for atypical nevus or seborrheic keratosis | High BRAF mutation rate (up to 56%) |
Nodular Melanoma (NM) | 15-30% | Trunk | Elevated, dome-shaped nodule; blue-black or blue-red, homogeneous color; 5% are amelanotic | Rapid vertical growth (weeks to months); lacks a clear radial phase | High BRAF mutation rate |
Lentigo Maligna Melanoma (LMM) | 10-15% | Chronically sun-damaged skin of face (cheeks, nose), neck, scalp, ears; elderly patients | Flat, slowly enlarging brown macule with irregular color variation (brown and tan shades); begins as lentigo maligna (melanoma in situ) before becoming invasive | Very prolonged radial phase | c-KIT aberrations (28%) more common than BRAF (6%); rarely associated with nevi |
Acral Lentiginous Melanoma (ALM) | 2-8% of melanoma in light-skinned; 29-72% in dark-skinned populations | Palms, soles, subungual areas; mean age ~65 years | Brown-to-black patch with irregular borders on acral skin; subungual variant presents as longitudinal melanonychia (brown-black nail streak) at great toe or thumb | Variable | BRAF (21%), c-KIT (13%), c-KIT copy number changes up to 36% |
Desmoplastic Melanoma (DM) | Uncommon | Head and neck in patients aged 60-70; chronically sun-exposed skin | Firm, sclerotic, or indurated lesion; ~50% amelanotic; ~50% associated with lentigo maligna | Tends toward perineural invasion; high local recurrence but low nodal metastasis | NF1 mutations (>90%); lacks BRAF/NRAS mutations; high UV-mutation burden |
Mucosal Melanoma | 1.3% | Conjunctiva, nasal/sinus cavity, oral cavity, genital/anorectal, urethral mucosa | Pigmented patches or bleeding masses on mucosal surfaces; often detected late | Variable | NRAS/KRAS mutations (5-30%); activates MAPK pathway |
Less Common Subtypes
Subtype | Key Features |
|---|---|
Nevoid Melanoma | Papule or light-brown nodule >1 cm; young adults; mimics benign nevus |
Spitzoid Melanoma | Resembles Spitz nevus but larger (>1 cm), thick invasive component (>2 mm), high mitotic activity, atypical cells; harbors HRAS mutations and BAP1 inactivation rather than BRAF/NRAS |
Rare types | Metaplastic, balloon cell, signet-ring cell, myxoid, rhabdoid, animal-type melanoma, malignant blue nevus |
The test-writer perspective here: SSM is the most common subtype overall, but in a vignette describing a dark-skinned patient with a pigmented lesion on the sole of the foot, the answer is ALM. A rapidly growing blue-black nodule on the trunk without a preceding flat phase points to NM. A slowly expanding flat brown patch on the face of an elderly patient with chronic sun damage is LMM. Do not confuse the subungual variant of ALM with subungual hematoma: a hematoma migrates distally with nail growth, while melanoma does not.
03Diagnostic Workup
Dermoscopy (best initial test for clinical evaluation)
Role
Non-invasive magnified evaluation of pigmented lesions
Key Findings
Atypical pigment network, negative network, atypical dots/globules, irregular streaks, regression structures, blue-white veil, shiny white lines, atypical blotch, polymorphous vessels; presence of at least one feature raises suspicion
Excisional biopsy with histopathology (gold standard/confirmatory)
Role
Provides definitive diagnosis, Breslow thickness, ulceration status, mitotic rate
Key Findings
Atypical melanocyte nests at dermo-epidermal junction, pagetoid spread of melanocytes above basal layer, loss of maturation with depth, confluent nests in dermis, predominance of single atypical melanocytes
Immunohistochemistry (IHC)
Role
Confirms melanocytic lineage in poorly differentiated or amelanotic tumors
Key Findings
S100, Sox10 (sensitive); HMB-45, Melan-A, MiTF (more melanocyte-oriented); DM typically expresses only S100 and Sox10; Ki-67 helps assess proliferation in nevoid melanoma
Serum markers (S100B, LDH)
Role
Monitoring disease course, not for primary diagnosis
Key Findings
S100B and LDH for prognosis and monitoring; LDH recommended for patients with distant metastasis (part of AJCC staging)
Imaging
Role
Staging and metastatic workup
Key Findings
CXR, USG/CT abdomen, bone scan, CT head (if indicated), CT thorax/abdomen/pelvis, PET/CT whole-body for advanced stages
Sentinel Lymph Node Biopsy (SLNB)
Role
Determines microscopic nodal spread
Key Findings
Recommended for Breslow >=1 mm; can be considered for thinner melanomas with additional risk factors (ulceration, high mitotic rate)
Investigation | Role | Key Findings |
|---|---|---|
Dermoscopy (best initial test for clinical evaluation) | Non-invasive magnified evaluation of pigmented lesions | Atypical pigment network, negative network, atypical dots/globules, irregular streaks, regression structures, blue-white veil, shiny white lines, atypical blotch, polymorphous vessels; presence of at least one feature raises suspicion |
Excisional biopsy with histopathology (gold standard/confirmatory) | Provides definitive diagnosis, Breslow thickness, ulceration status, mitotic rate | Atypical melanocyte nests at dermo-epidermal junction, pagetoid spread of melanocytes above basal layer, loss of maturation with depth, confluent nests in dermis, predominance of single atypical melanocytes |
Immunohistochemistry (IHC) | Confirms melanocytic lineage in poorly differentiated or amelanotic tumors | S100, Sox10 (sensitive); HMB-45, Melan-A, MiTF (more melanocyte-oriented); DM typically expresses only S100 and Sox10; Ki-67 helps assess proliferation in nevoid melanoma |
Serum markers (S100B, LDH) | Monitoring disease course, not for primary diagnosis | S100B and LDH for prognosis and monitoring; LDH recommended for patients with distant metastasis (part of AJCC staging) |
Imaging | Staging and metastatic workup | CXR, USG/CT abdomen, bone scan, CT head (if indicated), CT thorax/abdomen/pelvis, PET/CT whole-body for advanced stages |
Sentinel Lymph Node Biopsy (SLNB) | Determines microscopic nodal spread | Recommended for Breslow >=1 mm; can be considered for thinner melanomas with additional risk factors (ulceration, high mitotic rate) |
The clinical workup begins with visual inspection using the ABCDE criteria, which is the screening framework for any pigmented lesion. If a lesion raises concern, dermoscopy is the best initial test because it improves diagnostic accuracy without requiring tissue. The presence of at least one dermoscopic feature (blue-white veil, atypical pigment network, irregular streaks, regression structures) should prompt biopsy.
The gold standard is excisional biopsy with narrow margins (1-3 mm) for histopathologic analysis. The pathology report must include Breslow thickness (measured in millimeters from the granular layer to the deepest invasive melanocyte) and ulceration status, as both are essential for AJCC TNM staging. Shave biopsies that transect the base are unacceptable because they make accurate Breslow measurement impossible.
When a suspicious lesion is examined after biopsy, the surrounding area must be inspected for satellite lesions and in-transit metastases. All other skin surfaces including scalp, interdigital spaces, genitalia, and subungual areas should be checked for additional primary tumors. All regional lymph node basins must be palpated.
For staging workup in advanced melanoma (stage III-IV), imaging includes USG of regional lymph nodes, CT with contrast of the thorax/abdomen/pelvis (adding neck if clinically indicated), and/or PET/CT whole-body. BRAF mutation testing is recommended starting at stage III, as it determines eligibility for targeted therapy.
Serum markers S100B and LDH are used for disease monitoring rather than diagnosis. LDH is part of the AJCC M-category classification for stage IV disease.
04Management and Treatment
Excision Margins Based on Breslow Thickness
Breslow Thickness | Recommended Surgical Margin |
|---|---|
In situ | 0.5 to 1 cm |
Up to 1 mm | 1 cm |
>1 to 2 mm | 1 to 2 cm |
>2 mm | 2 cm |
Mohs micrographic surgery (MMS) can be considered for melanoma in situ or minimally invasive melanoma (T1a) in anatomically constrained areas such as the face, ears, or acral sites. For invasive melanoma, excision depth should extend to the fascia.
Management by Stage
0 in situ / IA (T1a)
Primary Management
Wide excision (1A)
Adjuvant/Systemic
None
Follow-up
Observation per education guidelines
IB (T1b)
Primary Management
Wide excision (1A); consider SLNB consultation (1B)
Adjuvant/Systemic
If SLNB positive, treat as stage III
Follow-up
Observation if SLNB negative
IB (T2a) / II (T2b-T4b)
Primary Management
Wide excision (1A); SLNB consultation (1B)
Adjuvant/Systemic
If SLNB negative: observation +/- radiation oncology consultation; if SLNB positive: treat as stage III
Follow-up
Per stage-based protocol
IIIA/IIIB/C/D (sentinel node positive)
Primary Management
Consider BRAF testing; routine regional nodal imaging q4-6 months OR CLND consultation
Adjuvant/Systemic
Adjuvant systemic therapy if available, OR observation
Follow-up
Imaging surveillance q4-6 months
III (clinically positive nodes)
Primary Management
Baseline imaging; BRAF testing; multidisciplinary consultation; FNA/core biopsy of nodes
Adjuvant/Systemic
Resectable: wide excision + TLND, then adjuvant systemic therapy or radiation. Unresectable: systemic therapy and/or palliative radiation
Follow-up
Per MDT recommendation
III (satellite/in-transit)
Primary Management
Baseline imaging; BRAF testing; multidisciplinary consultation
Adjuvant/Systemic
Resectable: wide excision, then adjuvant if NED. Unresectable: systemic therapy or local therapy (radiation, palliative excision, ablation)
Follow-up
Per MDT recommendation
IV (metastatic)
Primary Management
Biopsy metastatic lesion; BRAF testing; LDH; baseline imaging; multidisciplinary consultation
Adjuvant/Systemic
Oligometastasis: resection then systemic therapy if NED. Disseminated: systemic therapy, palliative/supportive care
Follow-up
Per MDT recommendation
Stage | Primary Management | Adjuvant/Systemic | Follow-up |
|---|---|---|---|
0 in situ / IA (T1a) | Wide excision (1A) | None | Observation per education guidelines |
IB (T1b) | Wide excision (1A); consider SLNB consultation (1B) | If SLNB positive, treat as stage III | Observation if SLNB negative |
IB (T2a) / II (T2b-T4b) | Wide excision (1A); SLNB consultation (1B) | If SLNB negative: observation +/- radiation oncology consultation; if SLNB positive: treat as stage III | Per stage-based protocol |
IIIA/IIIB/C/D (sentinel node positive) | Consider BRAF testing; routine regional nodal imaging q4-6 months OR CLND consultation | Adjuvant systemic therapy if available, OR observation | Imaging surveillance q4-6 months |
III (clinically positive nodes) | Baseline imaging; BRAF testing; multidisciplinary consultation; FNA/core biopsy of nodes | Resectable: wide excision + TLND, then adjuvant systemic therapy or radiation. Unresectable: systemic therapy and/or palliative radiation | Per MDT recommendation |
III (satellite/in-transit) | Baseline imaging; BRAF testing; multidisciplinary consultation | Resectable: wide excision, then adjuvant if NED. Unresectable: systemic therapy or local therapy (radiation, palliative excision, ablation) | Per MDT recommendation |
IV (metastatic) | Biopsy metastatic lesion; BRAF testing; LDH; baseline imaging; multidisciplinary consultation | Oligometastasis: resection then systemic therapy if NED. Disseminated: systemic therapy, palliative/supportive care | Per MDT recommendation |
Adjuvant Systemic Therapy (for resected stage III)
Agent | Dose and Schedule |
|---|---|
Pembrolizumab | 200 mg IV every 3 weeks, OR 400 mg IV every 6 weeks |
Nivolumab | 240 mg IV every 2 weeks, OR 480 mg IV every 4 weeks (not yet available in Indonesia) |
Dabrafenib/trametinib (BRAF V600+) | (Not yet available in Indonesia) |
Systemic Therapy for Unresectable/Metastatic Disease
Line | Options |
|---|---|
First-line | Pembrolizumab 200 mg IV q3w or 400 mg IV q6w; OR nivolumab 1 mg/kg + ipilimumab 3 mg/kg IV q3w x4 doses (not in Indonesia); OR nivolumab monotherapy (not in Indonesia) |
First-line if BRAF V600+ | Vemurafenib 720 mg or 960 mg PO BID / cobimetinib 60 mg, 80 mg, or 100 mg PO daily (various cycling schedules) (cobimetinib not in Indonesia); dabrafenib/trametinib (not in Indonesia); encorafenib/binimetinib (not in Indonesia) |
Disease progression or intolerance | Check for KIT, NRAS mutations. Options: repeat prior therapy, dabrafenib/trametinib + pembrolizumab, imatinib (KIT+), binimetinib (NRAS+), cytotoxic chemotherapy (CVD, temozolamide, paclitaxel, carboplatin/paclitaxel), palliative/supportive care |
Recurrent Disease
Recurrence Type | Approach |
|---|---|
True scar recurrence | Biopsy, restage, re-excise, then manage per new histopathologic stage |
Local satellite / in-transit | Biopsy, then treat as stage III (satellite/in-transit) |
Nodal recurrence (no distant mets) | Treat as stage III (clinically positive nodes) |
Distant recurrence | Treat as stage IV |
Wide local excision is the backbone of melanoma management across all stages. The single most important number to know is the Breslow thickness, because it dictates both excision margins and whether SLNB is indicated. For the exam, if a question gives you a melanoma with Breslow 0.8 mm without ulceration (T1a), the answer is wide excision with 1 cm margins and observation. If Breslow is 1.2 mm, SLNB enters the picture.
05Differential Diagnosis and Distractors
For Superficial Spreading Melanoma
Atypical (dysplastic) nevus
Why It Is Similar
Irregular borders, variable pigmentation
Key Discriminator
Nevi tend to be symmetric, have a more uniform color pattern, and lack dermoscopic features like blue-white veil or regression structures; stable over time
Seborrheic keratosis
Why It Is Similar
Can be darkly pigmented, irregular surface
Key Discriminator
"Stuck-on" appearance, well-demarcated borders, comedo-like openings and milia-like cysts on dermoscopy
Basal cell carcinoma (pigmented)
Why It Is Similar
Dark pigmented nodule
Key Discriminator
Pearly/translucent border, arborizing telangiectasia on dermoscopy, lacks true melanocytic dermoscopic features
Differential | Why It Is Similar | Key Discriminator |
|---|---|---|
Atypical (dysplastic) nevus | Irregular borders, variable pigmentation | Nevi tend to be symmetric, have a more uniform color pattern, and lack dermoscopic features like blue-white veil or regression structures; stable over time |
Seborrheic keratosis | Can be darkly pigmented, irregular surface | "Stuck-on" appearance, well-demarcated borders, comedo-like openings and milia-like cysts on dermoscopy |
Basal cell carcinoma (pigmented) | Dark pigmented nodule | Pearly/translucent border, arborizing telangiectasia on dermoscopy, lacks true melanocytic dermoscopic features |
For Nodular Melanoma
Blue nevus
Why It Is Similar
Blue-black color, dome-shaped
Key Discriminator
Stable, symmetric, uniform blue color; no recent growth or change
Pigmented Spitz nevus
Why It Is Similar
Dome-shaped, pigmented nodule
Key Discriminator
Typically in children/young adults, symmetric starburst pattern on dermoscopy
Pyogenic granuloma
Why It Is Similar
Rapidly growing nodule, may bleed
Key Discriminator
Bright red, vascular, homogeneous color; lacks melanocytic features
Merkel cell carcinoma
Why It Is Similar
Rapidly growing nodule on sun-exposed skin
Key Discriminator
Flesh-colored/red-violet, firm, typically in elderly/immunosuppressed
Differential | Why It Is Similar | Key Discriminator |
|---|---|---|
Blue nevus | Blue-black color, dome-shaped | Stable, symmetric, uniform blue color; no recent growth or change |
Pigmented Spitz nevus | Dome-shaped, pigmented nodule | Typically in children/young adults, symmetric starburst pattern on dermoscopy |
Pyogenic granuloma | Rapidly growing nodule, may bleed | Bright red, vascular, homogeneous color; lacks melanocytic features |
Merkel cell carcinoma | Rapidly growing nodule on sun-exposed skin | Flesh-colored/red-violet, firm, typically in elderly/immunosuppressed |
For Lentigo Maligna / LMM
Solar lentigo
Why It Is Similar
Flat brown macule on sun-damaged face
Key Discriminator
Uniform tan-brown, well-defined borders, no color variation or asymmetry
Pigmented actinic keratosis
Why It Is Similar
Pigmented macule on chronically sun-exposed skin
Key Discriminator
Rough/scaly surface, dermoscopy shows annular-granular pattern rather than melanocytic features
Flat seborrheic keratosis
Why It Is Similar
Flat brown patch on face
Key Discriminator
Sharp demarcation, fingerprint-like pattern on dermoscopy
Differential | Why It Is Similar | Key Discriminator |
|---|---|---|
Solar lentigo | Flat brown macule on sun-damaged face | Uniform tan-brown, well-defined borders, no color variation or asymmetry |
Pigmented actinic keratosis | Pigmented macule on chronically sun-exposed skin | Rough/scaly surface, dermoscopy shows annular-granular pattern rather than melanocytic features |
Flat seborrheic keratosis | Flat brown patch on face | Sharp demarcation, fingerprint-like pattern on dermoscopy |
For Acral Lentiginous Melanoma
Plantar wart (verruca plantaris)
Why It Is Similar
Lesion on the sole
Key Discriminator
Warts interrupt skin lines, have thrombosed capillaries ("black dots"), are flesh-colored/keratotic rather than pigmented
Subungual hematoma
Why It Is Similar
Dark discoloration under nail
Key Discriminator
Hematoma migrates distally with nail growth; positive for hemosiderin, no Hutchinson sign
Longitudinal melanonychia
Why It Is Similar
Dark nail streak
Key Discriminator
Benign melanonychia is uniform, narrow, and stable; melanoma shows widening, Hutchinson sign (pigment extending to nail fold), and irregular color
Onychomycosis
Why It Is Similar
Nail discoloration and dystrophy
Key Discriminator
Yellowish-white rather than brown-black, KOH positive, no pigmented nail fold involvement
Differential | Why It Is Similar | Key Discriminator |
|---|---|---|
Plantar wart (verruca plantaris) | Lesion on the sole | Warts interrupt skin lines, have thrombosed capillaries ("black dots"), are flesh-colored/keratotic rather than pigmented |
Subungual hematoma | Dark discoloration under nail | Hematoma migrates distally with nail growth; positive for hemosiderin, no Hutchinson sign |
Longitudinal melanonychia | Dark nail streak | Benign melanonychia is uniform, narrow, and stable; melanoma shows widening, Hutchinson sign (pigment extending to nail fold), and irregular color |
Onychomycosis | Nail discoloration and dystrophy | Yellowish-white rather than brown-black, KOH positive, no pigmented nail fold involvement |
For Desmoplastic Melanoma
Scar tissue
Why It Is Similar
Firm, fibrous, skin-colored
Key Discriminator
History of prior trauma/surgery at that site; no progressive growth
Dermatofibroma
Why It Is Similar
Firm dermal nodule
Key Discriminator
Dimple sign on lateral compression, stable, well-circumscribed
Desmoplastic nevus
Why It Is Similar
Firm, skin-colored papule
Key Discriminator
Smaller, symmetric, stable over time; lacks perineural invasion on histology
Differential | Why It Is Similar | Key Discriminator |
|---|---|---|
Scar tissue | Firm, fibrous, skin-colored | History of prior trauma/surgery at that site; no progressive growth |
Dermatofibroma | Firm dermal nodule | Dimple sign on lateral compression, stable, well-circumscribed |
Desmoplastic nevus | Firm, skin-colored papule | Smaller, symmetric, stable over time; lacks perineural invasion on histology |
06Traps and High-Yield Pearls
The most common way students get melanoma questions wrong is by fixating on skin color as a reason to dismiss melanoma. ALM is the predominant melanoma subtype in dark-skinned populations, and it occurs on palms, soles, and subungual areas, which are sites students often forget to consider. A vignette describing a dark-skinned patient with a changing pigmented lesion on the sole is testing whether you know that melanoma does not spare individuals with darker Fitzpatrick types.
Another frequent trap is confusing Breslow thickness with Clark level. Breslow thickness (measured in millimeters) is the primary prognostic factor and determines excision margins. Clark level (anatomic depth of invasion through skin layers) is older and no longer used in the current AJCC staging system. If a question stem provides both, use Breslow.
Students also stumble on the nodular melanoma presentation. Because NM lacks a prolonged radial growth phase, it can present as a rapidly growing, symmetric, uniformly dark nodule that does not fit the classic ABCDE criteria (no asymmetry, no border irregularity, no color variation). The vignette will describe a fast-growing, dome-shaped blue-black nodule. The "E" in ABCDE (Evolution) becomes the critical criterion here.
For management questions, the trap is ordering SLNB for melanoma in situ or T1a without additional risk factors. SLNB is recommended at Breslow >=1 mm. For thinner melanomas, it is only considered when additional risk factors are present (ulceration, high mitotic rate, lymphovascular invasion).
Finally, do not forget that LDH is a staging marker, not a diagnostic marker. It is checked in stage IV disease to classify the M category and to assess prognosis. S100B and LDH are for disease monitoring, not for making the initial diagnosis. The confirmatory diagnosis is always histopathology from an adequate excisional biopsy.