Sec 22 Melanocytic Tumors Flashcards
Presence of melanocytic cells in epidermal nests, defined as three or more melanocytic cells in direct contact (also known as thèque), within the dermis, or in other tissues
Melanocytic neoplasia
Increased melanocytes confined to the basal layer of the epidermis
Melanocytic hyperplasia
Represent a developmental abnormality of normal melanocytic development due to a mutation that occurs in a progenitor cell that results in the abnormal extensive accumulation of melanocytic cells along migration pathways during normal development
Congenital Nevomelanocytic Nevus
Present at birth but large variety appear between 1 month and 2 years of life, grows relatively proportionally, associated with loss of pigmentation, halo depigmentation, and regression
Congenital Nevomelanocytic Nevus
Congenital Nevomelanocytic Nevus: Small Medium Large Giant
Small <1.5 cm
Medium 1.5–19.9 cm
Large (≥20 cm)
Giant - as large as the patient’s palm if on the head and neck (and twice that area for other anatomic sites), 30% of the body surface, or 900 cm2 in adults
Have smooth, regular, and sharply demarcated border, and skin markings distort the skin surface; some relatively hairless; some have coarse, long, darkly pigmented; have a smooth, pebbly, rugose, verrucous, cerebriform, or grossly lobular surface
Congenital Nevomelanocytic Nevi
CNNs of the head, neck, or posterior midline, and/or the presence of multiple satellite lesions associated with large CNN may be complicated
Cranial and/or spinal leptomeningeal melanocytosis
Associated with giant CNN
Neurofibromatosis
Associated with the relatively sudden appearance of a dermal or subcutaneous nodule, very dark pigmentation, itching, pain, bleeding, or ulceration
Malignant degeneration of large CNNs
Histopathology: presence of nevomelanocytes in the epidermis as well-ordered thèques and/or nevomelanocytes in the dermis, which are present as sheets, nests, cords, and/ or single cells
Congenital Nevomelanocytic Nevus
Histopathology: appearance may be identical to typical acquired nevi, with nevomelanocytes in the epidermis as well-defined thèques and/or nevomelanocytes in the papillary dermis as sheets, cords, or nests; nevomelanocytes in the lower two-thirds of the reticular dermis and to be associated with appendageal and neurovascular structures
Nevomelanocytic type of large CNN
Histopathology: melanocytic elements take on the appearance of Wagner-Meissner corpuscles (lames foliacée), a palisaded arrangement of cells around a cellular mass of homogeneous material (Verocay body), and sheathing of nerves by neuroid tissue (neuroid tubes); may be responsible for lobulation and redundancy of tissue (pachydermatous or cerebriform appearance) due to the production of connective tissue elements such as reticulin, collagen, and sometimes mucinous stroma; may take on the appearance of a pigmented neurofibroma
Neuroid type of giant CNN
Histopathology: dermis may be infiltrated in whole or in part by nests or sheets of epithelioid cells and/or spindle cells; may have atypical cellular and architectural features, large epithelioid cells may comprise superficial papillary zones of the nevus, and smaller nevomelanocytes may appear in the same lesion in deeper zones of the reticular dermis, with a grenz zone separating the two elements
Spindle cell and/or epithelioid cell type of giant CNN
Histopathology: appearance may be that of a giant blue nevus, or the lesion may have elements of blue nevus (either common or cellular type) with heavily pigmented spindle-shaped melanocytic cells alone or intermixed with nevomelanocytes in the reticular dermis or deeper tissues
Blue (dermal melanocytic) type of giant CNN
Treatment goal in CNN
To remove as much of the nevus while preserving function and improving cosmetic appearance
Presents as a circumscribed macule/patch of tan background pigmentation (<1 cm to >10 cm in diameter) with features consistent with lentigo or café-au-lait macules including scattered, more darkly pigmented nevomelanocytic (or more hyperplastic) macular and/or papular elements
Nevus spilus
Associated with large varieties of nevus spilus
Multiple granular tumors Nevus flammeus Muscle atrophy Neurological disorders Phacomatosis pigmentokeratotica
Histopathology: consists of increased numbers of melanocytes in a lentiginous epidermal pattern
Electron microscopy: demonstrate melanin macroglobules
Nevus spilus - tan background pigmentation
Histopathology: demonstrate foci of increased melanocytic hyperplasia or melanocytic dysplasia (architectural disorder and variable cellular atypia)
Nevus spilus - flat, dark elements
Histopathology: usually contain collections of nevomelanocytes in the epidermis and/or dermis
Nevus spilus - raised elements
Develop after birth, slowly enlarge symmetrically, stabilize, and after a period of time may regress with majority develop during the 2nd-3rd decades of life
Common acquired nevomelanocytic nevi
Spontaneous and concurrent development of scattered nevomelanocytic nevi often similar in appearance
Eruptive nevi
Phenomenon of spontaneous development of a zone of depigmentation around a preexisting nevus, indicating the onset of involution and subsequent regression
Halo nevus Leukoderma acquisitum centrifugum Sutton’s nevus Leukopigmentary nevus Perinevoid vitiligo Perinevoid leukoderma
Lesions have a homogeneous surface and coloration pattern, round or oval shape, regular outlines, and relatively sharp borders; may be papillomatous, dome-shaped, pedunculated, or flat-topped and are usually skin-colored, pink, or brown
Common acquired nevomelanocytic nevi
May cause redness and even blistering in the perinevic halo
UV radiation
Process that results in the development of an eczematous dermatitis presenting as a red halo around nevi but no regression
Halo dermatitis
Meyerson’s nevus
Most common associated condition in halo nevus occurring in 18% to 26% of patients
Vitiligo
Associated with halo nevus
Poliosis Vogt-Koyanagi-Harada syndrome Pernicious anemia Prominent numbers of nevi Atypical nevi Personal or family history of melanoma
Relatively large number or numerous nevi are seen in
Turner syndrome
Noonan syndrome
Eruptive nevi suggests
Blistering disease
Immunosuppression
Nevomelanocytes in the deep dermis may be disposed within a collagenous framework that is loose, pale, and wavy in formations called
Neuroid tubes
Composed of peculiar foam cells comprising a portion or all of a given lesion; multinucleated balloon cells and multinucleated giant cells are seen frequently
Balloon cell nevus
Refers to the incontiguity association of different types of melanocytic nevi; most found in association with a benign compound nevus
Combined nevus
Name given to recurrent lesions after incomplete removal of a benign nevomelanocytic nevus; common after superficial destructive procedures
Recurrent melanocytic nevus
Histopathology: central nevomelanocytic nevus associated with a dermal band-like lymphohistiocytic infiltrate and a depigmented zone totally or almost totally devoid of epidermal melanocytes
Halo nevus
Useful in discriminating benign lesions from lesions with a metastatic tendency
FISH (fluorescence in situ hybridization)
CGH (comparative genomic hybridization)
In nevi, may help confirm a benign diagnosis
Low Ki67 activity and loss of HMB45 in dermal (deeper) cells
Associated with multiple blue nevi
Lentigines, cardiac myxoma, and mucocutaneous myxomas
[Carney complex/LAMB syndrome (Lentigines, Atrial myxomas, Mucocutaneous myxomas, and Blue nevi)]
Derived from a mutant precursor cell resulting in the accumulation and differentiation of the melanocytic cells in the dermis
Blue nevus
Mutation in blue nevus
GNAQ gene
Usually acquired, and once developed remain stable usually solitary, asymptomatic blue, blue-gray, or blue-black papules, usually less than 10 mm in diameter occur anywhere, but about half are present on the dorsa of hands and feet
Blue nevus
The blue-gray color of blue nevi is an optical effect of blue light backscatter from the skin over the dermal melanin
Tyndall effect
Associated with large plaque blue nevus (pilar neurocristic hamartoma)
Lentigo simplex
Darkly pigmented, blue-black papules or nodules, mostly on the head and neck or upper extremities, 2–9 mm in diameter, and occurring predominantly in the 1st four decades of life, including childhood
Deep penetrating nevi
Blue-gray or blue-brown nodules or plaques 1-3 cm in diameter, occasionally larger with surface usually smooth but may be irregular; one-half the cases are located on the buttocks or sacrum and may develop in association with CNN; more elevated, more aggressive locally, and occasionally associated with lymph node “benign metastasis”
Cellular blue nevi
Presents as an expanding dermal nodule with or without ulceration and may develop in contiguity with a cellular blue nevus, nevus of Ota, combined congenital blue nevus, or de novo
Malignant blue nevus (melanoma)
Histopathology: dermal melanocytes appear as melanin-containing fibroblast-like cells grouped in irregular bundles admixed with melanin-containing macrophages, associated with excessive fibrous tissue in the middle or upper reticular dermis, occasionally extending downward to subcutaneous fat or upward to papillary dermis; elongated melanin-producing dermal melanocytes lie with their long axis parallel to the epidermis
Common blue nevi
Histopathology: peripilar grouped arrangement of mostly spindle cells containing varying amounts of melanin, patterns of a common blue nevus and dermal melanocytosis (Mongolian spot), and presence of abnormal (granular) melanosomes
Plaque-like blue nevus (pilar neurocristic hamartoma)
Histopathology: may have both spindle and epithelioid cell forms and demonstrates deep extension into the dermis or subcutis in a wedge-shaped structure potentially tracking with neurovascular or adnexal structures
Deep penetrating nevi
Histopathology: a component of a common blue nevus plus fascicles of spindle-shaped cells with ovoid nuclei and abundant pale cytoplasm with little or no melanin, and often epithelioid cells, present in the dermis and often in subcutaneous fat in nests, bundles, and neuroid forms with little or no intervening stroma
Cellular blue nevi
Major complication of blue nevi
Potential risk of melanoma (highest - cellular blue nevus)
Common blue nevus that would require histopathologic examination
Sudden appearance of blue nodule
Expansion of a pre-existing blue nodule
Congenital blue nodule
Relatively large blue nodule or plaque >10mm in diameter
Acquired lesions, often during the third decade of life presents as sharply circumscribed, uniformly darkly pigmented papule
Pigmented spindle cell nevus
Dermoscopy: diffusely jet black with a sharp well defined border - should interface with the skin in a similar (uniform) manner for the full circumference of the lesion; pattern is often “starburst” in appearance
Pigmented spindle cell nevus
Histopathology: consists of vertically oriented fascicles of spindle-shaped, pigment-producing melanocytes; some pagetoid upward migration may be present, but the lesion can be distinguished from melanoma by uniform nuclei, uniform cellular detail, and distinctive pattern of growth; most cases have a lymphohistiocytic host response
Pigmented spindle cell nevus
Treatment: Pigmented spindle cell nevus
Excision with 3-5mm margin of normal skin
Dermoscopy: oval, uniform, and gray-blue in color; some have a central amorphous yellow appearance
Blue nevus
Presents most commonly as a solitary, asymptomatic, pink or red, hairless, firm, and dome-shaped; some may resemble a keloid with commonly smooth surface, and the borders may fade into surrounding skin; usually asymptomatic, but pruritus, tenderness, and/or bleeding may occur
Spitz nevus
Present as widespread eruptive lesions or in a grouped manner as multiple agminated lesions consisting of red, red-brown, brown, or dark-brown papules or nodules, with a fine stippled surface; often occur in the early years of life within a background of congenital macular pigmentation or occasionally within a hypopigmented plaque
Agminated spitz nevus
Histopathology: large melanocytic cells often twice the size of epidermal basal keratinocytes with prominent mononuclear or multinucleated giant cells in the epidermis and/or dermis which show progressive maturation with increasing depth, becoming smaller and more similar to ordinary nevomelanocytes with the overall distribution of cells in the dermis being wedge-shaped, with narrowing of the wedge toward the subcutaneous fat; coalescent eosinophilic globules (Kamino bodies) present; melanocytic elements are usually arranged in well- circumscribed nests; epidermis is usually hyperplastic, with elongated and bulbous pegs and knobs extending into the dermis
Spitz nevus
Markers for Spitz nevus
Gain of chromosome 11p
Amplification or activation of H-RAS
Treatment: Spitz nevus
Complete excision with a 3-5 mm clear margin of normal skin
Theories to the mechanism by which nevomelanocytes appear in regional lymph nodes
- Nevomelanocytes get trapped in developing nodal tissues
2. There may be passive transfer from the cutaneous lesion to the lymph node
Histopathology: nevomelanocytes largely confined to the nodal capsule; bear resemblance to the cells in the cutaneous lesion
Nodal nevi
Benign melanocytic neoplasia present in a lymph node. Nevomelanocytes are often located in the capsule but may also be present in the nodal parenchyma. Generally asymptomatic and found incidentally as a result of lymph node removal.
Nodal nevi
Sharply circumscribed, light-brown to very dark-brown macule
Lentigo simplex
Associated with Lentigo simplex
Peutz-Jeghers syndrome
LEOPARD syndrome (lentigines; electrocardiogram conduction defects; ocular hypertelorism; pulmonary stenosis; abnormalities of genitalia; retardation of growth, and sensorineural deafness)
LAMB/myxoma syndrome
Laugier-Hunziker syndrome
Lentigines are present at birth or shortly thereafter and may increase in number during childhood which occur on both sun-exposed and sun-protected sites, including genitalia, conjunctiva, oral mucosa, palms, and soles
Moynahan (LEOPARD) syndrome
Numerous lentigines may be present at birth or appear during early childhood with oral pigmentation usually persists whereas cutaneous lentigines usually fade after puberty; almost always present on the oral mucosa but other common sites of involvement include lips, nose, eyelids, anus, nail bed, and dorsal and ventral surfaces of hands and feet
Peutz-Jeghers syndrome
Lentigines on the lips and genital sites appear in early childhood and tend to persist and occur mainly on the face and genitalia as tan to black macules
LAMB syndrome
Lentigines are acquired during adulthood and persist indefinitely, not associated with somatic abnormalities which occur on the buccal and labial mucosa of the mouth, on fingertips and nail matrix
Laugier-Hunziker pigmentation
Presence of pigmented macules is restricted to a horizontal band across the central face
Centrofacial lentiginosis
First become manifest at birth or early childhood as small, circumscribed, light-brown macules, 2-10 mm in diameter, confined to a localized area of the skin, often in a segmental distribution and frequently in a curvilinear or swirled pattern
Agminated lentigines
Histopathology: intraepidermal melanocytic hyperplasia in the basal layer of elongated epidermal rete ridges, without nest formation; melanocyte number may only be minimally increased but pigmentary differences are marked or the number of melanocytes is sufficiently increased to begin forming nests, appearing similar to a junctional nevus
Lentigo simplex
Useful to demonstrate increased number of melanocytes confined to the basal layer and lacking junctional nest formation in Lentigo simplex
Mart-1
Mel-5
DOPA
Dermoscopy: simple well defined regular pigment network without any other dermoscopic findings, such as dots or globules
Lentigo simplex
Acquired lesions, generally in fair-skinned individuals, on sun-exposed skin surfaces which persist indefinitely; pigmented macule on skin exposed to natural sunlight or artificial sources of UVR, usually in the presence of similar lesions in the same location; may be tiny (<1 mm in diameter) or large (up to a few cm in diameter), with a tendency to confluence in severely sun-damaged skin and with smooth or irregular outlines
Solar lentigo
Histopathology: elongated epidermal rete ridges with club-shaped or bud-like extensions, frequent branching and fusing of rete ridges, a thinned or atrophic epidermis between rete ridges, and increased numbers of epidermal melanocytes without nesting; scant to moderate perivascular mononuclear cell infiltrate in the dermis, usually associated with scattered melanin-laden macrophages
Solar lentigo
Useful to demonstrate increased number of melanocytes confined to the basal layer and a lack of junctional nest formation in Solar lentigo
Mart-1
DOPA
Most common area for Dysplastic Nevus
Trunk particularly back
Clinical criteria for the diagnosis of a Dysplastic Nevus
- Diameter in one dimension at least 5 mm and a prominent at component
- (2 of 3) other features:
a. irregular, asymmetric outline,
b. indistinct borders
c. variable pigmentation
Histopathology: Architectural features - junctional component of scattered atypical melanocytes which may be most of the lesion, or an edge or shoulder extending several retia beyond a dermal component; rete ridges are elongated, with the nests of melanocytes at the tips or along the side of the retia with occasional bridging of the nests across retia; fibroplasia in the dermis, often concentric eosinophilic fibroplasia or lamellar fibroplasia; lymphocytes tend to be patchy and perivascular
Cytologic features - atypical melanocytes with abundant cytoplasm along the DEJ that are 1/3 to 1/2 larger than the melanocytes in the normal surrounding skin; nuclei may be slightly irregular or folded with hyperchromasia and clumping of chromatin; some may have prominent nucleoli.
Dysplastic nevus
An essential tool for clinical care of individuals with Dysplastic Nevus which serve as a medical record allowing determination to be made as to whether a lesion has changed
Total body photography (mole mapping)
New imaging techniques for Dysplastic Nevus
Confocal microscopy Multispectral imaging Optical coherence tomography Ultrasound Raman spectroscopy Melanin fluorescence
Major complication for Dysplastic Nevus patients
Melanoma
Most frequent complication for patients with Dysplastic Nevus
Scarring due to numerous biopsies
Treatment for Dysplastic Nevus
Observation
T or F: Removal of Dysplastic Nevus does not substantially decrease a patient’s risk of developing a melanoma
True
Major preventive intervention for the development of Dysplastic nevus
Decreased UV exposure
Most common type of cancer in young adults in the US ages 25-29, second most common cancer in adolescents and young adults 15-29 years old
Melanoma
Accounts for 75% of all skin cancer deaths
Melanoma
Major environmental cause of melanoma, especially in high-risk populations
Sun exposure (UV exposure)
Periodic, intense sun exposure rather than long, continued, heavy sun exposure is most important in melanoma causation
Intermittent exposure hypothesis
Serves as a surrogate measure of intermittent intense sun exposure
Sunburn history (blistering and peeling burns)
Melanoma incidence and mortality among Caucasians correlate inversely with latitude of residence and dose of UV radiation
Latitude gradient
Most common site for melanoma in men
Trunk, particularly the upper back
Most common sites in women
Lower legs, followed by the trunk
Most common location for melanoma in older persons
Face with the addition of the neck, scalp, and ears
Phenotypic features associated with an increased risk of melanoma
Light skin pigmentation Blond or red hair Blue or green eyes Prominent freckling tendency Tendency to sunburn with Fitzpatrick skin phototype I-II
Nevi at risk for developing melanoma
Adults with more than 100 clinically typical-appearing nevi
Children with more than 50 typical-appearing nevi
Any patient with atypical nevi
Patients with familial melanoma are estimated to account for how many percent of all patients with melanoma
10-15%
Account for approximately 40% of hereditary melanoma cases (≥3 melanomas in one lineage) and confer a 76% chance of developing melanoma (in US)
Germline mutations in the chromosome 9p21 tumor suppressor gene, cyclin-dependent kinase inhibitor 2A (CDKN2A)
Two gene products encoded by CDKN2A
- p16 (also known as INK4a, inhibitor of kinase 4a)
2. p14ARF (alternative reading frame)
A cell-cycle regulator that binds and inhibits cyclin-dependent kinases Cdk4 or Cdk6, thereby inhibiting progression of cells through the G1 phase of the cell cycle
p16
Inhibits a cellular oncogene Hdm2, which in turn accelerates the destruction of the p53 tumor-suppressor gene
p14
Serine/threonine kinase, which is a major player in the Ras-Raf-Mek-Erk mitogen-activated protein kinase (MAPK) signaling transduction pathway that regulates cell growth, proliferation, and differen- tiation in response to various growth factors, cytokines, and hormones
B-RAF
Tumor suppressor gene leads to enhanced Ras pathway signaling and downregulates signaling through the Akt arm of the Ras circuitry
PTEN/MMAC1
Transcription factor that appears to be a master regulator of melanocyte differentiation
MITF gene
Amplification of MITF gene appears to contribute to this novel carcinogenic mechanism
Lineage addiction
Five stages of malignant transformation and tumor progression in melanocytes
- Benign melanocytic nevi
- Atypical nevi
- Primary malignant melanoma, radial growth phase
- Primary malignant melanoma, vertical growth phase
- Metastatic malignant melanoma
Most common subtype, accounting for approximately 70% of all cutaneous melanomas diagnosed most commonly on intermittently sun-exposed areas, most frequently the lower extremity of women, and the upper back of men; may present subtly as a discrete focal area of darkening within a preexisting nevus
Superficial spreading melanoma
Second most common melanoma with trunk as the most common site remarkable for rapid evolution, often arising over several weeks to months typically appears as a uniformly dark blue-black or bluish-red raised lesion
Nodular melanoma
Subtype of melanoma in situ with a prolonged radial growth phase that may progress to invasive LMM with time; presents as slowly enlarging, brown, freckle-like macule with irregular shape and differing shades of brown and tan, usually arising in a background of photodamaged skin
Lentigo maligna
Most common site for ALM
Sole
Subtype of melanoma with distinct differences in frequencies seen between ethnic groups; presents as brown, black, tan, or red with variegations in color (most common color is brown-black) and irregular borders; often misdiagnosed as a plantar wart or hematoma
Acral lentiginous melanoma
Considered a variant of ALM, generally arises from the nail matrix, most commonly on the great toe or thumb; appears as a brown to black discoloration or growth in the nail bed
Subungual melanoma
A widening, dark, or irregularly pigmented longitudinal nail streak
Melanonychia striata
Finding of pigmentation on the proximal nail fold
Hutchinson sign
Most commonly develops in the sixth or seventh decade on sun-exposed head and neck regions with firm, sclerotic, or indurated quality, and 1/2 are amelanotic with higher rate of local recurrence due to a propensity to infiltrate perineurally
Desmoplastic Melanoma
Can arise on mucosal surfaces on the head and neck (conjunctival, intranasal, sinus, and oral), vulva, anorectal, or even urethral mucosa present most often with delayed detection and a deeply pigmented, irregular lesion
Mucosal Melanoma
Heterogeneous group of rare lesions that histologically resemble benign nevi by their symmetry and apparent maturation with descent in the dermis, thus with greater potential for misdiagnosis; marked hyperchromasia of the nuclei of the tumor cells, the presence of mitoses, and an expansile growth of the dermal cells
Nevoid melanoma
Subtype of melanoma that clinically and histologically resembles a Spitz nevus, but tends to be larger and have asymmetry and irregular coloration
Spitzoid melanoma
Second most common cancer in women of child-bearing age
Melanoma
ABCDE acronym for melanoma
A for asymmetry (one half is not identical to the other half)
B for border (irregular, notched, scalloped, ragged, or poorly de ned borders as opposed to smooth and straight edges)
C for color (having varying shades from one area to another)
D for diameter (i.e., greater than 6 mm, approximately the size of a pencil eraser)
E for evolving
A pigmented lesion that is different from other pigmented lesions on a particular individual should be approached with a high index of suspicion
Ugly duckling sign
A noninvasive technique in which a handheld device is used to examine a lesion through a film of liquid, usually immersion oil, using nonpolarized light (contact), or the lesion is examined under polarized light without a contact medium (noncontact)
Dermoscopy
Gold standard for diagnosing melanoma
Histopathologic evaluation of the biopsy specimen
Cytologic atypia necessary for the diagnosis of melanoma
Cellular enlargement Nuclear enlargement Nuclear pleomorphism Hyperchromasia of nuclei Nucleolar variability Presence of mitoses especially deep in the dermis
Major architectural features of melanoma
Asymmetry Poor circumscription (i.e., cells at the edge of the lesion tend to be small, single, and scattered) Large size (>5–6 mm)
Pagetoid spread
Melanoma Spitz nevi Spindle cell nevi Vulvar nevi Acral nevi
Histopathology: population of melanocytes appearing uniformly atypical
Superficial spreading melanoma
Histopathology: atypical melanocytes singly and in nests, predominantly confined to the basal layer of the epidermis, which become confluent without pagetoid spread, occurring in the background of photodamage; epidermis is thin and atrophic, with loss of rete ridges; variable cytologic atypia
Lentigo maligna
Lentigo maligna melanoma
Histopathology: characteristic lentiginous pattern of most cells being single and located near the dermal-epidermal junction; irregular acanthosis, and the melanoma cells are uniformly malignant and often dendritic
Acral lentiginous melanoma
Histopathology: demonstrates little tendency for intraepidermal growth; instead, there is a dermal mass of atypical melanocytes
Nodular melanoma
Expressed by almost all melanomas; but also by mela- nocytic nevi, Langerhans cells, and cutaneous neural tumors
S-100
Monoclonal antibody with high specificity for melanoma cells, although it is frequently negative in DM
HMB-45
Broadly expressed in benign and malignant melanocytic lesions but not in most DMs; more sensitive than HMB-45 and more specific than S100 for melanoma
Melan-A
Stain for Desmoplastic melanoma
Vimentin
S-100
Essential for determining optimal treatment and for
Accurate staging of melanoma
The single most important prognostic factor for survival and clinical management in localized stage I and II cutaneous melanoma
Tumor thickness
An independent prognostic factor for localized melanoma; confers a higher risk of developing advanced disease and lower survival rate
Ulceration
Independent predictor of survival (2nd most powerful predictor of survival); measured as the number of mitoses per square millimeter
Mitotic rate
Significantly increases the risk of relapse, lymph node involvement, distant metastases, and death
Vascular invasion
Correlate with a poorer outcome, and this has been retained in the current AJCC melanoma staging system
Microscopic satellitosis
Predictor of melanoma outcome
Sentinel lymph node status
Portends a worse prognosis with respect to overall survival rates
Increasing age (>60)
