CHAIRPERSON : Dr K DURGA(PROF.)

MODERATORS : Dr SHASHIKALA(ASSOC. PROF)

Dr NEELIMA (ASST. PROF)

HISTOPATHOLOGY OF MALIGNANT MELANOMA

By Dr Ajeta

Benign melanocytic tumors

Malignant melanoma

Superficial spreading melanoma

Nodular melanoma

Lentigo maligna

Acral lentiginous melanoma

Desmoplastic melanoma

Melanoma arising from blue nevus

Melanoma arising in giant congenital nevus

Melanoma of childhood

Nevoid melanoma

Persistent melanoma

Melanoma arising in association with dermal melanocytosis

Rare tumor

Between 20 to 60 years mean age 44yrs

Aggressive tumor with poor prognosis

Sites most commonly affected

scalp

orbit and face

Black nodule with satellitosis

Two components - benign and malignant

Benign – common blue nevus

cellular blue nevus

Common blue nevus – fascicles of dendritic melanocytes

melanophages and sclerotic bundles of

collagen between fascicles

Cellular blue nevus – solid aggregates of momomorphous ovoid

cells with abundant pale cytoplasm with little

or no melanin vesicular nucleus with

inconspicuous nucleoli

Malignant component - deep seated expansile asymmetric nodule

involving reticular dermis and subcutis

Neoplastic melanocytes – large spindled to epithelioid cells with

abundant cytoplasm pleomorphic

nuclei prominent nucleoli frequent mitotic

figures

DD

Nodular melanoma

Metastatic melanoma

Giant cellular blue nevus with subcutaneous cellular nodules

Ki-67

Bimodal age presentation

Most commonly on trunk

Presents as a firm nodule or dark

brown to black discoloured area in

the midst of the naevus

Can also present as a cyst

Sharply demarcated from adjacent congenital naevus

Epidermis – effacement of rete ridges , ulceration

Intraepidermal component – epithelioid cells with pigmentation

Dermal component – expansile nodules

spindle cells

nuclear hyperchromasia

prominent nucleoli

frequent mitoses

DD – proliferative nodules in giant congenital naevi

Melanomas developing prior to onset of puberty

Very rare

Risk factors - congenital naevi especially large varieties

atypical naevi

family history of melanoma

xeroderma pigmentosum

immunosuppression

Multiple matastasis from transplacental transmission

Trunk ,lower extremities ,head and neck

Features useful for the distinction of melanomas from naevi

Large size(i.e., >7 mm)

ulceration

high mitotic rate(>4 mitoses/mm2),

mitoses in the lower third of the lesion

asymmetry

poorly demarcated lateral borders

lack of maturation

marked nuclear pleomorphism

Conventional melanomas

Small cell melanomas

Melanomas simulating Spitz naevus

Small cell melanoma

Monomorphous small cells in

sheets and organoid

configuration

Basophilic round nuclei and

condensed chromatin

Aggressive tumors

DD – small round cell tumors

Mimic benign naevus clinically and histologically – symmetric

nested

devoid of radial growth

Discriminating attributes – high cellularity with sheet like growth

cytologic atypia

mitosis

adnexal infiltration

infiltrative growth in deeper dermis

absence of maturation

Scanner view

Persistent growth of residual, incompletely excised primary

malignant melanoma, of either the epidermal or the invasive

component, or both

Persistence or recurrence of a flat variably pigmented patch

adjacent to or surrounding the scar of the primary excision site.

DD - Metastatic melanoma involving scar

Pigmented basal cell carcinoma

Features to differentiate persistent melanoma from

metastatic melanoma

Epidermal component

inflammation

vascular invasion

mitotic rate

associated naevus

necrosis

fibrosis

scarring

VERTICAL GROWTH PHASE

If lesion is tumorigenic – atleast one cluster in the dermis is

larger than the largest intraepidermal cluster

(OR)

If there is dermal mitosis in the absence of tumorigenic growth

In thin , level II melanomas VGP is the only statistically significant

factor for metastasis

<0.76 mm – thin

0.76 mm – 4.00 mm – intermediate

>4.00mm – thick

Measured from granular layer to deepest extension of tumor

If ulcerated measured from base of ulcer overlying deepest point of

invasion

Metastasis in thin lesions very rare

Brisk TIL response – band of lymphocytes beneath tumor or

diffusely throughout its substance

NonBrisk TIL response

Absent TIL response

Non infiltrative lymphocytic infiltrate around tumor usually at its base

not associated with prognosis

Mitotic rate – In tumorigenic compartment , hot spot

0/mm2 – best prognosis

6/mm2 – worst prognosis

Ulceration – Poor prognosis

Vascular or lymphatic invasion – Tumor cells within vessels

Tumor cells within walls adjacent to endothelium

Angiotropism /Extravascular migratory metastasis

Strong predictor of positive sentinel lymph node

2nd most important predictor of survival

Satellite lesions – Discontinuous foci of tumor metastasis within 2cm

of primary melanoma

- Presence defines lesion as stage IV

- Microscopic satellites – worse prognosis

WHO Pathology and Genetics Of Skin Tumors

Lever’s Histopathology of Skin , Tenth Edition

Washington Manual Of Surgical Pathology