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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
Histopathology of malignant melanoma

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Histopathology of malignant melanoma

  • 1. CHAIRPERSON : Dr K DURGA(PROF.) MODERATORS : Dr SHASHIKALA(ASSOC. PROF) Dr NEELIMA (ASST. PROF) HISTOPATHOLOGY OF MALIGNANT MELANOMA By Dr Ajeta
  • 2.  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
  • 3.  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
  • 4. Black nodule with satellitosis
  • 5.  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
  • 6.
  • 7.  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
  • 8.
  • 9. DD  Nodular melanoma  Metastatic melanoma  Giant cellular blue nevus with subcutaneous cellular nodules
  • 10. Ki-67
  • 11.  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
  • 12.  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
  • 13.
  • 14.
  • 15.  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
  • 16.  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
  • 17.  Conventional melanomas  Small cell melanomas  Melanomas simulating Spitz naevus
  • 18.  Small cell melanoma Monomorphous small cells in sheets and organoid configuration Basophilic round nuclei and condensed chromatin Aggressive tumors DD – small round cell tumors
  • 19.  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
  • 21.
  • 22.  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
  • 23.  Features to differentiate persistent melanoma from metastatic melanoma Epidermal component inflammation vascular invasion mitotic rate associated naevus necrosis fibrosis scarring
  • 24.  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
  • 25.
  • 26.  <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
  • 27.  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
  • 28.  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
  • 29.  Satellite lesions – Discontinuous foci of tumor metastasis within 2cm of primary melanoma - Presence defines lesion as stage IV - Microscopic satellites – worse prognosis
  • 30.  WHO Pathology and Genetics Of Skin Tumors  Lever’s Histopathology of Skin , Tenth Edition  Washington Manual Of Surgical Pathology