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1.  Arise from skin, mucosa, retina and the leptomeninges
Def: Malignant proliferation of melanocytes

2. Epidemiology
App. 5% of skin malignancy ( 75 per cent of skin malignancy related deaths),
MM accounts for 3% of all malignancy worldwide,
 Most common cancer in young adults (20–39 years),
5% of all patients with MM will develop a second primary melanoma,
7% MMs present as occult metastases from an unknown primary
Increasing incidence over the years and equal in both sexes

3. Risk factors:
Hx of exposure to sunlight:
Intense intermittent exposure
Significant adult exposure
( associated with sunburn below
10)
Geographical location
(Australia and New Zealand)
Skin Factors:
Xeroderma pigmentosum (RR= 1000)
Past medical or family history of MM with dysplastic
naevi
Previous melanoma (RR= 84)
Multiple benign or atypical naevi
Dysplastic naevi (10% lifetime risk)
Red hair (RR= 3)
Tendency to freckle
Immunosuppression
Giant congenital pigmented naevus
Albinism
Genetic predisposition (CDKN2A gene)

4. Pathophysiology
 UV exposure is the major causal factor for developing MM
 Cumulative exposure favours the development of lentigo maligna
melanoma (LMM),
Whereas ‘flash fry’ exposure, typical of rapidly acquired holiday
tans – favours the other morphological variants

5. Diagnosis
History
• Change in size, shape and color
• Redness
• Itchy
• Tender
• Bleeding
• Crusting
• Ulceration
Examination:
• ABCDEs criteria
• Glasgow 7 point Criteria

6. ABCDEs Criteria
A- Asymmetry
B- Border irregularity/bleeding
C- Color Variation
D- Diameter (>6mm)
E- Elevation

7. Glasgow 7 point Criteria
• Major Features:
1. Change in size
2. Irregular shape
3. Irregular color
• Minor features:
1. Inflammation
2. Oozing
3. Change in sensation

8. Microscopic finding: Nevus
• nevus cells are arranged in nests.
• nuclei of nevus cells are uniform and rounded in contour and contain
inconspicuous nucleoli.
• the cells contain melanin pigment.
• little or no mitotic activity.

9. Microscopy: Melanoma
• melanoma cells are pleomorphic and have hyperchromatic nuclei
with prominent nucleoli.
• melanin pigment is present as fine granules.
• frequent mitosis.

10. 4 common variants of MM
1. Superficial spreading melanoma
2. Nodular melanoma
3. Lentigo maligna melanoma
4. Acral lentiginous melanoma

11. 1. Superficial spreading melanoma
• Most common type (70%)
• Most likely to arise in a pre-existing naevus, after several years
of slow change
• Followed by rapid growth in the preceding months before
presentation
• Typically it is a darker pigmented area in a junctional naevus
• Nodularity within superficial spreading melanoma heralds the
onset of the vertical growth phase

13. 2. Nodular melanoma
• Accounts 15% of all MMs
• male > female, arise typically de novo in skin
• More aggressive
• Shorter clinical onset
• Presenting in middle age and usually on the trunk, head or neck
• Appear as blue/black papules, 1–2 cm in diameter
• They lack the horizontal growth phase, tend to be sharply
demarcated

15. 3. Lentigo maligna melanoma
• Previously k/a Hutchison’s melanotic freckle
• Slow growing, varigated brown macule (a lentigo), on face, neck or hands of
the elderly
• Positively correlated with prolonged, intense sun exposure
• Women > men (5-10%)
• In situ melanoma in this variant is called lentigo maligna
• Less metastatic potential than other variants as they take longer to enter a
vertical growth phase

17. 4. Acral lentiginous melanoma
• Affects the soles of feet and palms of hands
• Rare in white-skinned individuals
• More common in the Afro-Caribbean, Hispanic and Asian populations
(35–60%)
• Usually presents as a flat, irregular macule in later life
• Twenty-five per cent are amelanotic may mimic a fungal infection or
pyogenic granuloma
• MM under the finger nail is usually SSM rather than ALM

18. • For finger or toe nail lesions, vital to biopsy the nail matrix rather than just the
pigment on the nail plate
• Feature of subungual melanoma- Hutchinson’s sign positive
(nail fold pigmentation which then widens progressively to produce a triangular
pigmented macule with associated nail dystrophy)
• The differential diagnosis is ‘benign racial melanonychia’, which produces a
linear dark streak under a nail in a dark-skinned individual

19. Fig: Acral lentiginous
melanoma on the sole of
the footFig: Subungual melanoma –
superficial spreading
melanoma.
Fig: Benign racial melanonychia

20. Miscellaneous Types
• Amelanotic melanoma (often arising in the GI tract and presenting with
obstruction, intussusception or as a metastasis from an unknown primary)
• Desmoplastic – mostly found on the head and neck region, has a propensity for
perineural infiltration and often recurs locally if not widely excised. May be
amelanotic clinically

21. Investigations
• Guidelines for staging are controversial
• Offering sentinel node biopsy to patients with clinical
stage II disease is prudent
• Investigations for stage III disease should be
directed to individual clinical presentation

23. Management
• focuses on:
Prolonging survival
Eliminating the cancer
Shrinking or stopping the growth of known metastases
Controlling symptomatic or risky sites of disease
Providing comfort
“Depending upon where and how big the metastases are, treatment may involve
drug treatments, surgery, and/or radiation therapy”

24. For Primary: Surgery is the main treatment
1. Handley’s wide local excision (WLE):
wide excision with clearance of margin as well as depth.
2. If primary area is wide, then amputation with one joint above is done.
3. In fingers and toes, disarticulation is required.

25. Regional lymph nodes
For biopsy positive nodal disease : block dissection of the regional lymph
nodes to remove all the lymph nodes in that regional basin

26. Drug treatments
3 main categories :
1. Immunotherapy – Drugs that stimulate or unleash your immune system to
attack and kill the cancer cells
2. Targeted therapy – Drugs that inhibit specific enzymes or molecules
important to the cancer cells
3. Chemotherapy – Drugs that stop or slow the growth of cancer cells by
interfering with their ability to divide or reproduce themselves

27. Immunotherapy
• (nivolumab [Opdivo], pembrolizumab [Keytruda], ipilimumab [Yervoy]),
which have largely replaced high-dose interleukin-2 (IL-2). These have
important benefits for some patients, although each can cause significant
side effects.
• Anti-PD-1 checkpoint inhibitors — The anti-PD-1 checkpoint inhibitors
(nivolumab, pembrolizumab) unleash the body’s immune system so that it
can be able reject the melanoma. Nivolumab is given once every two
weeks, while pembrolizumab is given once every three weeks.

28. Targeted therapy
• Three drugs, vemurafenib (Zelboraf), dabrafenib (Taflinar),
and trametinib (Mekinist) block this protein or the pathway it stimulates and
cause tumors with this specific mutation in BRAF to shrink.
• Generally, dabrafenib is given in combination with trametinib, as the two agents
together have been shown to be more effective and no more toxic than single-
agent dabrafenib or vemurafenib.

29. Chemotherapy
• dacarbazine or temozolomide to stop or slow the growth of cancer cells by
interfering with the ability of cancer cells to divide or reproduce.
• S/E on highly growing cells.
Chemotherapy is less effective than immunotherapy or targeted therapy, and it generally is not used as the initial
treatment for patients with advanced disease.

30. Prognosis
 Very aggressive tumor
The higher the mitotic index, the poorer the prognosis of the primary
tumor.
Once regional nodes are involved clinically, 70–85% of patients will have
occult distant metastases.
 Ageing, Females and Extremities melanoma better prognosis

31. References
• Bailey and Love’s Short Practice of Surgery; 26th Edition
• SRB’s manual of surgery; 5th edition
• Robbin’s Basis of pathology; 9th edition

32. Summary
• Definition
• Epidemiology
• Risk factors
• Diagnosis
• Types of melanoma
• Investigations
• Management
• Prognosis
The end