includes melanotic and non melanotic skin cancers discussed under varying headings. especially melanoma .

1. Skin Malignancies
Dr Suhas U

2. Introduction
• Most common form of cancer
• High incidence associated with environmental
exposure
• SCC and BCC – bulk of skin cancers
• Melanoma – M/C cause of skin cancer related
death

3. MELANOMA

4. • John Hunter – first published about melanoma
in 1787
• Rene Laennec – metastatic deposits in distant
viscera and called it “ cancer noire ” .

5. Epidemiology
• <2% of skin cancer
• 5th and 7th most common among males and females in
USA
• Skin – fair , blond or red hair, blue eyes – tendency
towards freckles and sunburn
• Gender – Males > females , better prognosis (females)
• Age – median age >60years(varying age)
• Prior history of melanoma or other skin cancers
• Precursor lesions – 40%

6. • Genetic
High risk skin types( Fitspatrick I and II)
Family history of melanoma
Xeroderma pigmentosum
• Environmental –
Intense intermittent sun exposures
Severe blistering sunburns
• Immunosuppression
• Upper socioeconomic status

7. UV radiation and melanoma
• UV light – UVA and UVB
• UVA
longer wavelength and penetrates more deeply into skin
Role in skin aging and wrinkling
Predominant wavelength in tanning beds and increased
melanoma
• UVB
Major source is sunlight
Damages superficial epidermal layer and cause for sunburn
Direct link between UVB and mutation driving
oncogenesis

8. Precursor lesions
Dyplastic Naevi
• 6-15mm macular pigmented lesions
• Indistinct margins and variable colour
• Difficult to identify neavus with dysplasia
• Most are benign
• Suspicious lesions require biopsy
• Histological types- mild, moderate and severe
• Moderate or severe – excision with negative margins
• Mild – observed over time

9. Congenital Naevi
• Risk proportional to number and size
• Small or medium – low risk and observation
• Giant size(>20cm)
 Rare
 Increased risk for melanoma , sarcomas
 Compete excision.

10. Spitzoid melanocytic lesions
• Wide range from spitz naevi to spitzoid melanoma
• Spitz naevus
Rapidly growing benign pink to brown lesion
Little or no progression to melanoma
• Spitzoid melanoma
Atypical features of size >10mm, asymmetry, poor
circumscription and ulceration

11. Pathogenesis
Gain of function mutations
• BRAF – 50%
• NRAS – 15%
• Tyrosine kinase receptor KIT – 20%
Loss of key tumour suppressor genes
• Inactivating mutation of CDKN2A – 25-40% familial
melanomas
CDKN2A codes for tumour suppressor genes INK4A
and ARF
• Loss of PTEN – 25-50%

12. Clinical presentation
• Irregular pigmented skin lesion that has grown or changed
over time
• ABCDE’s of melanoma – guiding diagnosis and decision
to perform biopsy
 Asymmetry
 Irregular borders
 Color changes
 Diameter >6mm
 Evolution or change over time

13. • History
Duration of primary melanoma, changes, symptoms
such as itching and bleeding
Sun exposure, tanning bed use , immunosuppression,
prior cancer history, and family history
• Examination
Complete skin examination
Primary lesion, in transit lesions and lymph nodes

14. Amelanotic melanoma
• Atypical melanoma
• Unpigmented raised pink or flesh colored skin lesions.
• A high index of clinical suspicion is needed.
• Indications for biopsy
Skin lesion that has changed in size, color, or shape
and is itching or bleeding.

15. Advanced melanomas
• Regional disease(10%)
 Lymphatic spread of tumor to the regional nodal basin.
 Set of lymph nodes receiving the first drainage from the site of
the primary tumor.
• In Transit disease
 Tumor spreads within the draining lymphatic channels and
becomes evident as cutaneous or subcutaneous nodules between
the site of the primary tumor and regional lymph nodes
• Diastant metastasis(5%)

16. Diagnosis
• Biopsy
Excisional Incisional
Smaller lesions Larger lesions
Narrow margin excison Punch biopsy
Local anaesthesia Local anaesthesia
Full thickness till subcutaneous
tissue
Through thicker area of lesion
and not on the edge of lesion

17. Histology
• All melanomas initially proliferate in the basal
layer
• Radial growth phase
Initial growth
Cells expand radially in the epidermis and superficial
dermis
• Vertical growth phase
Follows radial growth
Penetration into deeper structures
Invasion of blood vessels and lymphatics
Metastatic potential

18. Types Superficial
spreading
Lentigo maligna Acral lentiginous Nodular
Sun
expos
ure
Not
necessary
Yes Yes yes
Site Trunk,
Proximal
extremities
Face Subungual regions, palms
/ soles
Lesion Flat
pigmented
Radial
followed by
vertical
growth
Flat , dark , variable
pigmented lesion
with irregular
borders and slow
development
Pigmented lesion that
wont migrate with nail
growth and sometimes
causing streaks in nail
Raised papular
regions
Early vertical growth
Atypical
presentation not
ABCDE
Most
common
Large before
diagnosis
M/C in blacks Higher amelanotic
lesions
Proble
ms
•Cosmetic regions
•Histologic extent
extends beyond
clinical border
•Negative margin is
difficult
•Diagnosis usually at
advanced stages
•Poor prognosis in general
Greatest average
tumour thickness
and hence poor
prognosis

19. Superficial spreading

20. Lentigo maligna

21. Acral lentiginous

22. Nodular

23. Staging
Clarke’s classification – 1969
• extent of invasion into the anatomic layers of
the skin

24. Breslow’s thickness - 1970
• <1mm – thin
• 1-4mm – intermediate
• >4mm – thick
• As the thickness increases , prognosis will be
poor.

25. AJCC staging
Important prognostic factors
• Breslow’s thickness
• Ulceration
• Nodal stations and other lymphatic
manifestations
• Distant metastasis

26. TNM staging

28. Poor prognostic factors
• Older age
• Axial melanomas – trunk, head and neck
• Men
• Advanced TNM staging

29. Additional workup/ imaging
Indications
• Stage III with clinically detectable nodal mets
• Any stages with symptoms of metastasis
• Stage IV
Investigations
• PET CT
• MRI brain
• LFT and LDH

30. Treatment
Wide local excision
• Margins

31. Technique
• Anaesthesia
GA – SLN biopsy/ lymphadenectomy
LA
• Fusiform incision
• Depth –
skin, subcutaneous tissue till muscle fascia
Fascia – thick tumors
• Specimen sent for biopsy
• Closure
Primary closure
Complex flaps – rarely, head and neck melanomas

32. Tumours near nose , eye , ears
• Compromise of conventional margins to avoid
deformities/ disabilities
Subungual melanoma
• Amputation of distal finger with 1cm margin
• Ray amputation done rarely
Role of Mohr’s micrographic surgery
• Controversial
• Insitu lesions
• Lesions in cosmetic areas like face

33. Regional lymph nodes
• Elective lymph node dissection
No clinical evidence of nodal metastasis
No palpable nodes/ imaging doesn’t show
• Therapeutic lymph node dissection
Palpable nodes/ imaging detected
• Completion lymph node dissection
Nodal mets proved by SLN biopsy

34. SLN biopsy
Indications
• Intermediate lesions(20% nodal)
• Thin melanomas(5%)
Ulceration and mitotic index >1mitosis/mm2
Lesions >0.75mm thick(6.2% vs 2.7%)
• Thick melanomas
Increased risk of metastasis
Tumour negative SLN – better prognosis

35. • Involves preoperative Lymphoscintigraphy (Tc 99m
sulfur colloid(0.5mCi)
• Vital blue(isosulfan blue ) before incision
• Gamma camera with static and dynamic images
• Disadvantages
Unreliable nodal spread( head , neck and trunk)
Not improve 10year melanoma specific survival
• Advantages
Improved disease free survival and distant mets free
survival

36. Extent of lymphadenectomy
• Complete dissection as no effective adjuvanct
therapy
Axillary Dissection
• I, II , III lymph nodes
• Fibrofatty tissue around axillary vein,
thoracodorsal , medial pectoral neurovascular
bundle , long thorasic nerve
• Ligation of axillary vein, if tumor involves

37. Inguinal dissection
• Superficial + deep inguinal and pelvic nodes
• Superficial dissection sufficient for most cases
Pelvic dissection
Palpable pelvic nodes
Imaging proved pelvic nodes
Metastasis to Cloquet’s LN
multiple superficial nodes involved
Cervical dissection
Functional dissection sparing IJV and and spinal
accessory nerve is enough

38. Adjuvanct therapy
• Interferon therapy and radiotherapy
Interferon 2b alpha Radiotherapy
1month intravenous therapy and 11 month thrice
weekly subcutaneous therapy
Advantages
Prolong disease free survival
Disadvantages
No survival benefit
Toxicity
Influenza like symptoms
Fatigue, malaise
Anorexia
Hepatic toxicity
Melanomas are relatively resistant to
radiation
Indications
•One or more parotid nodes
•Two or more cervical nodes
•Three or more inguinal nodes
•Extranodal extension
•Maximum diameter lymph node >4cm
•Palpable nodal disease
•Desmoplastic melanoma

39. Follow up
• Depends on risk factors – initial stage and patient factors
• Most recurrences occur within 5years
• Periodical history and examination
• Imaging or lab investigations indicated in Stage IV regularly and
other stages if suspected
Stage 0, I and IIA Stage IIB, IIC and III
Risk for recurrence Low High
History and physical
examination
6monthly for 3years
Then anually
3-4monthly for 3years
6monthly for next 2years
Annually then

40. Treatment of recurrent disease
Local recurrence
• Tumors within 2cm from previous scar/ graft
• Represents aggressive tumor behavior
• Risk –
<0.75mm – 0.2%
0.75- 1.5mm – 2%
1.5-4mm – 6%
>4mm – 13%
• Treatment – surgical resection with negative
margins

41. In-transit disease
• Deposits within draining lymphatics
• Subcutaneous nodules between tumor and lymphatic nodal basin
• Investigations
 FNAC/ FNAB – confirm
 Imaging – distant metastatic disease
• Treatment
 Repeated resection – amenable lesions
 Not amenable to resection – intralesional injections(BCG, interleukin 2 ,
interferon alpha, PV-10.
 Other options – topical imiquimod application/ radiotherapy
 Extensive recurrent intransit disease confined to upper / lower extremity –
 HILP( hyperthermic isolated limb perfusion)
 Heated chemotherapy (42 C) using melphalan/ TNF alpha with tourniquets
 Through femoral or axillary vessel

42. Recurrent nodal disease
• Not had previous complete lymphadenectomy –
completion lymohadenectomy
• Previous CLND – excision of recurrence to negative
margins
• Adjuvanct radiotherapy may be considered

43. Stage IV - treatment
Systemic therapy- dacarbazine and interleukin 2 with
modest response rate but no overall survival benefit.
Immunotherapy –
• Focus on blocking negative feedback systems that
suppress T cell activity
• Ipilimumab – Monoclonal anti-CTLA-4 antibody
Prolongs T cell response
First systemic agent to demonstrate improved overall
survival with metastatic melanoma
• Programme death 1 inhibitors ar under study

44. Targeted therapy
• BRAF inhibitors – Vemurafenib, Dabrafenib
• MEK inhibitors – trametinib
Metastatectomy
• For limited metastatic disease

45. Special situations and melanoma
Unknown primary melanoma
• Stage III or IV disease with no preceding diagnosis
• <2% of melanomas
• Etiology
 Unknown primary that arises from benign naevus that is already trapped in
lymph nodes
 Melanomas that have spontaneous regression
 History of previous pigmented lesions/ excised lesions
• Diagnosis
 Thorough skin examination – perianal, scalp, external auditory canal, nail beds,
pelvic examination
 Endoscopic evaluation of oral cavity , nasal cavity, anus, rectum
 Ophthalmology examination
 PET CT/ MRI of brain
• Treatment – TLND

46. Melanoma and pregnancy
• 1/3rd of melanoma in women occur in childbearing age
• Any naevus of suspicious changes should be evaluated
• WLE can safely be performed with LA
• SLN biopsy can be performed if necessary by avoiding
vital blue dye

47. NON MELANOMA SKIN CANCER

48. • Most common type of malignant neoplasm
• 80% are BCC, almost 20% SCC and rest rare malignancies
• Sun exposure – predominant risk factor
• Increased risk for additional cancers like secon NMSC,
melanoma
• Hence long term periodic surveillance

49. Squamous cell carcinoma
Risk factors
• Prolonged sun exposure
• Cumulative effect of chronic UV radiation
• Fair skin, blue eyes individuals
• UV radiations
UVB increases the risk by direct carcinogenic effect on
keratinocytes – mutation and proliferation
UVB induced silencing of tumour suppressor gene p53
• Occupational and environmental factors
Arsenic
Organic hydrocarbons
Ionising radiation
Cigarrette smoke

50. • Genetic – albinism and xeroderma
• Chronic inflammation
 Burns scars (Marjolin’s)
 Chronic sinus
 Infection
 Non healing ulcers
• Immunosuppression
 Increases risk by 65times
 More aggressive and increases metastasis
 Intensity of suppressions and duration corelates the risk
 Acquired impairments of cell mediated immunity (Lymphomas,
leukemias)

51. Clinical presentation
• Most lesions – proliferation of keratin cells in basal layer of epidermis –
red/pink areas (Actinic keratoses)
Insitu lesions
• Bowen’s disease and erythroplasia of Queyrat
• Well-delineated pink papules or plaques
• Slow growth and do not progress to invasive disease, except except for
Bowen’s disease and erythroplasia of Queyrat where the risk of malignant
transformation is 3% to 5% and
• 10%, respectively
Invasive disease presents as
• Slightly pink or skin-colored, raised plaques.
• Bleeding of the lesion with minimal
• Painless ulcers with everted edges
• Grows horizontally and verically

53. Natural history
depends on location and characteristics
• Lesions associated with chronic inflammation and located at mucocutaneous
junctions metastasizes in 10% to 30% of cases
• In sun-exposed areas without adverse risk factors are less likely to spread and have a
better prognosis.
• Clinical risk factors for recurrence
 Presentation with neurologic symptoms
 Immunosuppression
 Tumor with poorly defined borders
 Tumor that arises at a site of prior radiation
 Perineural
• Histologic features indicative of aggressive disease
 Poor differentiation
 Thickness greater than 4 mm
 Adenoid, adenosquamous, and desmoplastic subtypes

54. Treatment
Field therapies
• Cryotherapy
• Curettage
• Cautery and ablation
• Drug therapy including imiquimod
• Radiation therapy
Surgical excision
• Standard surgical excision
• Mohr’s micrographic surgery

55. Standard surgical excision
• 4-6mm margin for low grade
• 10mm for high grade
• Factors rendering tumors high risk are
Size >2cm
Subcutaneous tissue involvement
Moh’s microsurgery
• Cosmesis or function preservation is critical
• Poorly differentiated tumors
• Invasive lesions
• Verrucous carcinomas.

56. Radiation therapy
• Poor surgical candidates
• Adjunct to surgical treatment in cases of lip carcinoma
• Microscopic positive margins,
• Perineural histology
• Underlying tissue invasion
• Multiple recurrences

57. Lymph nodes in SCC
• Regional palpable nodes should be removed along with
susceptible regional lymph node basins in patients with
SCC in the setting of chronic wounds.
• Management of lymph node disease involves surgical
resection and/or radiation therapy.

58. Basal cell Carcinma
• Arises from the basal layer of nonkeratinocytes
• M/C NMSC
• Site – sun exposed areas of head and neck
• Risk factors similar to SCC
• Intermittent intense exposure to UV radiation
• Mutation in hedgehog pathway
• No precursor skin lesions

59. Types
Nodular BCC
• The most common (60%)
• Raised, pearly pink papules
• Occasionally a depressed tumor center with raised borders (classic
“rodent ulcer”) appearance.
• Develop in sun-exposed areas of individuals over the age of 60years
Superficial BCC
• 15% of BCC
• Mean age of 57 years
• Trunk as a pink or erythematous plaque with a thin pearly border

60. Infiltrative form
• head and neck
• Late 60s with similar clinical appearance to the nodular variant.
Pigmented variant of nodular BCC
• difficult to differentiate from nodular melanoma.
• Other important subtypes include the morpheaform variant,
accounting for 3% of cases and characterized by indistinct borders
with a yellow hue, and fibroepithelioma .
• Histologic subtypes of BCC include nodular and micronodular (50%),
superficial(15%), and infiltrative.

62. Treatment
Surgery
• Standard surgery with 4-6mm margins
• Mohr’s micrographic surgery
Field therapy

63. Radiation therapy
• Poor surgical candidates
• Questionable resection margins
• Microscopic positive margins
Other field therapies include
• Topical 5flurouracil application
• Topical photodynamic therapy
• Cautery and ablasion

64. Other skin cancers
• Cutaneous angiomas
• Dermatofibrosarcoma protruberans
• Kaposi sarcoma
• Merkel cell carcinoma