for use by medical undergraduates for revision on skin maliganacy

1. SKIN MALIGNANCY
BY
DR FRANKLYN C BAGENDA
3RD YEAR GENERAL SURGERY

2. INTRODUCTION
Largest organ of the body (15% of body
Two main types–
epidermis
dermis
• connective tissue
Rests on subcutaneous layer or hypodermis
Normal thickness of 1-2 mm, up to 6 mm
• thicker skin (palms & soles) has stratum lucidum, no hair follicles or
sebaceous glandsfollicles or sebaceous glands

3. Anatomy
• Epidermis : ( 0.04 – 1.4 mm )
• Stratified squamous and cornfield.
• Keratinocytes
• Melanocytes
• Langerhan’scells
• Merkels cells

5. • Dermis
• Papillary & reticular dermis
• Non cellular Conective tissue
• Collagen
• Elastic fibres
• Nerves , blood vessels , lympahtics, muscle units, apocrine
unit eccrine sweat unit
• Contains : fibroblasts , mast cells , Langerhan cells and
lymphoctes

6. EMBROLOGY
Skin is derived from Ectoderm & Mesoderm
• Epitheleal structures derived
from ectoderm
• Epidermis
• Pilosebaceous & apocrine units
• Eccrine sweat units
• Nail unit
• Structures from the
neuroectoderm
• Melanocytes
• nerves
• Structures from the mesoderm
• Macrophages , mast cells
• Langerhan cells
• Merkel celss
• Fibroblasts
• Blood vessels
• Lymph vesssels
• Fat cells

8. Skin
whitening/bleaching
• is the use of
substances, mixtures, or
physical treatments to
lighten skin color.

9. •Overall incidence of skin cancer of
exposed skin is 15 times greater in
Caucasians than negroes

10. CLASSIFICATION OF SKIN TUMOURS
1. Epidermal tumours
A. Benign
 Papilloma
 Seborrhoeic keratosis
 Verrucous naevus
B. Malignant
 Basal cell carcinoma
 Epithelioma, Marjolin ulcer

11. CLASSIFICATION OF SKIN TUMOURS
2. Melanocytic tumours
A. Benign
 Junctional naevus
 Compound naevus
 Intradermal naevus
 Hutchinson's freckle
B. Malignant
 Melanoma
3. Sweat gland tumours (malignant)
Hidradenocarcinoma
 Adenoid cystic carcinoma

12. CLASSIFICATION OF SKIN TUMOURS
4. Sebaceous gland tumours
Sebaceous adenoma
Sebaceous carcinoma
5. Other tumours
Dermatofibrosarcoma protuberans
Trichofolliculoma (hair follicle tumour)

13. • Types of skin cancers:
• The most common types of skin cancer are:
Basal Cell Carcinoma (BCC)
Squamous cell (epidermoid) carcinoma (SCC).
Malignant melanoma

14. Basal cell carcinoma
• It is the most common skin cancer (80%)
• arising from the basal layer of epidermis and its appendages.
• referred to as "epitheliomas" because of their low metastatic potential.
• The incidence high in areas of ↑UV radiation (Australia,South africa)
• estimated lifetime risk of 33-39% for men and 23-28% for women
• Men >Women
• It increases with age (50-80 yrs )
• Rare in <40 yrs (5-15%)

15. Location BCC
• Majority are found on the face above a line from lobule of the ear to
the angle of mouth.
• Common sites
 Inner canthus of the eye
 Outer canthus of the eye
 Eyelids
 Bridge of the nose
 Around nasolabial foldmouth.

16. Epidemiology
• BCC is particularly common in Caucasians.
• lifetime risk of developing a BCC is 30 percent.
• The incidence in men is 30 percent higher than in women, particularly
with the superficial type.

17. Risk factors : a) UV radiation
• Sun exposure directly to a person's
sun exposure habits or susceptibility
to solar radiation.
• NB Childhood sun exposure
appears to be more important than
exposure during adult life
• Tanning beds using tanning beds
more than six times per year has
increased risk
• Therapeutic exposure to psoralen
plus ultraviolet A light (PUVA) for
cutaneous disorders

19. • b) Ionizing radiation
• Superficial therapeutic ionizing radiation, as for facial acne, psoriasis,
or tinea capitis, increases the risk of NMSC
• c) Immunosuppression
• Chronic immunosuppression (as occurs with solid organ
transplantation and with human immunodeficiency virus [HIV]
infection)
• d) Genetic variants —
• Genetic variation may play a role in susceptibility to BCC
• melanocortin 1 receptor (MCR1)

20. • e) Inherited disorders
• Basal cell nevus syndrome rare disorder of autosomal dominant
inheritance that is due to germline mutations of the human patched gene
(PTCH).
• Most have the following clinical features:
• Macrocephaly, frontal bossing, and hypertelorism
• Bifid ribs
• Palmar and plantar pitting (picture 2)
• Bone cysts, especially in the mandible
• Calcification of the falx cerebri

21. • BCC distrubution :
Head and neck 60%
Nose 14%
Trunk 30%
Extremities 10%
• There are several distinct clinical
types of
• BCC, and over 20 histological growth
• patterns of BCC
Nodular
Superficial
Morphoeic

22. Nodular Basal Cell Carcinoma
• most common 60 percent of cases
• begins as a small, slightly elevated papule
with a central depression which ulcerates,
heals over and then breaks down again
• Very mild trauma may cause bleeding
• One or more telangiectatic blood vessels are
usually seen coursing over the borders around
the central depression
• rolled edges representing tumor cells
spreading laterally beneath the skin
• Ulceration is frequent, and the term "rodent
ulcer"

23. Superficial basal cell carcinoma
• 30 percent of BCCs are superficial BCCs
• most commonly occur on the trunk
• typically present as slightly scaly, non-firm macules,
patches, or thin plaques
• pink to red-brown in color, often with central
clearing
• Erosion is less common than in nodular variety
• tend to grow slowly, and can vary in size from
macules measuring just a few millimeters in diameter
to lesions several centimeters in diameter

24. Morpheaform and infiltrating
basal cell carcinoma
• aggressive basal cell carcinoma subtypes
with sclerotic(scar like) plaques or papules
• 5 to 10 percent of BCCs.
• lesions are typically smooth, flesh-colored, or
very lightly erythematous papules or plaques
that are frequently atrophic
• border - not well defined and often extends
well beyond clinical margins
• Ulceration, bleeding, and crusting -
uncommon
• mistaken for scar tissue

25. Pigmented basal cell carcinoma
• In addition to features seen in lesions
of nodular basal cell carcinoma,
lesions of pigmented BCC contain
increased brown or black pigment
• seen more commonly in individuals
with dark skin

26. diagnosis
•Skin biopsy
• To confirm and diagnose bcc and its subtype
Shave biopsy
Punch biospy
• Cytology
• Histologic findings
• Laser doppler (eyelids tumor margins)

27. Management of BCC
• Non surgical
• Curettage
• Electrodessication
• Laser vapourisation
• Cautery and destruction.
• Surgical
• Moh’s microsurgery
• Wide local excision, 0.5-1cm margin free with
reconstruction procedure

28. FEATURES ASSOCIATED WITH HIGH RISK FOR
RECURRENCE
• treatment of BCCs with clinical
or pathologic features associated
with increased risk for
recurrence
• Recurrent BCC may reappear
months to years after initial
treatment
• leading to local tissue
destruction, morbidity, increased
risk for metastasis

29. CONT…
• The following characteristics have been proposed as factors
associated with increased risk for tumor recurrence
A) Location and size
• Greater than or equal to 6 mm in diameter in high-risk areas (eg,
central face, nose, lips, eyelids, eyebrows, periorbital skin, chin,
mandible, ears,
• Over 10 mm in diameter in other areas of the head and neck
• Over 20 mm in diameter in all other areas (excluding hands and feet)

30. B) Aggressive pathologic features
• Morpheaform, sclerosing, or mixed infiltrative
• Micronodular
• Basosquamous (keratinizing)
C) Lesions in sites of prior radiation therapy (RT)
d) Lesions in immunocompromised patients
E) Perineural invasion (tumor growth in or around nerves)
• occurs in up to 10 percent of BCCs is associated with an elevated risk
for lesion recurrence

31. Cutaneous squamous cell carcinoma (SCC)
• Common cancer arising from malignant proliferation of epidermal
keratinocytes
• 2nd most common skin Ca
• Malignant tumour of epidermal keratinocytes
• Can Metastasize
• Strongly related to sun exposure
• 70% occur on head and neck

32. Epidemiology
• Age > 50
• Fitzpatrick I and II
• Males
• Closer to equator

33. Risk Factors
• UV light exposure — Ultraviolet (UV) radiation
is absorbed by DNA and can result in DNA
damage , p53 tumor suppressor gene often
has point mutations
• NB cumulative sun exposure (principally UVB
radiation) is the most important
environmental cause of cutaneous SCC.
• Chronic inflammation — There is an increased
risk of cutaneous SCC in chronically inflamed
skin resulting from scars, burns, chronic ulcers,
sinus tracts,
• cutaneous SCC occurs in a chronic wound, it is
also known as Marjolin's ulcer.

34. Cont…
• HPV infection — Human papillomavirus
(HPV) infection can cause cutaneous SCC in
genetically predisposed individuals (eg,
epidermodysplasia verruciformis) and
verrucous carcinoma of the penis
• Radon — High concentrations of
environmental radon were associated with
increased rates of cutaneous SCC
• Selenium increased risk of cutaneous SCC
associated with dietary selenium
supplementation

35. Clinical features
• Most lesions are preceded by actinic keratosis.
• Typically, it is an ulcerative or cauliflower-like
lesion
• The edge is everted and indurated
• The base is indurated and it may be subcutaneous
tissue, muscle or bone.
• The floor contains cancerous tissue which looks
like granulation tissue.
Pale, friable, bleeds easily on touch

36. Clinical findings
• SCC in situ (Bowen's disease)
• typically presents as a well-demarcated,
scaly patch or plaque
• Intra-epidermal form of SCC
• SCC in situ: BM not invaded
• Well demarcated erythematous plaque
• Irregular border
• Surface crusting or scaling
• lesions are usually asymptomatic.
• SCC in situ lesions tend to grow slowly,
enlarging over the course of years

37. • Erythroplasia of Queyrat
• SCC in situ involving the penis
• presents as a well-defined, velvety, red
plaque
• Patients may experience pain, bleeding, or
pruritus.

38. • Invasive SCC
• clinical appearance of invasive SCC often
correlates with the level of tumor
differentiation.
• Well-differentiated lesions usually appear as
indurated or firm, hyperkeratotic papules,
plaques, or nodules.
• poorly differentiated lesions are usually
fleshy, soft, granulomatous papules or
nodules that lack the hyperkeratosis
• Lesions are usually 0.5 to 1.5 cm in diameter,
although some are much larger.

39. Cutaneous metastases
• most frequent site of metastasis for
cutaneous SCC is the regional lymph
nodes
• other potential sites for metastasis
include the lungs, liver, brain, skin, or
bone
• Metastases to the skin can present with
erythematous papules or nodules that
resemble primary lesions of cutaneous
SCC

40. Spread
 Local spread occurs by infiltration into the surrounding tissues.
 Lymphatic spread is the chief method of spread even though it
occurs relatively late. Regional nodes are involved first.
Blood spread is rare and late.

42. Investigations
• A wedge biopsy from the edge of the ulcer or growth
is taken.
• However, in proliferative lesions punch biopsy can also
be taken.

43. Management of SCC
• Treatment modalities for SCC include:
•Cautery and ablation,
•Cryotherapy,
•Drug therapy including imiquimod,
•surgical excision,
•Moh’s microsurgery, and
•Radiation therapy

44. Malignant Melanoma
• Accounting for about 3 to 4% of all diagnosed skin cancers,
melanoma begins in the melanocytes, cells within the epidermis
that give skin its color.
• The incidence is rising by 3% a year.
• Also: eyes, ears, GI tract, and oral and genital mucous
membranes
• 6th most common cancer in U.S.
• 1 in 60 lifetime risk of developing melanoma in Caucasians
• Highest incidence in Australia and NZ
• Incidence increasing worldwide.

45. Risk factors of melanoma
• Inttermittent Exposure to solar UV radiation
• Personal history of melanoma 10-fold increase
in risk.
• Family history of melanoma
• FAMMM
• Previous non-melanoma skin cancer
• Large number of moles/dysplastic moles

46. Common sites for melanoma
Men commonest site is the back
Women commonest site is the leg
Mucous mebranes eg lips or genitals
Under the nail
Eyes or mouth

47. Pathogenesis and Clinical Presentation.
• Melanoma growth most commonly starts as a localized, radial growth
phase followed by a vertical growth phase that determines metastatic
risk.

48. Clinicopathological subtypes
1. Superficial spreading melanoma,
2. Acral lentiginous melanoma,
3. Nodular melanoma,
4. Lentigo maligna melanoma,
5. Desmoplastic melanoma,
6. Amelanotic melanoma
7. Polypoid melanoma,
8. Mucosal melanoma,

49. Superficial spreading melanoma
• The most common subtype ( 70%).
• Presents with diffused borders, a
combination of several colors such as
brown, black, red, white, or others, and
an irregular and elevated surface.
• Characterized by laterally spreading
melanocytes within the epidermis.

51. Nodular melanoma
• 12-25%,
• More aggressive subtype.
• Presents with a relatively
sharp border as the
melanocytes extend vertically
rather than horizontally

52. Lentigo maligna or Lentigo maligna
melanoma
• Develops on sun-damaged skin (eg,
on the head and neck area of elderly
patients).
• Lentigo maligna is a melanoma in situ
• Distinction from “actinic
melanocytosis” can be difficult.
• Lentigo maligna melanoma invades
the dermis.

53. Acral lentiginous melanoma
• 7-15%. Less common, least
malignant.
• Occurs in old age and common in
face (Hutchinson’s melanotic
freckle).
• It is slow growing, variegated,
brown macule/ lentigo;
• Common in face/neck/hands
• common in elderly women.
• Lentigo maligna is in situ type.

54. Amelanotic melanoma:
• The worst type
because of the undifferentiation,
• It presents as rapidly progressive
pinkish fleshy tumour.
• It may mimic soft tissue sarcoma

55. Desmoplastic melanoma
• high affinity for perineural invasion
Common in head and neck with higher
recurrence rate.
• It is amelanotic melanoma with
thicker lesion
• Carrying poor prognosis due to
neural invasion.

56. Clinical features
• Changes in the preexisting mole
• Nonhealing ulcer.
 Painless , Bleeds on touch ,Edges and floor are
irregular.
 Pigmented .
 10% amelanotic melanoma.
 A halo may be present surrounding the ulcer.
Satellite nodules and in-transit lesion

57. In-transit lesion

58. ABCDE OF EVALUATING
A CHANGING MOLE
A- Asymmetry: One half does not
match the other
B -Border irregular: Ragged or blurred
C -Colour variation: Tan, black, brown
D -Diameter: > 6 mm
E -Evolving (elevation): Change in a
pre-existing lesion

59. Malignant melanoma

60. TNM STAGE
MELANOMA

61. Differential diagnosis of Malignant melanoma
• Seborrhoeic keratosis, dermatofibroma
• Pigmented BCC, pigmented SCC
• Naevus, sebaceous epidermal naevus
• Kaposi’s sarcoma, mycosis fungoides
• Cutaneous haemangioma
• Solar keratosis
• Pyogenic granuloma
• Cutaneous angiosarcoma

62. Classification
Breslow’s classification (1970):
Based on thickness of invasion
I. Less than 0.75 mm
II. Between 0.76 to 1.5 mm
III. 1.51 mm to 4 mm
IV. More than 4 mm

63. classification
Clark’s levels
• Level 1: Only in epidermis
• Level 2: Extension into papillary
dermis
• Level 3: Filling of papillary
dermis completely
• Level 4: Extension into reticular
dermis
• Level 5: Extension into
subcutaneous tissue

64. Investigations
• History and physical exam
• Excision biopsy of the lesion with free margin
• Nonspecific investigations to look for metastasis are:
 Chest X-ray-cannonball secondary
 CT scan is better
 Ultrasound abdomen-secondaries in liver
 X-ray of involved bone-osteolytic lesions
Whole-body PET-CT; or brain MRI.
• SENTINAL lymph nodes BIOPSY

65. Treatment of melanoma
• Surgical excision with safety margin
• Thicker melanomas>wider excision+/- sentinel node biopsy
• MOHS technique
• Regional Chemotherapy
• Immunotherapy

66. Prognostic factors
• Tumor thickness
<1mm, almost 100% 5year survival
>4mm, only 50% 5year survival
• Ulceration
• Mitotic rate
• Nodular involvement-
• Lactate dehydrogenase (LDH)

67. Kaposi’s Sarcoma
• Characterized by the proliferation and inflammation of
endothelial-derived spindle cell lesions.
• Primary tumour commonly occurs in skin, mucous
membrane, lymph nodes or viscera.
• It is linked with Human Herpes Virus 8(HHV8) as causative
agent.
• It is seen commonly in HIV patients due to
immunosuppression.

68. Types
1. Classic(Mediterranean),
2. African Kaposi‘s sarcoma.
3. AIDS associated Kaposi‘s sarcoma:
4. Transplant associated Kaposi‘s
sarcoma
5. HIV-negative men having sex with
men (MSM)–associated,

69. Clinical features
• Multiple reddish-blue nodules in the skin with ulceration over the
nodule.
• Lymph node enlargement.
• Koebner phenomenon is common in areas of trauma.

70. Differential Diagnosis
• Lymphomas.
• Cutaneous angiomatoses.
• Mycobacterial infection of skin.

71. Investigations
• Biopsy from the skin lesion.
• Tests for HIV infection.

72. Treatment
• Irradiation.
• Chemotherapy. Drugs used are adriamycin, bleomycin and
vinblastine.
• Antiretroviral therapy.
• Interferons.

73. Dermatofibrosarcoma Protuberans
• Rare, low-grade sarcoma of fibroblast
origin.
• It has low distant metastatic potential but
behaves aggressively locally with finger-
like extensions.
• Tumor depth is the most important
prognostic variable.
• Characteristically a slowgrowing,
asymptomatic, violaceous plaque
involving the trunk, head, neck, or
extremities.

74. Treatment dermatofibrosarcoma Protuberans
• Wide local excision with 3-cm margins down to deep underlying fascia
• Moh’s microsurgery in cosmetically sensitive areas
• Local recurrence occurs in 50% to 75% of cases,
• Clinical follow-up is important.

75. The END