3. Arise from melanocytes in basal layer in the epidermis
The worst prognosis and morbidity in all skin cancers
Incidence is increasing by every year (3-7% per year)
accounts for only 4% of all skin cancers, but responsible
for more than 77% of skin cancer deaths
Early detection and treatment important, because it
reduces the mortality and increases survival
Prognosis ( 5 years) Local disease > % 90
Regional disease 60 %
Distant metastasis 5%
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3074354/
3
4. Mostly arise from skin ( 95 % )
But also found in the eyes, ears, GI tract, and mucous
membranes
Unknown primary or metastasis (3 %)
4
8. Very fair skinned,
◦ particularly those with fair or red hair
Tendency to sun burn
Excessive childhood sun exposure
EX: blistering childhood sun burns
Age :
◦ the incidence steadily rises with age
◦ The highest incidence is in those over 80
The development of melanoma is multifactorial
and appears to be related to multiple risk factors
8
9. No of mole
◦ more moles you have on your body, the higher your
risk of melanoma
◦ more than 100 Atypical or dysplastic nevi
Born in a hot country
◦ Ex: Australia or Israel
Malignant melanoma in the first degree relative
◦ (3-10 %)
People who work outdoors and so are in the sun
Ex:sailors, farmers
9
13. People who have risk factors
should be follow and have
preventive efforts
13
14. A changing mole
◦ Most common warning sign
Pruritis
◦ most common early sign of melanoma is pruritis
Bleeding and ulceration are late signs showing
advanced disease
14
15. A- Asymmetry:
One half of the lesion does not match the other half.
B- Border irregularity:
The edges are ragged, notched, or blurred.
C- Color varieation:
Pigmentation is not uniform and may display shades of tan,
brown, or black; white, reddish, or blue discoloration is of
particular concern.
D- Diameter:
A diameter greater than 6 mm is characteristic, although some
melanomas may have smaller diameters; any growth in a nevus
warrants an evaluation.
E- Evolving:
Changes in the lesion over time
15
16. All suspected lesions are removed for
histopathologic examination
16
17. Excision
◦ (Golden standard)
*İncision biopsy
*Punch biopsy
Partial thickness or shaving biopsies are contraindicated
*All dermis layers should be removed
Balch CM, Houghton AN, Sober AJ, Soong S.
Cutaneous Melanoma. St Louis QMP 1998 17
19. most common subtype of melanoma, occurring in
approximately 70% of patients
most common on the trunk in men and on the legs in
women
most commonly seen in individuals aged 30-50 years
Manifest as a flat or slightly elevated brown lesion with
variegate pigmentation (ie, black, blue, pink, or white
discoloration)
generally greater than 6 mm in diameter
Irregular asymmetric borders are characteristic
19
21. Nodular melanoma is the second most common subtype
of melanoma, occurs in 15-30% of patients
Sseen most commonly on the legs and trunk
Rapid growth occurs over weeks to months
Lack of an identifiable in situ (or radial growth) phase
Rresponsible for most thick melanomas
Mmanifests as a dark brown-to-black papule or dome-
shaped nodule, which may ulcerate and bleed with
minor trauma
Tends to lack the typical ABCDE melanoma warning
signs
21
23. accounts for 4-15% of cutaneous melanoma cases
typically located on the head, neck, and arms (sun-
damaged skin) of fair-skinned older individuals (average
age 65 y)
grows slowly over 5-20 years
Only 5% to 8% of lentigo maligna are estimated to
evolve to invasive melanoma.
Lentigo maligna appears as a tan to brown macule or
patch with variation in pigment or areas of regression
that appear hypopigmented clinically.
Lentigo maligna melanoma is characterized by nodular
development within the precursor lesion.
23
25. Acral lentiginous melanoma is the least common
subtype, representing only 2% to 8% of
melanoma in Caucasians,
It typically occurs on the palms or soles or
beneath the nail plate (subungual variant).
Irregular pigmentation, large size (>3 cm
diameter), and plantar location are characteristic
features of acral lentiginous melanoma.
25
26. Subungual melanoma may be confused with a
benign junctional nevus, pyogenic granuloma, or
subungual hematoma.
Rapid onset of diftuse nail discoloration or a
longitudinal pigmented band within the nail
plate warrants biopsy of the nail matrix, from
which these melanomas arise.
The additional presence of pigmentation in the
proximal or lateral nail folds (Hutchinson's sign)
is diagnostic of subungual melanoma
26
29. Spread of melanoma with the depth of invasion
from its origin in the epidermis. There are five
levels of invasion
classification
of the Melanoma by Clark
29
30. Level I — the atypical melanocytes are confined
to the epidermis (in situ melanoma);
Level II — the atypical melanocytes have extended into
the papillary dermis but have not reached
the reticular dermis;
Level III — the atypical melanocytes have penetrated to
the interface between the papillary dermis and
the reticular dermis but do not extend into the
reticular dermis;
Level IV — the atypical melanocytes have extended
into the reticular dermis;
Level V — the atypical melanocytes have reached into the
subcutaneous fat.
30
31. According to the thickness of the lesion
as measured by an ocular micrometer
from the top of the granular zone of
the epidermis to the base of the neoplasm
clasification by Breslow
31
32. Level 1: less than 0.76 mm thick
Level 2: between 0.76– 1.50 mm
Level 3: between 1.50 - 4.00 mm
Level 4: exceed 4.00 mm in thickness
32
36. Stage I : No metastasis (Local Disease)
Stage II : Nodal metastasis (Regional Disease)
Stage III : Distant Metastasis (Systemic Diasese )
36
37. T Staging: Primary tumor thickness
T1 : </= 1 mm a) no ulceration, mitosis < 1mm2
b) ulceration exist, mitoz > 1mm2
T2 : 1-2 mm a) no ulceration
b) ulceration exist
T3 : 2,01-4 mm a) no ulceration
b) ulceration exist
T4 : >4 mm a) no ulceration
b) ulceration exist
TNM Classification
AJCC 2009
37
38. TNM Classification
AJCC 2009
N Staging : Lymph node status
N1 : 1 Lymph Node
N2 : 2-3 Lymph Node .
N3 : > 4 metastatic nodes, or matted nodes, or in
transit metastases/satellites with
metastatic nodes
38
39. M Staging: Distant Metastases
M1 : Distant skin,subcutaneous or lymph node
Normal LDH
M2 :Pulmonary metastases Normal LDH
M3 : Visceral Organ or other distant metastases
Normal LDH
TNM Classification
AJCC 2009
39
43. Suggested surgical margins:
(according to breslow thickness)
In-situ MM 0,5-1 cm
Breslow thickness < 1mm : 1 cm
Breslow thickness 1-4 mm: 2 cm
Breslow thickness >4 mm: > 3 cm
43
44. METASTATIC MALIGNANT MELANOMA
LYMPHATIC METASTASES
HAEMOTOGENIC METASTASES
IN –TRANSIT METASTASES
LOCAL SATELITE METASTASES
44
45. Effect of Lymph Node metastases on
Survival
10 years Survival
%
Microscopic Lymph
Node metastases
48
No Lymph Node
metastases
65
Palpabl Lymph Node
metastases
12
45
46. Treatment of Lymph Nodes
Wait and see (no treatment)
Elective Lymph Node Dissection
Sentinel Lymphadenectomy
46
47. Elective Lymph Node Dissection
Removing the regional lymph nodes for
prevention in no clinical palpable lymph node
There is no consensus on survival advantage of
Elective Lymph Node Dissection (ELND)
47
50. Sentinel Lymphadenectomy
Morton introduced for Stage I Melanoma
patients in 1992
Vital blue dye intradermal injection was used for
lymphatic mapping
Lymphatic drainage of primary tumor goes
specific lymph node in regional lymph basin.
This is the first node in the basin. This is called
as sentinel lymph node
50
51. Sentinel lymph node shows the regional node
status
If sentinel lymph node negative, others lymph
nodes in the basin are also negative
If sentinel lymph node contains tumor cells, It
means disease spread to the regional nodal
basin
51
53. Sentinel Lymphadenectomy
Intradermal injection of tc99 m labeled sulfur colloid
and lymphoscintigraphy
intra-operative vital blu dye injection
Removing blue stained and hot lymph node as
sentinel nodes
Serial section of nodes, immunohistopathologic
examination by S 100, HMB 45 (melenoma spesific)
54
54. Advantages of Sentinel
Lymphadenectomy
Provides staging
Prevents of Electice Lymph node dissection
morbidity
Gives a specimen to pathologist to examine in detail
Provides psychological support
Can be done by local anesthesia
Less costly
55
57. Treatment of Distant Metastases
Soliter skin and distant lymph nodes are
removed
İsoleted pulmonary metastases can be removed
in selected cases
Brain and GI metastases are removed for
palliation
Radiotherapy may be benefical for selected
patients (mainly for pain treatment)
58
58. Avarege life expentancy is 6-9 months
There is no real treatment for Stage IV patients
Most realistic goal is palliation and preservation of
quality of life
59
60. Most common cancer in the world
Represents the most common form of cancer in
Caucasians
Continuing increase in incidence worldwide
Currently2–3 million new cases are diagnosed
worldwide every year
Most common risk factors is exposure to ultraviolet
(UV) light
BCC accounts for 75% of cases of NMSC
SCC accounts for the remaining majority of NMSC
61
62. UVB radiation
Sun light exposure
Increase in incidence in sunnier climates
lower rates in darker skin types
BCC has been more associated with
intermittent and childhood sun exposure
SCC more related to chronic UV exposure
63
63. UV light is thought to induce direct DNA
mutation
Use of tanning devices is associated with
2.5-fold increase in SCC risk and 1.5-fold
increase in BCC risk
Phototherapy, utilized in the treatment of
various skin diseases, is also associated
with increased risk of NMSC
64
64. UV effect reduced by hair, thick stratum
corneum, and melanin
More pigments protect the UVB , absorbs the
light
Exposure as child increases risk
Exposures to arsenic, organic hydrocarbon,
ionizing radiation, and cigarette smoke have
been associated with increasing risk for SCC
65
65. Genetic mutations are cofactor in the
development of NMSC
Mutation of patched gene on chromosome
9q22 associated with multiple BCC
Mutations of PTCH have been found in
70% of sporadic human BCC
66
66. Mutation of cytochrome450 (CYP),
glutathione S-transferase (GST) and p53
are associated with BCC
CYP and GST are known to detoxify
mutagens
p53 has an important function as a tumor
suppressor gene regulating the cell cycle
67
67. Actinic keratosis (AK) and Bowen’s disease
are precursor for SCC
72% of SCC have been noted to develop
within AK or actinically damaged skin
Errors in p53 signalling and mutations of
p53 have been identified in 69% to over
90% of invasive SCC
Other reported mutations for SCC include
WNT, p16INK4, NF-κB and c-Myc
68
68. Fair or red hair, blue eyes, increasing
number of melanocytic naevi
Human papillomavirus(HPV) pathogenic
for SCC
HPV prolong keratinocyte cell cycle, with
degradation of p53
69
69. Impaired immunity, especially cell-
mediated , is a well-established cause of
SCC
Chronically immunosuppressed patients
who undergone organ transplantation
Immunosuppressive drugs such as
azathioprine, cyclosporine, and prednisone
increase the risk for SCC by 50%
70
70. After 10 years of immunosuppression,
NMSC develop in 10% of patients ,after
20 years increases to 40%
Acquired impaired cell-mediated immunity,
including lymphomas, leukemias, post
radiotherapy, autoimmune diseases and
human papillomavirus(HPV)infection are
risk factor for SCC
71
71. Old scar, old burn scar
Actinic keratosis
Common above middle age and elderly
Characterized by papule or plaque with rough
surface
May develop cutaneous horn or become malignant
10-20% of lesions progress to SCC
72
72. Cutaneous Horn
Hard, yellowish brown, horny outgrowth,
often curved with circumferential ridges.
Surrounded by acanthotic collarette
Seen on exposed areas specially upper
part of face and ears
73
73. Bowen's disease
An early stage intraepidermal SCC
Common above 60 years
Common at genitalia
Typically presents as a gradually enlarging,
well-demarcated erythematous plaque with
irregular border, crusted or scaling surface
74
75. BCC
Tumour size greater than
2cm
Infiltrative, micronodular
Histological subtype
Perineural invasion
Anatomic site over central
face
SCC
Tumour size greater than 2
cm
Tumour thickness greater
than 4 mm
Moderate or poor histological
differentiation
Anatomic site over ear,
lip,Genitalia
Perineural invasion,
Lymphovascular invasion
Immunosuppressed patients
Tumours arising from chronic
scars or ulcers
76
81. Basel cell nevus
syndrome
Childhood onset
Autosomal
dominant
Multiple
Associate with
other
anomalies(skin pit
on palm,sole,bifid
fid rib)
82
82. Sun exposed area
Squamous epithelial cell ivade the dermis
with well differentiated keratinization
Poorly differentiated, keratinization and
inflammation minimal or absent
Poorly differentiated lesion may have
pseudo glandular appearance
83
84. In classical cases diagnosis can be made
clinically
Curretage biopsy
Local anaesthesia
Scrap with dermal curet
Tumor cell group soft and easily removed
85
85. Shave biopsy
Upper half of dermis sampled with
minimal deformity
Punch Biopsy
3-4 mm sufficient for diagnosis
May destroy normal dermal barrier and
allow extension into deeper structures
86
86. Excisional Biopsy
Treatment of choice for primary BCC or
pigmented lision
Impractical for large tumor when border
are not clear
Deep wedge biopsy is helpful in diagnosis
and depth
87
87. Choice of treatment dependent on
Risk stratification of the tumor, patient
preference or suitability, and availability of
local services
High-risk tumor have greater risk of
recurrence and require more aggressive
treatment
88
88. The gold standard for high-risk BCC and
SCC is Mohs micrographicsurgery (MMS)
If MMS is not available, excision with
predetermined wide margins
Radiotherapy may be considered
89
89. Under local anesthesia
Margin for resection is not well defined
Commonly 3-4 mm of normal appearing
skin
Local recurrence is greater then 90 %
90
90. Mohs micrographic surgery(MMS)
First developed by Frederic Mohs in1941
In standard surgical excision (SE) with
predetermined margins
100% of the peripheral and deep margin is
analysed to confirm the presence or absence of
any residual tumor
Once complete clearance is achieved, the wound
is repaired direct closure, local skin flap or skin
graft, secondary intention
91
92. Curettage and cautery( C and D)
Removing epidermis and dermis containing
tumour tissue
This process can be repeated immediately once or
twice
Effective treatment of low-risk NMSC
Increasing diameter, cure rates significantly
decreased
High cure rates for low risk
93
93. Cryosurgery
Delivery of liquid nitrogen to freeze and
then thaw the target tumour tissue
Local cellular destruction
High cure rates have been reported for
NMSC
94
94. Low cure rate for high-risk NMSC
Recommended for low-risk BCC
Not recommended for SCC as HCC have a
potential for metastasis
Cryosurgery will also manifest a
hypopigmented scar
95
95. Photodynamic therapy
Effective therapy for BCC or low-risk
nodular BCC of less than 2 mm thickness
Topical application of 5- aminolaevulinic
acid (ALA) or methyl aminolaevulinic(MAL)
Uptake of the drug into the tumour cells
preferentially, distruction occur
Excellent choice of treatmentfor BCC
96
96. Radiotherapy
Effective treatment modality for patients with
unable to undergo surgery
Efficacy is overall lower than with MMS
Beneficial for postoperatively tumors with
perineural invasion
When complete margin excision is not possible
Increase the risk of subsequent BCC and SCC
97
