Skin

cancer
Desak G. A Suprabawati
Divisi Bedah Onkologi
Departement of Surgery
RSU Dr. Soetomo/FK UNAIR
 Adalah keganasan yang berasal dari
kulit dan adneksa kulit kecuali yang
berasal dari genitalia
Classification
Non melanoma skin cancer (NMSC)
- basal cell carcinoma (BCC)
- squamous cell carcinoma (SCC)
- skin adnexa
Melanoma
melanoma

Malignant neoplasm arises from

melanocyte cell
Skin and mucosal
All ages : > 35 55 years
 Introduction

Malignant melanoma has now become

more common.
In United States,
1935 1 : 100.000 people
1991 12.9 : 100.000 people
1998 18.3 : 100.000 for white males
13.0 : 100.000 for white females
 The American Cancer Society has
estimated that 68,720 cases of
melanoma will be diagnosed in the United
States in 2009.
Queensland, Australia, has the highest
incidence of melanoma in the world,
57 cases per 100,000 people per year.
Israel also has one of the highest
incidence, 40 cases per 100,000 people
annually.
 Although melanoma accounts for
only 5 % of skin cancer, it is
responsible for 3 times as many
deaths each year as non
melanoma skin cancers
 pathogenesis

Melanoma arises from transformed

melanocytes and occur anywhere that
melanocytes have migrated during
embryogenesis.
The eye, central nervous system,
gastrointestinal tract, and even the
gallbladder have been reported as
primary sites of the disease.
 Risk factors
Increased exposure to sunlight (UV
radiation) (intermittent, intense sun
exposure, particularly in fair-skinned, light-
haired individuals).
individuals who have 100 benign nevi
5 nevi, > 5 mm
50 nevi, > 2mm
History of sunburn, especially in childhood
familial history of this cancer (10%)
 Race : Whites > blacks and asians.
White people with blond or red hair and
profuse freckling, blue eyes.
Xeroderma pigmentosum
gene mutations~ development of
melanoma : CDKN2A, PTEN, NRAS, BRAF.
Male : female = 1.2 : 1
The average age : 57 years.
 Clinical history

Familial history :
10 % of patients with melanoma have a
family history of melanoma (familial
multiple mole melanoma FAMMM, mutation
in the CDKN2a tumor supressor gene).
Develop melanoma at an earlier age
Tend to have multiple dysplatic nevi, and
multiple primaries.
 Patient history:
Any previous history of melanoma ~ risk
of developing 2nd melanoma.
Sun exposure (severe sunburns in
childhood, the capacity to tan)
Moles (change in size, border, color,
symmetry, bleeding, ulceration, itchy,
location)
Clinical Appearance

A : Assymetri
B : Border : irregularity
C : Color : variety
D : Diameter : diameter > 6 mm
E : Evolving on enlarging
In transit metastase
Satellite nodule
Physical examination

Skin examination
Lymph node examination :examine all
lymph node groups.
Melanoma may disseminate through the
lymphatics (~ regional lymph nodes) and
hematogenously (~ any node basin on
the body).
 Common sites of metastases : lung, liver,
bone, subcutaneous areas, and in late
stages, brain.
Patients who present with lymph node or
metastatic involvement without any
obvious primary site ~ spontaneous
remission of the primary ( degree of
immune system involvement).
Histopatological Type

Superficial spreading: 70%

Nodular type :15-30%
Lentigo melanoma maligna:4%-
10%
Acral lentiginous melanoma: 2%-
8%
Amelanotic melanoma : jarang
1 Superficial spreading melanoma
- 70% of cutaneous melanoma
- often arise from a pigmented dysplatic
nevus
- develop from a long-standing stable
nevus changes (ulceration, enlargement,
color change)
- may be found in any body surface,
especially the head, neck, and trunk of
males and the lower extremities of
females
 2. Nodular melanoma

10-15% of melanoma
Commonly found on the trunk of males.
Has an early vertical growth phase ( a
high-risk lesion)
5 % of all nodular melanomas are
amelanotic melanomas (should be
examined with the immunochemical
stains S-100 and HMB-45)
3. Lentigo malignant melanoma

10-15% of melanomas.
Flat, large (1-5 cm) lesions
located on the arms, hands, and face
of the elderly (median age 70 years)
(sun-exposed area)
Has a relatively longer radial phase.
4. Acral lentiginous melanoma
3-5% of cases
Have an equal frequency among blacks and
whites
Most commonly seen in individuals with darker-
pigmented skin.
Occur on the palms, soles, and subungual
areas.
Extremely aggressive, rapid progression from
the radial to vertical growth phase.
Pathological Staging
( Micro staging )
Clark s Level ( Wallace Clark ): invasion tumor into
dermal layer
- Invasion level : I V
- thickness of the skin invasion
- deeper level means greater of recurrence
Breslows Level ( Alexander Breslow ): evaluate
depth of tumor invasion tumor in mm
- thickness of the primary tumor
- more prognostic informative than Clark
- more reproducible and less subjective than Clark
 staging
Clark staging
Level 1 : all tumor cells above
basement membrane (in situ)
Level 2 : tumor extends into
papillary dermis
Level 3 : tumor extends to
interface between papillary
and reticular dermis
Level 4 : tumor extends into
reticular dermis.
Level 5 : tumor invasion of
subcutaneous tissue
 Breslow classification (thickness):
1: 0,75 mm
2: 0,76 1,5 mm
3: 1,51 4 mm
4: 4 mm
 Tumor Primer ( T )
Klasifi Ketebalan Status ulkus
kasi T Melanoma
Tx Tidak dpt diperiksa karena shave biopsy atau melanoma yg
mengalami regresi
To Tidak ditemukan tumor primer
Tis Melanoma in situ
T1 < 1,0 mm
a.Level II atau III, tanpa ulcerasi
b.Level IV atau V atau ada ulcerasi

T2 1,01-2,0 mm a. Tanpa ulcerasi

b Dengan ulcerasi
T3 2,01-4,0 mm a. Dengan atau tanpa ulcerasi
b. Dengan ulcerasi
T4 > 4,0 mm a. Tanpa ulcerasi
b. Dengan ulcerasi
 Kelenjar Getah Bening Regional ( N )
Klasifikasi Jumlah metastasis N Massa metastase nodul
N

Nx Kgb regional tidak dapat

diperiksa

N0 Tidak ada metastasis kgb

regional

N1 Metastasis ke 1 kelenjar
getah bening a.Metastasis mikroskopik,occult secara klinis
b.Metastasis mikroskopik, tampak secara klinis

N2 Metastasis ke 2 atau ke 3
kgb regional atau a.Metastasis mikroskopik,occult secara klinis
metastasis intra limfatik b.Metastasis mikroskopik, tampak secara klinis
regional tanpa metastasis c.Lesi satelit atau metastasis in-transit tanpa
kgb regional metastasis kgb
N3 Metastasis pada >4 kgb
regional, atau metastasis
kgb yang bersatu,
metastasis in-transit atau
lesi satelit dg metastasis
kgb regional
 Metastasis Jauh ( M )
Klasifikasi M Tempat
Mx Metastasis jauh tidak dapat
Diperiksa

M0 Tidak ditemukan metastasis

jauh

M1 Metastasis jauh a. Metastasis ke kulit, jaringan subkutan atau

kgb yang jauh
b. Metastasis ke paru
c. Metastasis ke tempat visceral lainnya atau
metastasis jauh ke tempat manapun yg
disertai peningkatan kadar LDH (lactic
dehydrogenase serum)
 Stadium Klinik & Histopatologik
Stadium Klinik Stadium Histopatologik
Stadium 0 Tis N0 M0 Stadium 0 pTis N0 M0
Stadium IA T1a N0 M0 Stadium 1A pT1a N0 M0
Stadium IB T1b N0 M0 Stadium 1B pT1b N0 M0
T2a N0 M0 pT2a N0 M0
Stadium IIA T2b N0 M0 Stadium IIA pT2b N0 M0
T3a N0 M0 pT3a N0 M0
Stadium IIB T3b N0 M0 Stadium IIB pT3b N0 M0
T4a N0 M0 pT4a N0 M0
Stadium IIC T4b N0 M0 Stadium IIC pT4b N0 M0
Stadium III Tiap T N1 M0 Stadium IIIA pT1-4a N1a M0
Tiap T N2 M0 pT1-4a N2a M0
Tiap T N3 M0
Stadium IIIB pT1-4b N1a M0
pT1-4b N2a M0
pT1-4a N1b M0
pT1-4a N2b M0
pT1-4a/b N2c M0

Stadium IIIC pT1-4b N1b M0

pT1-4b N2b M0
Tiap pT N3 M0

Stadium IV Tiap T Tiap N M1 Stadium IV Tiap pT Tiap N M1

 Dif. MM from Benign Moles
Characteristic Melanoma Benign Moles
A Asymmetry Asymmetry Symmetry
B Border Irregular, Regular, round
Irregularity notched

C Color Very dark- Uniform, tan,

variable brown
D Diameter > 6 mm < 6 mm
Diagnostic procedure

Phisical examination
Radiology imaging :
- routine : thorax, abdominal USG
- indication: CT scan, MRI
Citologi : FNA, inprint citology
Biopsy:type, differentiation , depth of
invation
Laboratory studies

CBC count
Chemistry panel (complete)
Alkaline phosphatase (metastatic disease
to bone or liver)
AST/ALT
Total protein and albumin (overall health,
nutritional status)
Renal function test.
 Lactate dehydrogenase
may indicate distant metastase,
(especially lung and liver)
If elevated ~ poor prognosis
Part of of the staging system for
melanoma
 Penatalaksanaan

MM masih localized
-Wide excision: dengan safety margin 2 cm
-Diseksi kelenjar getah bening regional
-Sentinel lymph node biopsy , intra operative
lymphatic mapping
-Adjuvant therapy
 TERAPI
Primary lesion : wide excision

melanoma Safety margin

1 In situ 0.5 cm
2 0,76 mm 1 cm
3 0,76-1,5 mm 1 cm
4 > 1,5 mm 2 cm
5 subungual Amputasi proximal
interphalangeal joint
MM dengan local recurrence

Wide excision ulang : amputasi

In transit metastase:
Hyperthermic Isolated Lymph Perfusion
dengan melphalan
Isolated limb infusion: melphalan dan
actinomycin-D
MM metastase jauh

Pembedahan bila memungkinkan

(metastatektomi)
Radioterapi
kemoterapi
 Adjuvant therapy
Interferon -2b: bila resiko terjadi rekurensi tinggi
Radioterapi
Kemoterapi : dacarbazine monoterapi, Dartmouth
regimen (dacarbazine, cisplatin, carmustine dan
tamoxifen) atau temozolomide
Vaccine dan terapi biologi : BCG
Antibodi monoclonal
Vaksin tumor : pada advanced melanoma dan high
risk patient
Terapi sel : infus sel dendritik
Imunoterapi
Biokemoterapi
chemotherapy
Single agent chemotherapy :
Dacarbazine :
200 mg/m2 IV on days 1-5 every 3 weeks or
750 850 mg/m2 IV on days 1 every 4-6
weeks.
+ Cisplatin : 100 mg / m2 IV every 3 weeks
+ taxanes.
paclitaxel 135-215 mg/m2 every 3 weeks
+ temozolomide ( an oral imidazole) 150-200
mg/m2 PO daily for 5 days every 28 days
 Multiagent chemotherapy
In 1990s, the Dartmouth regimen was the
most commonly employed chemotherapy
regimen in stage IV melanoma
Carmustine 150 mg/m2/day on day 1 every
6 weeks
Cisplatin 25 mg/m2/day on day 1-3 every 3
weeks
Dacarbazine 220 mg/m2/day on day 1-3
every 3 weeks
Tamoxifen 20 mg PO daily
 TERAPI
Melanoma maligna Safety margin
1 In situ 0.5 cm
2 0,76 mm 1 cm
3 0,76-1,5 mm 1,5 cm
4 > 1,5 mm 2 cm
5 subungual proximal amputation of
interphalangeal joint
 Non melanoma
skin cancer (NMSC)

Basal cell carcinoma

Squamous cell carcinoma
Karsinoma adneksa kulit
Basal cell carcinoma
(BCC)
Neoplasma maligna yang berasal dari
non keratinizing cell pada basal
epidermis
Terbanyak
Wajah (hidung, dahi, pipi)
Jarang metastase
Invasi lokal tinggi
Faktor resiko

Radiasi sinar ultra-violet : + mutasi

gen p53
Imunosupresi
Intoksikasi arsen kronis dan tar
Fairy skin, albino
Sindroma nevus basal (autosomal
dominan)
KLASIFIKASI
HISTOPATOLOGI
Superficial BCC
Nodular BCC
Infiltrative (morpheaform, aggresive
growth) BCC
Pigmented BCC
Cystic BCC
Fibroepitelioma of Pinkus (FEP)
PROSEDUR DIAGNOSIS

Anamnesis: lesi kehitaman, borok

Pemeriksaan fisik : ulcus rodent:borok
dengan tepi tidak rata, kehitaman,
jarang meta ke KGB
Pemeriksaan penunjang
- foto polos, CT scan, MRI
Squamous cell carcinoma
(SCC)

Neoplasma maligna dari keratinizing

cell
Potensial untuk metastasis regional
maupun jauh
FAKTOR RESIKO
Lesi prakanker : keratosis senilis, compound
nevus, multiple dysplastic nevi
Paparan sinar ultra-violet
Bahan karsinogen : arsen, tar, hidrokarbon
polisiklik
Fairy skin
Ulkus kronik, jaringan parut, fistula yang tidak
sembuh-sembuh
Kelainan genetik : xeroderm apigmentosum,
nevoid basal cell syndrome, albino
Marjoline ulcer
GEJALA KLINIK

Lesi kulit progresif yang tumbuh

menonjol dengan borok seperti bunga
kol, mudah berdarah, berbau khas.
Dapat disertai dengan metastasis ke
KGB regional atau metastasis jauh
(hati, paru-paru dll)
PROSEDUR DIAGNOSTIK
Pemeriksaan klinis
-Anamnesis
-Pemeriksaan fisik
Pemeriksaan penunjang
-Radiologis : x-foto toraks, x-foto tulang,
CT scan, MRI
Biopsi
-Lesi 2 cm dilakukan biopsi eksisi
-Lesi > 2 cm dilakukan biopsi insisi
PROSEDUR TERAPI

Terapi untuk SCC hampir sama

dengan BCC tergantung dari ukuran
lesi, lokasi anatomi, kedalam invasi,
gradasi histopatologi dan riwayat
terapi
rekonstruksi dengan memperhatikan
fungsi dan kosmetik terutama di
daerah wajah; tutup primer, tutup
dengan graft atau flap