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Skin Cancers. Malignant Melanoma
Skin Cancers. Malignant Melanoma
Cutaneous malignant
melanoma is a
neoplasm arising from
the melanocytes that
can occur de novo or
from a preexisting
lesion such as a
congenital, acquired, or
atypical (dysplastic)
nevus.
Biologic progression of melanoma
Melanocyte nevus
dysplastic nevus меlanoма “in situ”
superficial spreading melanoma
nodular melanoma metastatic
melanoma
Professional education:
students
family doctors
dermatologists
surgeons
cosmetologists
morphologists
oncologists !
nurses
ABCD-test
Screening:
Precursor Lesions
ABCDE rules:
'A' is Asymmetry
If the border or
edges of the mole
are ragged, blurred,
or irregular, have it
checked by a
dermatologist.
Melanoma lesions
often have uneven
borders.
'C' is for Colour
A mole is suspicious
if the diameter is
larger than 6 mm.
Benign moles are
usually less than 6
millimeters in
diameter.
'E' is for Evolving
Asymmetry of lesion;
Border irregularity;
Color change;
Diameter larger than
6 mm;
Evolving (surface
changes [raised,
bleeding, crusting] or
symptomatic [itchiness
or tenderness]).
Melanoma can vary in appearance
Dermatoscopy:
Dermatoscopy: ABCD
ЕЛМ
Diagnostics system MoleMax:
Growth patterns of melanoma:
TNM:
Metastatic cells
1 2
3 4
Metastatic melanoma
Palliative - therapy
Hormonotherapy
Supportive care
Survival rates:
J Clin Oncol 2001;19:3635-3648.
BCC, T1
The following are exposure-related risk factors
in the development of cutaneous cancers:
UV radiation exposure (high cumulative dose of
sunshine, tanning beds, or medical UV treatments)
Immunosuppression (eg, HIV), including iatrogenic
immunosuppression (eg, transplant recipients)
Ionizing radiation (eg, medical treatments,
occupational or accidental radiation exposure)
Infections (eg, HPV, osteomyelitis, acne conglobata,
hidradenitis suppurativa, dissecting cellulitis of scalp,
lupus vulgaris, lymphogranuloma venereum,
granuloma inguinale, and chronic deep fungal
infection)
Chemical carcinogens (eg, arsenic, tar, polyaromatic
hydrocarbons)
Host responses that influence cutaneous SCC
development include the following:
Genetic susceptibility and dermatoses (eg, xeroderma
pigmentosum, dystrophic epidermolysis bullosa,
epidermodysplasia verruciformis, xeroderma pigmentosum,
oculocutaneous albinism, dyskeratosis congenita,
porokeratosis [Mibelli type, disseminated superficial actinic
type, linear type], nevus sebaceous, and KID syndrome
[keratitis, ichthyosis, deafness])
Susceptibility to UV radiation (eg, fair skin [Fitzpatrick skin
types I and II], blond or red hair, light-colored eyes)
Chronic inflammation, such as nonhealing burns or scars
(eg, Marjolin ulcer, burn scar or thermal injury, venous
ulcer, lymphedema, discoid lupus erythematosus, erosive
oral lichen planus, lichen sclerosis et atrophicus, mutilating
keratoderma, and necrobiotic lipoidica)
The biggest cause of skin cancer is sun
exposure
SCC in situ:
Greater than 2 mm
thickness or Clark level IV
or higher
Perineural invasion
Primary anatomic location
on the ear or non–hair-
bearing lip
Poorly differentiated or
undifferentiated cellular
histology
Precancerous lesions: Actinic (Solar) Keratosis)
Clinical case:
Basal Cell Carcinoma,
T1N0M0
(ulcer pattern)
Basal Cell Carcinoma
Clinical case:
Ear Squamous Cell
Carcinoma,
T4N0M0
TNM-Classification of Skin Cancer:
Squamous Cell
Carcinoma of lower
eyelid with invasion
in bulbar
conjunctiva,
T4N0M0
Skin Cancer
Squamous Cell
Carcinoma of Cheek,
T4N0M0
Skin Cancer
Results after
half course of
gamma-
therapy, 45 Gy
SCC of back: scheme of surgery
Surgery of skin cancer: flap plasty of wound
after complete excision of cancer
Skin Squamous Cell Cancer of Neck:
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