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Skin cancer.  Melanoma. Skin cancer.  Melanoma.

Skin cancer. Melanoma. - PowerPoint Presentation

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Skin cancer. Melanoma. - PPT Presentation

Precancerous diseases Odessa National medical university С hair of Radiation Diagnostics Therapy and Oncology Head of chair prof  Sokolov VN Head of Oncology cycle prof Bondar ID: 917318

cancer skin cell melanoma skin cancer melanoma cell keratosis sun carcinoma squamous nevus basal people lesions disease exposure malignant

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Slide1

Skin cancer.

Melanoma.

Precancerous

diseases.

Slide2

Odessa National medical university

С

hair of Radiation Diagnostics, Therapy and Oncology

Head

of chair, prof. 

Sokolov

V.N

.

Head of Oncology cycle, prof.

Bondar

O.V.

Docent,

Kuznetsova

O.V.

Slide3

Epidemiology

The incidence of skin cancers is rising in people of Caucasian descent due to increased sun exposure and ageing population.

Skin cancers are usually referred to as melanoma, basal cell carcinoma and squamous cell carcinoma.

Non melanoma skin cancer is the most common cancer in humans.

Highest incidence of melanoma in Australia.

The melanin in skin affords protection, resulting in a lower incidence in those darker skin colours.

Slide4

What causes it?

While the full answer still has not been unravelled, what is sure is that excessive sun exposure plays a leading role in the development of this type of skin cancer.

Severe, blistering sunburns especially in childhood are thought to play an initiating role. However, recent research shows that sunburns at any time during life can also increase the risk.

While anybody can get melanoma, fair skinned people who have sun-sensitive skin that burns rather than tans are more likely to get this disease.

People with freckles and red hair fall into this group, as do some blonds and those with blue or green eyes.

Slide5

Development of skin cancer depends on

Sun exposure

Environmental agents

Ionising radiation

Genetic predisposition (xeroderma pigmentosum, Gorlin's syndrome)

Immunosuppression

Slide6

Slide7

Statistics

BCC

SCC

MM

All other

1,000,000

350,000

55,000

1,285,000

Basal cell carcinoma, Squamous cell carcinoma and Melanoma

Slide8

Slide9

Keratosis

Keratosis occurs on skin as a result of uneven growth of keratin. It results when the keratin in the skin grows in form of clusters instead of growing uniformly. Keratosis is more common in fair skinned people than dark toned people. Although, usually keratosis isn’t very harmful but excess occurrence reflects some serious dangers such as cancer. keratosis is classified in various forms such as

Actinic keratosis

Hydrocarbon keratosis

Keratosis pilaris

Slide10

A

seborrheic keratosis

is a benign skin growth that originates in keratinocytes.

The lesions appear in various colors, from light tan to black. They are round or oval, feel flat or slightly elevated (like the scab from a healing wound), and range in size from very small to more than 2.5 cm

.

O

nly the top layers of the epidermis are involved, seborrheic keratoses are often described as having a "pasted on" appearance.

Some dermatologists refer to seborrheic keratoses as "seborrheic warts"; are usually not associated with HPV.

Slide11

Keratosis pilaris.

Keratosis pilaris occurs as a result of excessive production of keratin. This excess keratin results in formation of bumps that can be a bit itchy and irritating.

Keratosis can be prevented by keeping the skin clean and maintaining a healthy life style. In order to treat keratosis pilaris various options are available. By keeping the skin moisturized , using retinoid and choosing photodynamic therapy keratosis pilaris can be treated.

Slide12

Arsenical keratosis

is a growth of keratin on the skin caused by arsenic, which occurs naturally in the earth's crust and is widely distributed in the environment

.

Arsenical compounds are used in industrial, agricultural, and medicinal substances. Arsenic is also found to be an environmental contaminant in drinking water and an occupational hazard for miners and glass workers.

A

rsenical keratosis

Slide13

Arsenic may also causes

other conditions including: Bowen's disease, cardiovascular diseases, developmental abnormalities, neurologic and neurobehavioral disorders, diabetes, hearing loss, hematologic disorders, and various types of cancer.

Arsenical keratoses

may persist indefinitely, and some may develop into invasive squamous cell carcinoma. Metastatic arsenic squamous cell carcinoma and arsenic-induced malignancies in internal organs such as the bladder, kidney, skin, liver, and colon, may result in death.

Slide14

A

ctinic keratosis

A

lso known as solar keratosis or senile keratosis, is a very common lesion occurring susceptible persons as a result of prolonged repeated solar exposures. The action of ultraviolet radiant energy, principally UVB, results damage to the keratinocytes and produces single or multiple, discrete, dry, rough, adherent scaly lesions. These premalignant lesions may

progress to squamous cell carcinomas.

It causes the formation of reddish -brown spots or patches on skin. Cryosurgery, photodynamic therapy, electrocautery and laser are some of the common treatments available.

Slide15

Hydrocarbon keratosis

HK is also another well -known type of keratosis. It occurs in people who are more exposed to chemical compounds such as poly-aromatic hydrocarbons or poly -nuclear aromatic hydrocarbons. It is a very dangerous form of keratosis and can also result in cancer. Also known as “tar keratosis” or “tar warts” this skin lesion occurs primarily in workers dealing with tar , oil , fuel and lubricating oils. Consulting a dermatologists as soon as you observe changes in your skin is very important .

Slide16

Leukoplakia (smoker's keratosis)

it is visible as adherent white patches on the mucous membranes of the oral cavity, is not a specific disease entity.

Leukoplakic lesions are found in approximately 3% of the world's population. Like erythroplakia, leukoplakia is usually found in adults between 40 and 70 years of age, with a 2:1 male predominance.

Leukoplakia is primarily caused by the use of tobacco. Other possible etiological agents implicated are HPV's, Candida albicans and possibly alcohol. Most result from chronic irritation of mucous membranes by carcinogens

Slide17

Leukoplakia

5% to 25% of leukoplakias are premalignant lesions; therefore, all leukoplakias should be treated as premalignant lesions by dentists and physicians - they require histologic evaluation or biopsy. Hairy leukoplakia, which is associated with HIV infection and other diseases of severe immune deficiency can go on to develop lymphoma when associated with HIV.

Treatment involves avoidance of predisposing factors — tobacco cessation, smoking, quitting betel chewing, abstinence from alcohol — and avoidance of chronic irritants, e.g., the sharp edges of teeth. Taking beta-carotene orally seems to induce remission in patients with oral leukoplakia.

Slide18

Xeroderma pigmentosum

XP is an autosomal recessive genetic disorder of DNA repair in which the ability to repair damage caused by ultraviolet (UV) light is deficient. In extreme cases all exposure to sunlight must be forbidden, no matter how small.

Multiple basaliomas and other skin malignancies frequently occur at a young age in those with XP. In fact, metastatic malignant melanoma and squamous cell carcinoma are the two most common causes of death in XP victims.

Slide19

Symptoms of XP include:

Often occurring during a child's first exposure to sunlight.

Development of many freckles at an early age

Rough-surfaced growths (solar keratoses), and skin cancers

Eyes that are painfully sensitive to the sun and may easily become irritated, bloodshot, and clouded

Blistering or freckling on minimum sun exposure

Spidery blood vessels

Oozing raw skin surface

Limited growth of hair on chest, legs

Scaly skin

Irregular dark spots on the skin

Slide20

Bowen's disease

BD

(also known as "squamous cell carcinoma in situ") is a neoplastic skin disease, it can be considered as an early stage or intraepidermal form of squamous cell carcinoma.

It was named after Dr John T. Bowen, the doctor who first described it in 1912.

Causes of BD include solar damage, arsenic, immunosuppression (including AIDS), viral infection (human papillomavirus or HPV) and chronic skin injury and dermatoses.

Slide21

Bowen's disease

BD typically presents as a gradually enlarging, well demarcated erythematous plaque with an irregular border and surface crusting or scaling.

BD may occur at any age in adults but is rare before the age of 30 years - most patients are aged over 60. Any site may be affected, although involvement of palms or soles is uncommon.

BD occurs predominantly in women (70-85% of cases). About 60-85% of patients have lesions on the lower leg.

Slide22

BOWENOID PAPULOSIS

is a cutaneous condition characterized by the presence of pigmented verrucous

papules on the body of the penis.

They are associated with human

p

apillomavirus, the causative agent of genital warts. The lesions have

a typical dysplastic

h

istology and are

generally considered benign, although

a small percentage will develop

malignant characteristics.The term "Bowenoid papulosis" was coined in

1977 by Kopf and Bart and is named after dermatologist John Templeton Bowen

Slide23

Slide24

Erythroplasia of Queyrat

is a form of squamous cell carcinoma in situ arising on the glans or prepuce, possibly induced by HPV

.

Slide25

KERATOACANTHOMA

is a common, rapidly growing but benign tumor that will involute spontaneously, even if untreated. It is believed to originate from the hair follicles.

Slide26

Extramammary Paget disease

EPD

characterised by a chronic eczema-like rash of the skin around the anogenital regions of males and females.

M

ost commonly occurs in women aged between 50-60 years.

It is most often an in-situ tumour of the apocrine glands. However, about 25% of

EPD

is associated with an underlying cancer, either adenocarcinoma in situ or a more widespread invasive cancer.

Sometimes

EPD

may be present for 10-15 years before evidence of cancer or metastases appear.

Slide27

H

PV – papules

HPV induced premalignant papules are

рremalignant lesion

s

of the anogenital epithelium, such as bowenoid papulosis and condyloma acuminata, were recently found to be closely linked tiologically

to infection with certain types of HPV

.

Slide28

E

pidermodysplasia verruciformis

EV

is a rare, multifactorial disorder consisting of genetic, immunologic, and extrinsic (UVB) components in addition to infection with specific HPV types. Beginning in the third or fourth decade of life, patients may develop multiple in situ and/or invasive squamous cell carcinomas.

Slide29

Nevus

(

birthmarks

,

moles

)

is

a

chronic benign lesions of the skin. However, 50% of malignant melanomas (a skin cancer) arise from pre-existing nevi. Using the term nevus and nevi loosely, most physicians and dermatologists are actually referring to a variant of nevus called the "melanocytic nevus", which are composed of melanocytes.

Epidermal nevi are derived from keratinocytes or derivatives of keratinocytes. Connective tissue nevi are derived from connective tissue cells like adipocytes and fibroblasts. Vascular nevi are derived from structures of the blood vessels.

Slide30

Diagnosis of nev

us

Clinical diagnosis of a melanocytic nevus from other nev

us

can be made with the naked eye using the ABCD guideline, or using dermatoscopy.

The main concern is distinguishing between a benign nevus, a dysplastic nevus, and a melanoma.

A

skin biopsy is required when clinical diagnosis is inadequate or when malignancy is suspected.

Slide31

Diagnosis of nev

us

All melanocytic nev

us

will change with time - both congenital and acquired nev

us

. The "normal" maturation is evident as elevation of the lesion from a flat macule to a raised papule.

The color change occurs as the melanocytes clump and migrate from the surface of the skin (epidermis) down deep into the dermis. The color will change from even brown, to speckled brown, and then losing the color and becomes flesh colored or pink.

During the evolution, uneven migration can make the nevi look like melanomas, and dermatoscopy can help in differentiation between the benign and malignant lesions

Slide32

The ABCDE's of

malignant melanoma will aid in early detection.

Asymmetry

The shape on one side

is different than

the other side.

Slide33

ABCDE’s of Skin Cancer

Border

The border of visible edge is irregular, ragged and imprecise.

Slide34

ABCDE’s of Skin Cancer

Colour

There is a colour variation with brown, black, red, grey or white areas within the lesion

Slide35

ABCDE’s of Skin Cancer

Diameter

The growth of the diameter or width is common in malignant melanomas.

Slide36

ABCDE’s of Skin Cancer

Evolution

There is a change in the size, shape, symptoms

(such as itching or tenderness)

, surface

(especially bleeding)

or colour.

Slide37

Attributes of malignisation:

1)

Change of color, sharp pigmentation (black color)

2) Non-uniform coloring

3) Infringement or full absence of skin figure, peeling of nevus

4) Inflammation around nevus

5) Change of borders

6) Increase in the sizes and condensation of nevus

7) Small nodules in the basis of nevus with necrosis in center

8) Itch, burning or pressure in area of nevus

9) Cracks, ulcers or bleeding from nevus

Slide38

Basal Cell Cancer

Slide39

Basal Cell Skin Cancer

What does it look like?

Basal cell skin cancers usually appear on sun exposed areas, most commonly the face and neck, but also on the trunk, arms and legs. The appearance of this type of skin cancer can vary.

Slide40

The early warning signs to look for are:

A firm, flesh coloured or slightly reddish bump, often with a pearly border.  It may have small blood vessels on the surface which gives it a red colour.

A sore or pimple-like growth that bleeds, crusts over and then reappears.  Any sore that does not heal within four weeks should be examined by your dermatologist.

A small, red scaling patch seen most often on the trunk or limbs.

Slide41

What causes it?

Ultraviolet radiation from the sun is the prime cause of this skin cancer. Frequent severe sunburns and intense sun exposure in childhood increase the risk of basal cell skin cancer in adulthood.

Slide42

Who is at risk?

A large group of the population is much more susceptible to getting this form of skin cancer.

Fair-skinned people with blond or red hair and skin that usually burns when out in the sun are most at risk.

The incidence increases as people get older, especially over the age of 50. However, these tumours are now being seen in teenagers and in people in their early twenties.

Slide43

B

asal cell carcinoma

It is

composed of cells that arise

from the epidermis and the appendages which

resemble the basal layer of the epidermis and is

associated with a characteristic stroma.

It tends to grow slowly and invade locally over many years, which eventually leads to ulceration,

hence the name “rodent ulcer.” Account for more than 75% of keratinocytic skin cancers diagnosed in USA

each year.

Slide44

Types of basal cell carcinoma

Nodulo-ulcerative or nodular

Superficial multifocal

Morpheaform or sclerosing

Pigmented

Fibroepithelioma

5

2

3

1

4

Slide45

S

quamous cell carcinoma

It is a

malignant tumor

arising from epidermal or appendageal keratinocytes

or from the squamous mucosal epithelium.

There is often a history of damage by

exogenous agents acting as carcinogens, such as

sunlight, ionizing radiation, local irritants, or

arsenic ingestion. The tumor cells have a tendency toward keratin formation. Bowen disease is an in situ squamous cell carcinoma.

Verrucous carcinoma is a variant of low grade squamous cell carcinoma with a clinicopathologically distinct warty appearance.

Slide46

Squamous Cell Skin Cancer

What does it look like?

Squamous cell skin cancers appear as thickened, red, scaly bumps or wart-like growths. They may also look like an open sore or crusted skin.

Slide47

Where does this cancer appear?

SCC may grow quickly over a period of a few weeks.

It appears on chronically sun-exposed areas such as the head and neck, arm, back of the hand and leg.

Areas to be particularly careful to check for this cancer include the rim of the

ear and the lip

since the cancer can be more aggressive at these locations.

Slide48

What causes it?

Frequent sun exposure is the leading cause of this disease.

However, people whose immune systems are suppressed through taking anti-rejection drugs face a higher risk for this disease.

Slide49

MELANOMA

Slide50

Types of melanoma

Superficial melanoma (70%) – dark area arising in pre-existing naevus, classically asymmetrical with variable colour

Nodular (20%) – dark nodule, uniform in colour, although may be amelanotic, majority arise in normal skin

Lentigo maligna melanoma (5%) – occurs on face and neck of older patients in areas of sun damage

Acral-lentiginous (5%) – palms and soles,

subungual location

Slide51

Melanoma

Familial human melanoma

is characterized

by an increased risk of developing primary

melanoma, a higher incidence of multiple primary

melanomas, and an earlier age at onset.

These characteristics are common to many other heritable malignant and premalignant conditions such as retinoblastoma, Gardner syndrome,

xeroderma pigmentosum, and nevoid–basal cell carcinoma. In individuals with familial melanoma, the locus for cutaneous malignant melanoma–dysplastic nevus resides on the distal

portion of the short arm of chromosome.

Slide52

Slide53

Biopsy

Slide54

Slide55

Classification of Clark and Breslow

Level I

– melanoma lies in the epidermis above an intact basal lamina.

Level II

– melanoma has penetrated the basal lamina into the papillary dermis.

Level III

– melanoma involves the papillary dermis and may extend to the papillary-reticular dermis interface.

Level IV

– melanoma extends into the reticular dermis.

Level V

– melanoma extends into the subcutaneous fat.

Breslow’s microstaging method

, which is simpler and more reproducible than Clark’s method, uses an ocular micrometer to measure the vertical thickness of the primary tumor from the granular layer of the epidermis, or the base of an ulcer, to the deepest identifiable contiguous melanoma cell.

Slide56

Slide57

Slide58

Melanoma. Treatment.

Slide59

Melanoma. Treatment.

Slide60

Prevention

Decreasing sun exposure !!!!!!

Liberally applied sun cream with a sun protection factor of at least 15, limited sun exposure between 10 a.m. and 4 p.m. and wearing protective clothers from the basis of most sun protection advice.

Slide61