Malignant skin tumors

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Skin tumors

Actinic Keratosis

Actinic keratosis (AK) (solar keratosis) is a squamous cell carcinoma insitu confined to the
epidermis. The lesions are commonly sun -induced, and increase in number with age. Most lesions
remain superficial. Lesions that e xtend more deeply to involve the papillary and/or reticular dermis are
termed squamous cell carcinoma (SCC).
Risk factors included: -
Individuals with light complexions are more susceptible than those with dark complexions.
Years of sun exposure are requi red to induce sufficient damage to cause lesions .
Immunosuppression is a risk factor. HPV infection, and chemical substances.

Clinical features.

the lesion started as area of slightly rough. Texture is the key to diagnosing early lesions. They
are bet ter recognized by palpation than by inspection. Very gradually an adherent, yellow, sharp scale
forms. Removal of the scale may cause bleeding . Most lesions vary in size from 3 to 6 mm. The extent
of disease varies from a single lesion to involvement of t he entire forehead, balding scalp, or temples.
Complicated cases will progress to SCC.

Management

Avoid sun exposed and use sun screens
Cryotherapy. chemical cuteraiztion.
Surgical removal.
Topical topical chemothe rapy with 5 -fluorouracil, topical immiquimod , diclofinac gel,

Basal Cell Carcinoma (Rodent Ulcer)

Basal cell carcinoma (BCC) is the most common malignant cutaneous neoplasm found in
humans. The most common presenting complaint is a bleeding or ulcera ted sore that heals and recurs.
BCC advances by direct extension and destroys normal tissue. Left untreated or inadequately treated,
the cancer can destroy the whole side of the face or penetrate subcutaneous tissue into the bone and
brain. Up to 80% of BC Cs occur on the head and neck. About 15% occur on the shoulders, back, or
chest. Men have a significantly higher incidence than women.

Risk Factor

Physical characteristics
Blond or red hair
Blue or green eyes
Light skin color
Exposures
Arsenic
Coal tar
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Ionizing radiation
Smoking
Tanning –bed use
Ultraviolet light

Genodermatoses

Albinism
Xeroderma pigmentosum
Nevoid basal -cell carcinoma syndrome (Gorlin’s Syndrome)
Immunosuppression
Recipients of solid -organ transplants

Cli nical Type of basal Cell Carcinoma

• Nodular BCC (the most common variant) is characterized by skin -colored, dome -shaped
papules with telangiectasias and a pearly border. The lesions may be crusted or ulcerated, and
they may be associated with intermittent b leeding.
• Pigmented BCC .
• Superficial BCC .
• Morpheaform (sclerosing or infiltrating).
Management: There are several factors to consider before choosing the best treatment
modality. The most important are clinical presentation, cell type, tumor size, and lo cation . Biopsy must
be done before initiating the treatment
Surgical:
• Curettage (usually with electrodesiccation).
• Excision surgery.
• Cryosurgery.
• Mohs’ micrographic surgery.
Radiation.
Topical Therapy :
• Imiquimod 5% cream.
• 5- Fluorouracil.
Intralesional th erapy
• Interferone -Alfa.
• Photodynamic therapy (PDT).
• Intralesional Zinc sulphate 2%.(Iraqi study)
Squamous Cell Carcinoma

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It is a malignant tumor of epithelial keratinocytes (skin and mucous membrane )

etiology and risk factors.

UVB radiation is important for the induction of SCC. Risk factors include exposure to sunlight
during childhood, sunburns, ionizing radiation, light skin , blue eyes , blonde or red hair , outdoor
occupations, freckling, or facial telangiectasia, and psoriasis treatment with oral psor alen and
ultraviolet A radiation (PUVA). Arsenic , used in medications in the past, and in drinking water
produces tumors and carcinoma in situ.
Human papillomavirus types 6 and 11 are found in tumors of the genitalia and type 16 in
periungual tumors. Im munosuppression leads to a great increase in the risk of SCC. Renal -transplant
recipients have a 253 -fold increase in the risk of SCC.

Clinically as Usually isolated but may be multiple. keratotic and/or ulcerated lesions , indurated lesion
most commo nly in sun -exposed areas . SCCs are common on the scalp, backs of the hands, and the
superior surface of the pinna; BCC is rarely found on these sites.

History: Slowly evolving tumor. "Any isolated keratotic or eroded papule or plaque in a
suspect Patien t that persists for over a month is considered a carcinoma until proved otherwise".

Management: After the diagnosis has been confirmed by biopsy ,

The tumor should be excised with a 0.5 –cm border of normal skin.
Mohs micrographic surgery is useful for high risk tumors
Radiotherapy is effective in frail and the elderly.
Carcinoma in situ : cryotherapy,or 5 -fluorouracil topically.

Malignant Melanoma

One of the most dangerous tumors, malignant melanoma arises from cells of the melanocytic syste m.
Melanoma has the ability to metastasize to any organ, including the brain and heart. Therefore, it is
imperative that all physicians be familiar with the features of early preinvasive melanoma and includes
a complete skin examination as part of routine physical examinations.
With early detection and local surgery it may be cured in over 92 percent of cases. So what do
we look for? It is as simple as ABCDE.

A = asymmetry;

B = border irregularity;
C = color variability;
D = diameter greater than 0.6 cm.
E= elevation irregularity

Etiology

Sun exposure , genetic factor , PUVA,,,
Types
Lentogo maligna(melanoma in situ)
Superficial spreading melanoma
Acral lentigenous melanoma
Nodular melanoma

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Treatment with surgical excision after a ssessment grading of disease.

Kaposi sarcoma
(KS) is a multisystem vascular neoplasia characterized by mucocutaneous violaceous lesions
and edema as well as involvement of nearly any organ. Many individ uals with KS are in some degree
immunocompromised, especially those with HIV disease.
Etiopathogenesis
Type 8 (HHV -8), has been identified in tissue samples of several variants of KS.
Clinical Variants of KS
1-Classic Kaposi sarcoma
2-African Cutaneous KS (endemic)
3-African lymphoadenopathic.(endem ic)
4-AIDS related KS (epidemic)
5-Kaposi’s sarcoma associated with immunosuppressive states .
Clinical features Kaposi sarcoma may develop at any time during the course of HIV infection.
Generally, the greater the immunosuppression (e.g. with CD4 cel l counts less than 200/mm3) the more
extensive the Kaposi sarcoma will be.
Kaposi sarcoma presents as red to purplish spots (macules) and raised bumps (papules and nodules).
They are generally first seen on the skin, commonly on legs or feet. They also o ccur in the mouth.
Initially, the lesions are small and painless but they can ulcerate and become painful. Their visible
presence may cause considerable anxiety. Kaposi sarcoma lesions can also occur internally; in the gut,
lungs, genitals and lymphatic sy stem. These internal lesions may cause symptoms e.g. discomfort with
swallowing, bleeding, shortness of breath, swollen legs, etc.
The appearance of Kaposi sarcoma lesions is often typical but a skin biopsy of a lesion allows a
definite diagnosis.
Ma nagement:
Teatment underlying conditions
Lcal Treatment with cryotherapy, electrocuterization, radiotherapy, surgical excision
Iteralesioanl treatment with interferon, bleomycin , vincristin,,
Sstemic treatment with interferon, retinoid, ,,

Cutaneous T-Cell Lymphoma

The term cutaneous T -cell lymphoma (CTCL) encompasses a group of distinct lymphomatous
neoplasms of helper T cells that present in the skin but later may involve lymph nodes, peripheral
blood cells, and the viscera. Mycosis fungoides, Séza ry syndrome, and lymphoma cutis are all
examples of CTCL. The malignant cells have a marked affinity for the skin, particularly the epidermis,
often leading to formation of Pautrier’s intraepidermal abscesses.

Mycosis fungoides

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The name mycosis fungoide s is misleading because the disease is not fungal in origin. MF is a
rare T -cell lymphoma that appears to originate in the skin. MF is twice as common in men as in
women. Most cases are diagnosed in the fifth and sixth decades.

The course is unpredictabl e, sometimes lasting less than 1 year or lingering for decades. There
are three phases in the evolution of the disease:
Patch stage: Macules and patches, slightly erythematous and scaly (eczematous like lesions) .
Predilection sites include buttocks, tru nk, upper thighs, upper arms .

Plaque stage: Gradual thickening of patches with increased scale (psoriatic like lesions)

Tumor stage: Usually after many years, abrupt development of thick, often ulcerated tumors
arising from the plaques or even from norm al skin.

Some patients have only plaques and tumors. Other patients may have all stages in the same time.
Lymphadenopathy may develop at any stage. Survival time is less than 3 years once the tumor phase
begins.
Despite the new laboratory diagnostic met hods, recognition of the physical signs of the disease by the
clinician is still the most sensitive method of detection.

Treatment

Topical with steroid, nitrogen mustard, PUVA , retinoid radiotherapy
Systemic with MTX , retinoid ,,,