Skin carcinomas

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Introduction /Classification:

  • Skin cancers are common, observed in the subject of clear phototype with variable incidence in the world: incidence peaks recorded in American whites and Australian whites
  • Primary skin cancers include two main groups:

Epithelial cancers: keratinocyte deriver, epithelioma or carcinomas: basal and spinocellular carcinoma

Non-epithelial cancers: drifts from other cells: melanoma (melanocyte), sarcoma (fibroblast)

  • Epithelial skin cancers are the most common.
  • Skin melanoma is less common but has a dreadful prognosis; it's the largest purveyor of death


  • Different alterations occur on the skin cell (keratinocyte, melanocyte, other cells) will lead to the cancer cell
  • Cell transformation is the result of genetic events inducing irreversible genomic abnormalities disrupting cell proliferation

Exogenous agents: cause alterations in cellular DNA, resulting in a mutation leading to a cancer cell: ultraviolet aorlysic rays A or B, ionizing radiation or oncogenic viruses

Chemical agent: aromatic polycyclic hydrocarbons, pesticides

  • Genesis and skin cancers:

Genes responsible for cell transformation: abnormal, only in tumor cells, precise carcinogenic factors, ultraviolet rays

Genes that confer a genetic predisposition to cancer: genodermatosis that exposes the risk of developing skin tumours, mainly Xeroderma pigmentosum, mutations are carried by all cells of the body. Early age

Tumor suppressing genes (P53 gene): controls the smooth running of the cell cycle, it is a true guardian of the genome, stopping the cell cycle after genotoxic stress (UV), which allows to repair the genomic damage suffered before continuing mitoses

  • Tumorigenesis by default repair of cellular alterations: the normal individual has an enzymatic equipment capable of repairing previous alterations, however, during some genetic diseases this enzyme equipment is (Xeroderma pigmentosum). The normal individual as he progresses in age sees weakening his means of repairing cellular alterations (frequency peak in the elderly)
  • No elimination of abnormal cells: in its normal state, the antitumor immune system ensures the elimination of any abnormal cells. Severe immune deficits will allow the emergence of tumor clones

Basal cell carcinoma

Skin carcinomas 2

  • Malignant epithelial tumour from keratinocyte
  • More common in subjects of clear phenotype with a history of intense sun exposure.
  • Strict skin cancer, occurs immediately on healthy skin
  • Photo-exposed areas, never touches mucous membranes
  • Favorable prognosis (never metastasis)
  • The invasive potential is purely local (local malignancy)
  • Surgical treatment


  • The most common epithelial cancer alone accounts for 70% of epithelial cancers.
  • High incidence in high-sun countries (Australia)
  • Subject aged, 40 years old, from clear phenotype to history of intense sun exposure
  • Risk factors:

Sun: major carcinogen, repeated sun exposure (holidays, sports activity) – prevention and school education measures

Skin carcinomas 3Genetic predisposition: are more common in light-skinned subjects, phototype I/II

MC1R: gene involved in skin pigmentation (photo-protective melanin), certain variants are risk factors for skin cancer

Geno-dermatoses predispose to basal cell carcinomas: Xeroderma pigmentosum

Immunodepression: Organ transplants cause more basal cell carcinomas, HIV

Clinical aspects:

  • Elemental lesion: a small papule of transparent (translucent) normal skin color, revealing the vessels of the underlying dermis in the form of telangiectasies, this lesion is called "epithelioma pearl"

Seat: photo-exposed areas, in 80% of cases: head, neck, face

  • Clinical forms:

Nodular shape: the elemental lesion may remain unique and increase in size giving a pink-coloured nodule traversed by fine telangiectasies, the most common form

Scar plane: the elemental lesion multiplies, several epitheliomama beads will match in rosary and take a rounded layout: smooth atrophic center and elevated periphery by the juxtaposition of pearls

tattooed basal cell carcinoma: the elementary lesion will pigment, brown spots, covering the surface of the tumor – nodular melanoma

Sclerodermiform shape: whitish, hard and shiny imprecise boundaries, the surface is depressed and retractable, covered with telangiectasies. Recidivism

Ulcerated shape (ulcus rodens): nail-stroke ulceration, slowly extended, with beaded border

Waxing form: digging ulceration with a large necrotic crater that can lead to severe mutilation


  • Positive diagnosis:

Clinical: in front of the fixedness of the lesions, the beaded border and the presence of telangiectasies

Histology: a proliferation of small, clear-limit basaloid cells reminiscent of epidermal basal layer cells. These cells cluster in compact cell clusters and take on a palisadic peripheral arrangement.  The tumour remains well delineated compared to the rest of the dermis

  • Differential diagnosis: spinocellular carcinoma, malignant melanoma (in pigmented forms)

Evolution / Prognosis:

  • Slow, exceptional metastases
  • Basal cell carcinoma has an essentially local evolution

Ulcerated form: destruction of tissue under the skin, cartilage tissue or underlying bone tissue creating a gateway to overinfection germs and complicating itself with naso-sinus infection or septic meningitis causing mortality


  • Surgery: treatment of choice, allows histological control of the margins of exeresis: complete surgical exeresis – regular monitoring for recurrences
  • Other therapeutic weapons: in case of topography at risk and/or multiple lesions or subject to risk: radiotherapy, cryotherapy with liquid nitrogen, dynamic phototherapy


Uses effective photoprotection:

  • Clothing: wearing covering clothes, hat
  • Use of sunscreens: allows less photoprotection, it requires repeated applications of high index sunscreens

Spinocellular carcinoma

Skin carcinomas 4Definition:

  • Malignant epithelial tumour, primitive of keratnocytic origin, sdresmous carcinoma
  • De novo or on precursor (precancerous lesion), skin and mucous membranes
  • Local, locoregional and remote extension
  • 2nd in frequency of keratnocytic carcinomas, 20% of epithelial skin cancers.
  • Observed in the elderly subject, after 60 years of clear phototype and living in sunny areas


  • Male – female, age 60
  • Very high incidence in Australia, incidence increases with age
  • The risk of stodbroid carcinoma is related to two factors: cumulative dose of sun exposure, phototype

Skin carcinomas 5Etiological factors (precancerous lesions)

  • Precursors of skin shaded carcinomas:

Actinic Keratosis: Frequent lesion on photo-exposed areas: face, extremities, scalp. Elderly, fair skin, erythematous lesion, brownish, rough

Radio-induced Keratosis

Keratosis of aromatic polycyclic hydrocarbons: incomplete combustion of wood, coal or oil (refining products, fuels, tar…)

Skin scars: burns, radiodermites – regular monitoring

Chronic sores: chronic leg ulcers – risk of degeneration

  • Precursors of shadercardo carcinomas of the mucous membranes:


Chronic Actinic Cheilitis: professionals exposed to the sun: atrophy, erosion, dander, lower lip

Smoking Cheilitis: smoker, keratosic plaque, whitish

Anogenital mucous membrane:

Infectious Origin:

HPV: oncogenic types, Bowen's disease, carcinoma in situ

Mucous Dermatosis:

Sclerotic lichen: chronic dermatosis, pruritus, vulva, whitish lesion, sclerosis


  • Onset: spinocellular carcinoma often develops on a precancerous lesion: actinic keratosis, Bowen's disease, burn scar, radiodermite, chronic ulceration. The constructed lesion combines 3 components: budding, ulceration, infiltration

Ulcero-vegetative shape: more frequent, protruding and infiltrating tumour, irregular surface, seat of a budding and bleeding ulceration, undeed edges

  • Seat of lesions: discovered regions (head, neck), lower and upper limbs, damage to mucous membranes and half-mucous membranes: tongue, lips, vulva and acorn

Clinical forms:

The tumour combines the different semiological elements in varying proportions:

  • Ulcer-vegetative form: the most common
  • Pure ulcerated shape
  • Vegetable shape: cauliflower, easily hemorrhagic
  • Nodular shape: nodular, warty and crusty protruding lesion

Positive diagnosis:

Clinic – histology

  • Sdamous cell carcinoma should be suspected in the presence of any precancerous lesions, crust, budding, bleeding, skin induration, underlying infiltration. The presence of any of these signs should require a skin biopsy to confirm the diagnosis
  • Histology: proliferation of large cells with many cyto-nuclear mitoses and atypies, these cells cluster in lobules or spans poorly delineated, there is a keratinizing differentiation in the form of cornate globes, the underlying derme is often invaded

Evolution / Prognosis:

  • Potentially invasive cancer, local extension from near to near
  • Clinical examination: search for adenopathy in the lymphatic drainage air of the tumour because lymph node metastases are early. In the face of any call, paraclinical examinations will be performed for blood, liver and lung metastases.


  • Surgical exeresis: complete set to hypodermis – small and prognostic tumours.

In case of topography at aesthetic and/or functional risk cryosurgery, radiotherapy, laser…

In case of metastases: surgery, palliative treatments


  • Solar photoprotection.
  • Treatment of any precancerous lesions.
  • Screening and monitoring of high-risk subjects.

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