DefinitionThis section has been translated automatically.
From the epithelial cells of the skin, outgoing malignant tumours, characterised by destructive and infiltrating growth, spreading to neighbouring organs and organ systems. In an extended definition, the term "non-melanoma skin cancer" is also used to describe other malignant tumours of the integument that do not originate from the epithelial cells(cutaneous B and T cell lymphomas, Kaposi's sarcoma, Merkel cell carcinoma, etc.
ClassificationThis section has been translated automatically.
Carcinoma of the skin (classification)
- In situ squamous cell carcinoma of the skin
- In situ carcinoma of the actinic keratosis type
- In situ carcinoma of the Bowen's disease type
- Invasive squamous cell carcinoma of the skin
- Squamous cell carcinoma of the skin - classic type -
- Acantholytic SSC
- Mucinsecreting SSC
- Desmoplastic SSC
- Small cell SSC
- Clear Cell SSC
- Lymphoepithelioma-like carcinoma of the skin.
- Verrucous carcinoma:
- Nodular basal cell carcinoma (>50% of cases)
- Superficial basal cell carcinoma (15% of cases)
- Sclerodermiform basal cell carcinoma (about 25% of cases)
- Pigmented basal cell carcinoma
- Ulcerated basal cell carcinoma
- Destructive basal cell carcinoma (Ulcus terebrans) (<1% of cases)
- Premalignant fibroepithelioma (Pinkus tumor)
- Eccrine adnexal carcinomas:
- Apocrine adnexal carcinomas:
- Follicular adnexal carcinomas:
Neuroendocrine differentiated carcinoma:
In general medical terminology, carcinomas of the skin/mucosa are also named according to their location. Common names are:
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EtiopathogenesisThis section has been translated automatically.
The development of malignancies, which begins with the transformation of the cell into a tumour cell, is now understood as a multiphase phenomenon that can last for years or even decades. It is a gradual disturbance of biological equilibrium processes, at the beginning of which the transformation (by chemical, physical, viral etc. influences) of gene sequences (proto-oncogenes) into oncogenes takes place (initiation). In epidermal malignancies, the p53 gene is the best known tumour suppressor gene. 60-75% of squamous cell carcinomas show alterations of the p53 gene. Mutations in the p53 gene are typical UV damage. They cause that UV damage is no longer repaired to a sufficient extent. Oncogenes of the ras family (mutations in the ras gene lead to growth impulses) and bcl-2 (apoptosis inhibitors) are also involved.
The transformation area generally remains without growth tendency at first; only with further exposure to carcinogens or unspecific damage (co- and syncarcinogenesis) does the tissue transform towards preneoplasia (see below precancerosis, AIN, KIN, CIN, PIN), which may persist for a long time as a precursor of the malignant tumour (latency phase) or even regress. Finally, preneoplasia turns into primary neoplasia, the malignant tumour, which sooner or later manifests itself clinically.
Remarkably, there are differences to basal cell carcinoma in the behaviour of the tumour cell assemblies when stained with the antibody BerEp4, which detects the "epithelial cell adesion molecule" EpCAM. Since this antibody is not expressed in squamous cell carcinomas, it represents an important differentiation possibility between the two tumour entities.
Predisposing factors in the development of malignant epithelial tumours:
- Physical carcinogenesis: UV rays, ionizing rays, infrared rays
- Chemical carcinogenesis: methylcholantrenes, benzpyrene, azo dyes; by means of corrosive agents Food, exhaust fumes and cigarette smoke can spread carcinogenic substances.
- Viral carcinogenesis: Oncogenic viruses (human papilloma viruses: HPV 5, 16, 18) can cause malignant tumours. Viral genes are transferred into the genome of host cells, causing a transformation of the infected cells.
- Immunological carcinogenesis: Mutation of one or more cells to malignancy is assumed. The properties changed by mutations are transferred to the daughter cells. This process is suppressed when the immune system is functioning normally. A tumor disease only develops when individual tumor cells temporarily elude the immune system's grip and can grow into a larger tumor cell complex through cell division.
- Chronic inflammation: Tumour formation due to the chronic inflammatory stimulus, e.g. lichen planus, lichen sclerosus et atrophicus, lupus vulgaris, porokeratosis, chronic ulcers, fistulas.
- Genodermatoses: Xeroderma pigmentosum, epidermodysplasia verruciformis, albinism
- Individual factors: light skin, ray scars.
HistologyThis section has been translated automatically.
- Degree x (Gx): no determination possible
- Grade 1 (G1): < 25%
- Grade 2 (G2): 25-50%
- Grade 3 (G3): 50-75%
- Grade 4 (G4): > 75%.
- tumour thickness >2mm
- Penetration depth from Clark level 4
- Degree of de-differentiation from grade 3
- Perineural invasion
TherapyThis section has been translated automatically.
See under the respective entities.
Operative therapieThis section has been translated automatically.
In the case of invasively growing carcinomas of the skin, a surgical procedure will generally be regarded as the first choice therapy.
In principle, "the bigger the better" applies. This basic principle bears the danger of overtherapy. In this respect, the safety distance of the first excision is individually selected, adapted to the localisation, tumour size and type, growth behaviour - continuous or discontinuous - as well as the age of the patient. This "individualized" procedure requires a high level of competence in histological workup. The complete visualization of the excision margins by means of a three-dimensional examination technique (3D-histology) is superior to any other histological procedure in terms of sensitivity. A surgical procedure secured in this way can reduce the local recurrence rate to below 2%. If necessary and sensible, it allows to work with small safety margins during primary excision and still avoid local recurrences. In the case of an R1 resection, topographical preparation of the excidate and assignment of a tumour excision allows a precise and gentle follow-up operation until the tumour is free.
Each tumor entity and its subtypes has its specific local infiltration patterns. Often they are asymmetrical, not distributed over the entire circumference and thus clinically difficult to assess. This must be taken into account especially in the case of desmoplastic squamous cell carcinoma (high local recurrence rate) or even in the case of very large tumour nodes.
|Entity||Depth of cut|
|Squamous cell carcinoma||Flat ablation, epidermis, dermis, subcutis (depending on size)|
|Merkel cell carcinoma||deep ablation, possibly musculature|
|Carcinoma of the adnexes||Subcutis|
|M. Bowen (genital/perianal)||Cutis / subcutis|
|Squamous cell carcinoma||0.2-1.0 cm|
|Merkel cell carcinoma||0.5-1.0 cm|
|Carcinoma of the adnexes||0.5-1.0 cm|
|M. Paget||0.5-1.0 cm|
|M. Bowen (genital/perianal)||0.5-1.0 cm|
TablesThis section has been translated automatically.
TX: Primary tumor cannot be assessed
T0: No indication of primary tumour
Tis: Carcinoma in situ
T1: Expansion < 2 cm, <2 high-risk parameters
T2: Expansion > 2 cm with or without additional high-risk parameters; or: Expansion of any dimension with 2/>2 high-risk parameters
T3: Tumor with invasion of the maxilla, mandible, orbita or temporal bone.
T4: tumour with invasion of the skeleton or perineural invasion of the skull base
NX: Regional lymph nodes cannot be assessed
N0: No infestation of regional lymph nodes
N1: Infection of regional lymph nodes
MX: The presence of distant metastases cannot be assessed
M0: No distant metastases
M1: Remote metastasis
Stage 0: Tis N0 M0
Stage I: T1 N0 M0
Stage II: T2 N0 M0 and T3 N0 M0
Stage III: T4 N0 M0 and each T N1 M0
Stage IV: every T and every N M1
Note(s)This section has been translated automatically.
LiteratureThis section has been translated automatically.
- Boehringer A et al (2015) Analysis of incomplete excisions of basal-cell carcinomas after breadloafmicroscopy
compared with 3D-microscopy: a prospective randomized and blindedstudy
. J Cutan Pathol doi: 10.1111/cup.12535Breuninger
H (2011) Project Sentinel Node in squamous cell carcinoma. Abstract CD 46th DDG meeting AKS23/04
- Breuninger H (2015) Safety distances for malignant skin tumours. derm 21: 203-212
- Farasat S et al (2011) A new American Joint Committee on cancer staging system for cutaneous squamous cell carcinoma: Creation and rationale for inclusion of tumor (T) characteristics. J Am Acad Dermatol in press
- Mieczko A et al (2011) BerEP4-negative basal cell carcinoma of the palm: Case report and literature review. JDDG 9:140-143
Incoming links (21)Albinism oculocutaneous tyrosinase-negative; Atrophy, tight; Bowen's disease; Carcinoma; Carcinoma in situ; Carcinoma scirrhosum; Carcinoma simplex; Cd10; Cheek ulcer, neurotic; Cutaneous carcinoma; ... Show all
Outgoing links (40)Adenoma aggressive digital papillary; Adnexal carcinoma microcystic; Ain; Albinism (overview); Basal cell carcinoma (overview); Carcinoma cuniculatum; Carcinomas of the sweat glands; Carcinoma verrucous (overview); Cin; Cribriform apocrine carcinoma of the skin; ... Show all
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