Carcinoma of the skin (overview) C44.L

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Synonym(s)

Light skin cancer; NMSC; Non-melanocytic skin cancer; Nonmelanoma skin cancer; Skin cancer; Spinocellular carcinoma; Squamous cell carcinoma; White skin cancer

Definition
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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.

Classification
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Carcinoma of the skin (classification)

Squamous cell carcinoma of the skin (SCC)

Basal cell carcinoma of the skin

  • 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)

Adnexal carcinoma:

Neuroendocrine differentiated carcinoma:

In general medical terminology, carcinomas of the skin/mucosa are also named according to their location. Common names are:

Etiopathogenesis
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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.

Histology
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S.u. carcinoma, spinocellularProliferationof epithelial dressings originating from thesurface epithelium with keratinocytes that are undifferentiated to varying degrees, which infiltrate the different layers of the dermis or subcutis and the underlying structures in the form of fingers or in broad dressings. According to Broders, a distinction is made according to the proportion of atypical cells:
  • Degree x (Gx): no determination possible
  • Grade 1 (G1): < 25%
  • Grade 2 (G2): 25-50%
  • Grade 3 (G3): 50-75%
  • Grade 4 (G4): > 75%.
In the AJCC classification (2010) the following histological parameters are considered "high-risk" findings:
  • tumour thickness >2mm
  • Penetration depth from Clark level 4
  • Degree of de-differentiation from grade 3
  • Perineural invasion

Therapy
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See under the respective entities.

Operative therapie
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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
Proposals for the primary depth of cut for the primary excision (n. Breuninger)
Squamous cell carcinoma Flat ablation, epidermis, dermis, subcutis (depending on size)
Merkel cell carcinoma deep ablation, possibly musculature
Carcinoma of the adnexes Subcutis
M. Paget Cutis/Subcutis
M. Bowen (genital/perianal) Cutis / subcutis

Proposals for the safety distances for primary excision (n. Breuninger). For 3D histology the smaller safety distance applies
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

Tables
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TNM Classification

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

Staging

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)
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Squamous cell carcinoma is the most common skin tumour capable of metastasis. The global metastasis rate is low at about 4 %. If risk classes are defined by measuring the tumour thickness, a "high-risk class" can be defined from a tumour thickness of 5-6 mm. Here the risk of metastasis is about 16 %. For this risk group, an early diagnosis by means of sentinel lymph node biopsy seems to be useful (see also carcinoma, spinocellular).

Literature
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  1. 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
  2. Breuninger H (2015) Safety distances for malignant skin tumours. derm 21: 203-212
  3. 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
  4. Mieczko A et al (2011) BerEP4-negative basal cell carcinoma of the palm: Case report and literature review. JDDG 9:140-143

Disclaimer

Please ask your physician for a reliable diagnosis. This website is only meant as a reference.

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Last updated on: 29.10.2020