PATH 09 - SKIN NEOPLASMS

1) Epidermal - Seborrhoeic keratosis, wart, squamous papilloma

2) Melanocytic origin– Lentigines, naevi (junctional, compound, dermal)•

3) Skin adnexal origin – Syringoma, trichofolliculoma

4) Soft tissue origin – Dermatofibroma, hemangioma, neural tumours, lipomas

Basal cell carcinoma (BCC)

• Common skin neoplasm (most common skin Cx)
• Related to exposure to sunlight
• AKA = basal cell epithelioma, (bc rarely metastasises)

While certain factors can result in higher-grade behaviour, in most cases earlier detection and treatment have made extensive local destructive neoplasm a thing of the past

Excellent if appropriate Tx.

Recurrent Cxs harder to cure.

Although basal-cell carcinoma rarely metastasizes, it grows locally with invasion and destruction of local tissues.

Can impinge on vital structures like nerves --> loss of sensation or loss of function or rarely death.

Most cases successfully treated before serious complications occur.

Arise from pluripotent cells lodged in the epidermis and follicular epithelium.

Mutations of p53 gene may play a role in the development of BCC.

• depressed centres and rolled borders
• Slow growth rate
• lesion starts as "pearly" or ivory in appearance
• As it grows, ulcerates --> crusting

• Cutaneous squamous cell carcinoma (SCC) is a malignant atypia of keratinocytes in the skin.
• Tumour of epidermis char'd by 2 types- in situ amd invasive.

• Sunlight causes SCC
• Areas affected - neck 75%, hands 15%

Similar to premalignant skin tumours such as actinic keratoses, the incidence of non-melanoma skin tumours varies dramatically depending on skin phototype or constitutive pigmentation, cumulative sun exposure, and geographic latitude. In addition to solar UV exposure, other factors are known to increase the risk of SCC, such as ionising radiation, burns, previous psoralen, and UV-A light therapy for psoriasis, hereditary skin conditions, environmental toxins such as arsenic and tar, human papillomavirus and compromised immune responses

SCC

SCC arises in keratinocytes that have undergone uncontrolled proliferation.

UV light is absorbed by skin ---> erythema, sunburn and, ultimately, solar elastosis and/or skin cancer.

Chronic UV exposure may cause mutations in cellular DNA. The accumulation of genetic abnormalities leads to tumour formation.

SCCs develop through a multi-step process that involves the activation of proto-oncogenes and/or inactivation of tumour suppressor genes. 

Usu presents as ulcerated lesion, w hard, riased edges, in sun exposed sites

May begin w solar keratoses

Can metastasise to lymph nodes (rare)

Prog depends on depth of tumour invasion, histological pattern, and immunological status of the patient.

Metastasis - Generally the metastatic potential of SCC is low at 3% but ic w size.

Metastases are more common in tumours of the ear (10%) or lip (30%), scalp and extremities, esp if rcvd immunosuppressive therapy.

Metastatic disease --> long-term prognosis extremely poor.