Skin Neoplasms Flashcards
Firm outgrowth of keratinocytes and a thick keratin layer with a ‘church spire’ architecture, associated with HPV Infection?
Benign proliferation of keratinocytes with horn cysts. Presents as single or multiple, sharply demarcated pigmented lesions that protrude above surface of skin with a soft, tan-black, “greasy” surface
Atypical enlarged keratinocytes that do not invade into dermis. Occurs in immunosuppression commonly in sun exposed areas
Hyperkeratosis with full thickness aplasia that can progress to SSC?
Risk factors and prognosis for Invasive Squamous Cell Carcinoma?
Arises from hair follicular epithelium rather than squamous cells in epidermis and can be associated with Gorlin Syndrome?
Neoplasms arising from epidermis?
- Seborrheic keratosis
- Verruca vulgaris / viral wart
- Actinic keratosis (pre-malignant)
- Bowen’s disease / squamous cell carcinoma in-situ (SCCis)
- Squamous cell carcinoma (SCC)
- Basal cell carcinoma
Neoplasms arising from Melanoocytes?
- Benign naevi (more commonly called moles)
- Dysplastic naevi
- Melanoma
What is Dysplastic Naevus Syndrome?
- Genetic mutation
- Presentation
Risk factors for malignant Melanoma?
– UV light exposure.
– Family history (10% of melanoma patients)
– Multiple naevi (e.g. >25 increase risk x 4)
– Immunosuppression
Measuring Stage of Melanoma
Measuring Depth of the Melanoma Invasion
Clark Level
- Confined to epidermis
- Invades papillary dermis
- Invades and expands papillary dermis
- Invades reticular dermis
- Invades subcutis
Malignant Melanoma Therapies
BRAF Inhibitor Therapy: High clinical stage tumours are tested for genetic mutations in the BRAF V600 gene. 60% of malignant melanoma eligible
PDL1 Inhibitor Therapy: PDL1 is a protein that allows some cancer cells to avoid attack from our own T lymphocytes. PDL1 extends from the surface of the tumour cells and binds to the PD1 and B7.1 surface proteins that reside on T lymphocytes. This union is known as an immune checkpoint => instructs T lymphocytes to leave the cancer cell alone. One approach to fighting cancer is to block the PDL1 receptor on the tumour cells.
Adnexal Neoplasms may arise from:
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Adnexal Neoplasms may arise from:
- Sebaceous Glands
- Hair Follicles
- Sweat Ducts
Syndromes associated with Adnexal Neoplasms?
- Brooke Spiegler Syndrome (Chr 16 Mutation)
- Muirr-Torre Syndrome (Autosomal Dominant mutation in MLH1 + MSH2 mismatch repair genes. Variant of Lynch Syndrome)
- Cowden Syndrome (Autosomal dominant mutation PTEN tumour suppressor gene)
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Burt Hogge-Dube Syndrome (Autosomal dominant alteration in the
BDH/FLCN on chromosome 17 encodes a protein called folliculin)
Syndrome associated with Adnexal neoplasms that arises from germline mutation in the cylindromatosis gene on chromosome 16 presents with Cylindromas, spiradenomas, and trichoepitheliomas on scalp, face, and neck.
What are patients at an increased risk for?
Syndrome associated with Adnexal neoplasms that arises from autosomal dominant alteration in MLH1 and MSH2 mismatch repair genes and is considered a variant of Lynch syndrome.
What are patients at an increased risk for?
Muir-Torre Syndrome
Patients at risk for:
- Colorectal adenocarcinoma
- Endometrial adenocarcinoma
- Cutaneous sebaceous tumors (sebaceous and sebaceous carcinoma)
Syndrome associated with Adnexal neoplasms that arises autosomal dominant mutation in the PTEN tumor suppressor gene and presents with multiple hamartomas?
What are patients at an increased risk for?
Cowden Syndrome
Patients at risk for cancers of the:
- Thyroid
- Breast
- Endometrium
- Colorectum
- Melanoma
Syndrome associated with Adnexal neoplasms that arises from autosomal dominant alteration in BDH/FLCN genes on Chromosome 17 that encodes for the protein folliculin.
What are patients at an increased risk for?
Burt Hogge-Dube Syndrome
Patients are also at risk for developing:
- lung cysts with pneumothorax
- renal cell carcinoma (bilateral chromophobe renal cell carcinoma and oncocytoma)
