Skin Cancer Flashcards
Leser-trelat sign
- Explosive development of brown papules
- Paraneoplastic syndrome
- Brown “stuck on” papule that well circumscribed
- immature bland basaliloid keratinocytes with hyperkeratotosis acanthosis, keratin filled horn cysts
- seborrheic keratosis
- activating mutation in FGF-3
- Soft, flesh colored, bag-like polyp
- fibrovascular covered by normal tissue
- acrochondron (skin tag, fibroepithelial)
Well demarcated papule with central punctum
- recapitulate hair follicle
- epidermoid cysts ( aka sebaceous cyst)
- cyst will recur if entire lining is not excised
Cyst with a stratified squamous cell layer that includes granular layer
Epidermoid cyst
- many call them sebaceous cysts
Cyst with a stratified squamous cell layer that doesn’t include granular layer
Pilar cyst
- Lesion of disorganized keratinocytes in the lower layers of epidermis
- does not involve full thickness of epidermis
- actinic keratosis
- premalignant: can turn into squamous cell carcinoma
- Full thickness dysplasia
- irregular hyper chromatic nuclei
Squamous Carcinoma in situ
- excision is curative
- sun exposure is number 1 risk factor
- Cup shaped lesion with central crater
- dome shaped nodule with central crater and keratin plug
Keratoacanthoma
Most common skin carcinoma
Ulcer with rolled boarder or pink pearly papule with talengectasia
Slow growing, circumscribed
Basal cell carcinoma
Gorlin syndrome
- nevoid basal cell carcinoma syndrome
- PTCH mutation (9:22)
- two hit pathology
Lentigo vs. freckle
- lentigo: darker, doesn’t darken in sun, larger, includes mucous membrane
- freckle: smaller, darkens in sun, lighter, not on mucous membranes
Nevi
- p16/INK4a, CDNK2 mutation
- benign
- moles
- melanocytes Nevis: nests of melanocytes in basal epidermis
- compound Nevis: junctional and intra dermal nests of melanocytes
Fused nests of atypical melanocytes between rete pegs
Linear lamellar fibrosis of papillary dermis
Dysplastic Nevus
Risk factors for malignant melanoma (genetic and environmental)
- CDNK2a gene mutation
- RAS/BRAF and PI3K
- sun exposure, lightly pigmented, giant congenital nevi
Atypical melanocytes within epidermis, esp migrating in stratum spinosum, confluent single melanocytes at basal layer
Melanoma-in-situ
Dysplastic melanocytes involve epidermis and invade the dermis
Malignant Melanoma
Vertical growth down into dermis
- primary prognostic factor
- increases the risk in localized melanoma
- Breslow thickness (measured from granular layer)
Tan-brown-red firm papule commonly on extremities
Fibroblasts and foamy histeocytes trap individual collagen bundles at periphery
Benign fibrous histyocytoma
Condition involving optic gliomas and pigmented Hartomas in iris, cafe-au-lait spots on skin
Neurofibroma (NF-1: loss of RAS)
AD
Cafe-au-lait spots without but no lisch nodules in the iris
NF-2
Plexiform rubbery mass
NF tumor
Firm solid nodule/plaque on trunk, uniform spindle cells/storiform fascicles invading subcubitus
Dermatofibrosarcoma protuberans
- unlikely to metastasize -> Fibrosarcoma may metastasize
Chronic non-healing lesions on trunk
- atypical T cell infiltration with cerebriform nuclei
- beads on a string lining up on DE junction
Mycoses fungoides
- prognosis depends on % body coverage
- moves into blood -> sezary syndrome
Dome shaped papules on nodules and forehead
- jigsaw like puzzle islands of basaloid cells with small ductal lumen and surrounding hyaline sheath
Cyclindroma, turban tumors
Slow-growing flesh colored papule on head and neck of older adults
- well circumscribed dermal nodule of sebocytes and outer layer if basaloid germanitive cells
Sebaceous Adenoma
- may be associated with HNPCC
Solitary asymptomatic skin colored papules on face
- associoated with PTEN mutation
- trichilemmomas
Tumor suppressor genes associated with skin cancer (2)
- p53
- PTCH
Solar elastosis
- elastic fibers get damaged and become disorganized
- not full thickness
Insitu Squamous vs actinic keratosis
- generally size
- squamous cell is also full thickness with basal layer is intact (in situ)
Sunlight damage
- UV -> pyrimidine dimers -> p53 activation (most common mutation in people who develop SCC) -> arrest cell division and corrupt cell dies
- chronic immunosuppression increases risk factors
- long term chronic lesion also increases risks
Large light pink keratinocytes in well circumscribed cup
- keratoacanthoma
BCC transformation
- main issue is damage to local tissue
- BCC rarely metastasize (.5%)
BCC pathenogenesis (3 options)
- most are sporadic p53 mutation
- 30% are PTCH
- gorlin syndrome: Nevoid BCC, one hit mutation in all cells
Long thin rete pegs, non-nested single large myelocytes
- lentigo
BRAF-RAS path mutation
- Nevus
- often accumulates p16 (melanoma have decreased)
Nests of melanocytes
Nevus
- junctional-> compound -> intradermal
Decreased p16/ increase in RAS -> increase in BRAF
- associated with malignant melanoma
17q11
- NF1
- eyes
RAS mutation
- plexiform
22q11
- acoustic fibromas
- NF2
- no lisch nodules
Mycoses fungoides prognosis
- % body coverage
- stage (patch, plaque, nodule)
Pautrier abcess
- mycoses fungoides
- lymphocytes infiltrating
Association with lynch syndrome
- sebaceous Adenoma
Oncogenes tumor suppressor genes
- oncogenes: Dominant expression, gain of function (kinases, GFs et al)
- tumor suppressors: (p53, PTCH) resistive expression, loss of function
Bowen’s syndrome
- squamous cell carcinoma in situ
- unlike Actinic keratosis (which rarely transforms), Bowens transforms in 26 % of cases
Trt of AK
5-FU: lights up areas affected
Eminems CD is Not Killer
Malignant melanoma
- CDNK2a
Gore PiTCHed his Nevil scheme in Philadelphia
Nevoid basal cell carcinoma: gorlin syndrome: PTCH: t9;22
