name a few benign epithelial tumors

• seborrheic keratoses- hyperkeratosis, Leser-Trelat sign
• acanthosis nigricans:hyperpigmented
• fibroepithelial polyp:acrochordon, papilloma
• epithelial cyst
• adnexal tumor

definitive Dx w/ histological biopsy

squamous cell carcinoma

basal cell carcinoma

melanoma=most deadliest

lentigo

melanocytic nevus

dyslastic nevi

melanoma

• arise spontanoeusly in mid-age, older pt.
• presentation: round impacted with keratin, flat, coin-like plaques, appear "stuck on" may easily peel off. dermacated sharply from epiermis, variable melanin pigmentation
• hyperkeratosis: a lot of keratin, pseudo horn cyst.
• small sheet of cells, resembling basal cells of normal epidermis
• sign of leser-Trelat: rpaid increase in number, phenotypic marker for stomach adenocarcinoma.

• thicked, hyperpigmented zones of skin
• flexural areas: axillae, skin folds of neck
• 2 types:

1. benign (80%): childhood, early puperty
2. malignant association (20%): underlying adenocarcinoma, mid-aged, older individual.

• NO melanocytic hyperplasia

• acrochordon, squamous papiloma, skin tag.
• neck, trunk, face, intertriginous area
• attached to skin by a small, often slender stalk.
• morphology: fibrovascular cores covered by benign squamous epithelium.
• may see ischemic necrosis.
• a/w diabetes, DM and intestinal polyposis

Fibroepithelial polyp

fibrovascular core covered by benign squamous epithelium

• wen-swelling or growth on skin
• downgrowth of epithelium into dermis layer.
• cystic expansion of epidermis-->epithelium forming hair follicle.
• cyst filled with keratin, firm , dermal, movable.
• morphology:

1. epithelial inclusion (wall resemble normal epidermis)
2. Pilar/trichilemmal (wall resembles follicular epithelium)- no granulosum epi layer.
3. Dermoid (similar to epidermal cyst, multiple appendages)
4. Steatocystoma (well resembling sebaceous gland duct)

• neoplasm of: hair follicle, eccrine gland, apocrine gland.
• Morphology: cylindroma (ductal appocrine/eccrine differentiation), syringoma (eccrine differentiation), trichilemmoma (cowden dz-mutation in tumor suppressor gene PTEN)

• this is a extreme case of eccrine cylindroma
• type of adnexal tumors
• clinical appearance of multiple dermal eccrine cylindroma extensively involving the scalp and other sites of the head and neck. AKA turban tumor.
• Histology showing "jig saw" puzzle pattern.

• type of adnexal tumors
• characterized by small, multiple tan papules in the vicinity of the lower eyeslid.
• histology show small glandular structures with little 'tail'. DNS

• a type of adnexal tumor (gland neoplasm)
• the tumr represents as a lobular growth of glycogen-rich clear cell.
• cowden disease-mutation of suppressor gene PTEN

• this is an extreme case of premalignant epithelial tumor- actinic keratosis
• this is a solar keratosis. chronic exposure to sunglight-->build up of excess keratin.
• occur on lightly pigmented individual.
• THIS IS WHAT WILL BECOME SQUAMOUS CELL CARCINOMA IN SITU.
• Morphology: basal cell alyer atypia, marked hyperkeratosis (thicken stratum corneum). Parakeratosis (nuclei retention in cells of stratum corneum). superficial dermis has elastosis
   (thickened, blue-gray elastic fibers)

• This is keratocanthoma!
• rapidly develop neoplasm, mimic squamous cell carcinoma. men> women. sun exposed area.
• morphology: dome shaped nodule, keratin filled crater surrounded by proliferating epithelial cells
• epithelium-enlarged cells showing reactive cytologic atypia.
• cells are glassy, eosinophilic cytoplasm and produce keratin.

• a common malignant epithelial tumor.
• sunlight affects DNA, causing transient immunosuppression (langerhans cells)-->favoring tumorigenesis and profession.
• pathogenesis: UV-->DNA damage, transient immunosuppressed--> increase risk to ocogenic virus HPV (type 5 and 8)--> increase risk for development of SCC

• In situ: not invaded through basement membrane of dermoepidermal junction. cels are enlarge, atypical nuclei.
• invasive lesion: cell broken through basement membrane, nodular and ulcerated, show hyperkeratosis.

• a common, slow growing malignant epithelial tumor
• rarely metastasize
• lightly pigmented patient, sun-exposed.
• clinically: pearly papules often with telangiectasias.
• morphology: tumor cells resemble basal cell, arise from epidermis not occur on mucosal surface. these cell arranged into nest (w/ pallisaded arragement of cells around the periphery)that infiltrate into dermis. 

• a melanocytic tumor.
• benign hyperplasia of melanocytes, occur in all age. unknown pathogenesis.
• "liver spot" solar lentigo.
• histology: linear, melanocytic hyperplasia restricted to cell layer immediately above the basement membrane.
• produce hyperpigmented basal layer

• a melanocytic tumor
• AKA moles
• congenital
• junctional nevi: aggreagates of round cells growing along DE junction
• compound nevi: growing INTO underlying dermis
• intradermal nevi: older lesion, aggregates are lost.
• compound and intradermal= more elevated
• sequence of maturation is of diagnostic importance in distinguishing bening nevi from melanoma. (compared to benign nevi, melanoma does not mature as it goes deeper into dermis)
• melanocytic nevi matures as it goes deep into dermis. 

1. superficial nevi are larger, grow in nest and produce melanin.
2. deeper nevi are smaller, produce little or no pigment, resemble neural tissue=nneurotization.

• a form of melanocytic nevi
• precursor to melanoma
• NOT ALL melanomas originate from dysplastic nevi.
• Morphology:  nuclear englarged, hyperchromasia
• single nevus cell replace normal basal cell-->producing lentiginous hyperplasia
• dyplastic nevi are larger than ordinary moles, irregular border, not uniform colored.
• may a/w dysplastic nevus syndrome-AD
• patogenesis: mutation CDKN2A, CDK4, NRAS, BRAF

• common, very deadly
• cured surgically
• usually asymptomatic
• most are >10mm
• ABC: asymmetry, Irregular Border, Variegate Color
• 2 periods of growth:

1. radial growth: horizontal spread of melanoma with epidermis and superficial dermis, lack ability to metatasize,
2. vertical growth: invade into deeper dermal layers, appear as nodules, emergence of clone cells with metastatic potential; unlike melanocytic nevus, melanoma does not mature as it goes deeper.

• pathogenesis: mutation diminishing activity of retinoblastoma (RB) tumor suppressor protein. aberant increases in the RAS and PT-3K/AKT signaling
• TX: excision of entire lesion, use HMB-45 monoclonal ab to assess if tissue is of melanocytic origin, used as a tumor marker for melanoma.