skin cancers Flashcards by M K

lifetime risk of nonmelanoma skin cancer?

1 in 5 lifetime risk in US

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what is the most common invasive neoplasm in the US?

basal cell carcinoma

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what is the frequent mutation in Basal cell carcinoma?

PTCH mutations(30%) in sporadic tumors

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what is the function of PTCH

tumor suppressor gene: regulator of basal epidermal cell proliferation

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what are five risks for acquiring basal cell CA?

UV exposure, fair complexion, h/o sunburns(especially blistering), family history of BCC and immunosuppression

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what is the classic appearance of a basal cell carcinoma?

pearly nodular characteristic, centrally ulcerated, and studded with talengectiasies (dilated BVs)

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describe the cells of basal cell carcinoma

basophillic hyperchromatic cells that form nodules, extending from the surface epidermis; cells at the periphery of the aggregations form a palisade

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what are tumor nodules set in?

set in a mucnious stroma with retraction from that stroma (clefting, or retraction artifact)

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what is the most common subtype of basal cell CA?

nodular

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describe the appearance of classic BCC(nodular)

well circumscribed nodule with pearly rolled border and central erosion. note telangiectasias as well

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only _____of BCC presents before age 50, and it is rare prior to age 35.

20%

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what is Basal cell nevus syndrome aka Gorlin syndrome? what is the mutation in this cancer? at which age do ppl usually present with BCCs?

autosomal domiant and rare. 1 in 56,000 people

characterized by mutation in PTCH1: tumor suppressor gene

BCCs at early age (~23yo)

MSK defects and jaw cysts

increased risk for other neoplasms: medullobastoma, fibrosarcoma

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how often does BCC metastasize?

rarely! 0.0028% to 0.55% of cases

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what is the most common treatment of BCC?

excision = most common treatment

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what are other common treatment of BCC?

electrodessication and currentage

cryosurgery

radiaiton

topical tx for superficial BCC: 5-fu and imiquimod(inhibitor of TLR7 and TLR8 also involved in inhibitng sonic hedgehg pathway)

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name one targeted therapy for advanced BCC. what is its MOA?

vismodegib. MOA: small molecle inhibitor. competitive antagonist of SMO.

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what is vismodegib approved for?

approved for advanced BCC (metastatic disease, recurrent disease(post surgery) and non-surgical candidates)

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how common is squamous cell carcinoma?

second most common skin CA

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what are three categories of squamous cell carcinoma?

minimal atypia = actinic keratosis
full thickness of epidermal atypia confined above the basement membrane (SCC in situ) (Bowen’s disease, erythroplasia of Queyrat)
Invasice SCC (well differentiated, moderately differentiated, poorly differentiated)

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in actinic keratosis, what is the clue to the superficial nature of the lesions?

lack of inducration

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t/f. parakeratosis (keratiznation characterized by retenion of nuclei in the stratum corneum) is a characteristic of actinic keratosis

true

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describe squamous cell carcinoma

hyperchromatrophic, pleomorphic nuclei, disorganied growth, mitoses and invasion through basal layer.

cells are pink, keratinizing, like hte stratum spinosum

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what is the etiology of SCC

no specific SCC oncogene or tumor suppressor gene has been indentified; increased p53 mutation only

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name three risk factors for development of SCC

UV radiation

HPV

immunosuprression (esp with transplant patients)

others: chornic inflammation, certain scars(burns), chemical exposure, especially arsenic, radiaiton exposure, leukoplakia

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KNOW: what is the risk of metastasis in cutaneous SCC related to? (4)

tumor size, depth of invasion into dermis, anatomic site, host immune status

size and depth of tumor that are at high risk for metastasis in SCC

larger than 2cm clinically, greater the risk; greater than 4mm in depth or subcutaneous extension higher risk on lips and ears

what is the overall risk of metastasis of SCC?

\<5% (closer to 0.5-1% for actinic induced non-mucosal skin)

in SCC what are some high risk metastasis scenarios?

actinic induced on lip: 2-16% Marjolin's ulcers 10-30% vulvar, perineal, penile HPV-induced 30% leukoplakia

two common locations of SCC metastasis

lungs and lymph nodes

name 2 subtypes of SCC

keratoacanthoma and marjolin's ulcer

what is a keratoacanthoma? which cancer is it related to? how does it grow? is it painful? can it involute?

neoplasm of keratinocytes related to SCC, possibly a subtype rapidly grows over 2-6 weeks painful may involute spontaneously

what is marjolin's ulcer?

an ulcerated invasive scc arising on a background of chornic inflammation, scarring, radiation, trauma

what does SCC treatment depend on?

degree of progression

what is the tx for actinic keratosis?

topical therapy, cryotherapy

what is the tx for SCC in situ?

topical therapy, intralesional, exicision

how do you treat invasive SCC

exicision

who is at highest risk to get melanoma?

old white men

t/f. most melanomas develop de novo

true (about 20% develop from pigmented lesions)

where do melanomas have to be in order to metastasize?

have to be in the dermis

what are the three types of melanocytic nevi?

junctional, compound, intradermal

do melanomas mature with descent into the dermis (cells get smaller)?

no, melanomas do not mature with descent into the dermis

do nevi have melanocytes above the basal layer?

not usually, melanocytes above the basal layer is more characteristic of melanoma

both nevi and melanoma are comprised of \_\_\_\_\_\_\_\_

melanocytes

both nevi and melanoma share which mutations?

BRAF

t/f. high numbers of nevi (\>50) can incerase risk of melanoma

true (melanocyte burden)

t/f. melanoma can develop from pre-existing nevi

~20% develop from nevi ~80% develop de novo

identify three multifactorial etilogies for melanoma

genetic predisposition (CDNK2, BRAF) environment (UV) underlying immune status

what are 9 common melanoma risk factors?

1. large number of common nevi (esp \>50) 2. giant congenital nevi 3. atypical nevi 4. history of blistering sunburns 5. family histor of melanoma 6. light complexion, tanning bed use 7. underlying immune dysfunction

the ABCDE of melanoma + 2 more signs

A - asymmetry B- borders: irregular, scallped C- color: mottled, variegated, not uniform D- diameter \>6mm E- elevation changing mole and ugly duckling sign

what are the five subtypes of melanoma?

acral lentigous - arises in palms or soles, often in dark skinned individuals, not related to UV light expsoure lentigo maligna melanoma - nodular superficial spreading amelononic - non-melanin producing

what are three prognostonic indicators for melanoma

1. whether they are in the dermis 2. how far they go into the dermis 3. wehtehr or not they are ulcerated

describe lentigo maligna

melanoma of older patients on sun-exposed skin slow growing, still in radial pahse, still melanoma in situ

what defines acral lentiginous melanoma?

defined by anatomic location on plantar, palmar, and subungal skin most common melanoma in dark-skinned pts.

what heralds the progression of the an situ lesion of lentigo maligna melanoma to an invasive one?

when a nodule arises on the backgroud on lentigo maligna

nodular melanoma. what is the location? do they have preceding preceding radial growth? what is their epidemiology?

usually on sun exposed skin, no preceding radial growth; 15% of MM, 2x men\>women

characteristis of a superficial spreading melanoma

wider variation in color, diameter \> 6mm, elevated

where are melanocytes derived from?

neural crest cells

melanoma metastasis is often via \_\_\_\_\_

lymphatics, but not exclusively

what is the #1 organ site for melanoma metastasis?

skin

what is the most common cause of death in melanoma involvement

CNS involvement

KNOW: what is the single most important prognostic factor in melanoma metastasis?

lymph node involvement

KNOW: what is the single most important histological prognostic factor in melanoma?

breslow thickenss and ulceration

what is breslow's thickness?

distance of involvement from the stratum granulosum (top) to the deepest tumor cell (bottom)

how do you treat melanoma?

catch it early and cut it out!

50% of melanoms harbor which mutaiton

BRAF

MOA for vemurafenib?

small molecule inhibitor of BRAF V600E mutation

what is vemurafenib approved to treat?

unresectalbe or metastastic (stage 4) melanoma provides survival benefit (although modest) initial response impressive, but melanoma adpats new trials focused on combo therapy esp with ipilimumab

what is the MOA for ipilimumab?

blocks CTLA4 --\> immune stimulatin

what is role of sunlight in SCC, BCC, and melanoma?

SCC - cumulative lifelong expsoure clearly related to development BCC - UV important but not clearly related to cumulative doses --\> intermittent? melanoma -- certainly plays a role, along with genetics, other environmental facotrs, and immune system

xeroderma pigmentosum: incidence

autosomal recessive: 1 in 1 millin in US

what is the defet in xeroderma pigmentosum

defects in gene that function in nucleotide excision repair of thymine dimers

xeroderma pigmentosum leads to increased risk in skin cancers by which mech?

by increased sensitivity to UV light

Summary: skin cancer is common and incidence is increasing amenable to prevention and early detection genetic advances have led to targeted therapies in advanced disease

skin cancers Flashcards

(74 cards)