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MSK II Exam 1 > 2-15 Pre-Malignant and Malignant Lesions > Flashcards

2-15 Pre-Malignant and Malignant Lesions Flashcards

1
Q

What are some pre-malignant and malignant lesions?

A

I.Dysplastic nevi and malignant melanoma

II.Actinic keratosis

III.Squamous cell carcinoma

  • Keratoacanthoma type

IV.Basal cell carcinoma

V.Dermatofibrosarcoma protuberans

  • Bednar tumor

VI.Leukemia/lymphoma

VII.Mastocytoma

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2
Q

What is a dysplastic nevus?

A

AKA Clark Nevus

•Gross appearance is worrisome for melanoma

–Asymmetric

–Border irregular

–Color uneven

–Diameter > 6 mm

•Occur on non-sun or sun exposed skin

–Melanocyte nests (theques) at the tips of rete ridges

–Rete ridges are often “bridged” (connected at their bases)

–Reactive fibrosis of papillary dermis

•Two forms

–Sporadic: not prone to malignancy

–Familial: dysplastic nevus syndrome

  • Autosomal dominant
  • 50% chance of melanoma by age 60
  • CDKN2A and CDK4 mutations (also seen in familial melanoma syndromes)
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3
Q

What is dysplastic nevus syndrome?

A

AD inheritance

50% chance of melanoma by age 60

CDKN2A and CDK4 mutations

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4
Q

What is a malignant melanoma?

A

malignant neoplasm of melanocytes

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5
Q

What are the subtypes of malignant melanoma?

A

•Subtypes

–Lentigo maligna (in situ sun exposed area)

–Lentigo maligna melanoma (invasive lesion similar to lentigo maligna)

–Superficial spreading (invasive, mostly horizontal growth phase)

–Nodular (invasive, mostly vertical growth phase)

–Acral lentiginous (palms, soles and subungual; non-caucasian; in situ or invasive)

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6
Q

When and where do most melanomas occur?

A
  • Most melanomas occur in sun damaged skin (also occur in non-sun exposed skin)
  • May occur in any skin location and occasionally in the eye, mucous membranes of the genitalia, anus, oral cavity, or other sites

–Occurs primarily in adults; beginning in 3rd decade

–90% originates de novo as an isolated lesion

–Can arise adjacent to a pre-existing melanocytic nevus

–Aggressive malignancy that metastasizes widely with significant mortality

•Metastasizes to regional lymph nodes, liver, lungs, and brain

(Vertical growth – invasion

Horizontal – unlikely to metastasize, called superficial spread, usu flat

Nodular – goes deep

Acral – means distal, occurs in hands and feet and have bad prognosis, not associated with sun exposure, so it’s different mutations than other melanomas)

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7
Q

What are the risk factors for malignant melanoma?

A

•Caucasians with fair skin

–Albinism or genetic syndrome such as xeroderma pigmentosa dramatically increases incidence (50X-100X)

•Prolonged MCB UV exposure with

repeated sunburn

•3 episodes of “peeling” or severe

sunburn before age 20

•Male gender

(Clinically tested mutations:

BRAF V600 found in 50%

NRAS found in 20%

KIT found in <5% (non-sun exposed)

Please recall that BRAF and NRAS mutations are also present in benign melanocytic nevi and are not sufficient for malignant transformation)

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8
Q

What percentage of melanomas are familial? What types of mutations are present?

A

~10% to 15% of melanomas are familial

Many (but not all) also have dysplastic nevi

Increased telomerase activity from mutated TERT gene is present in 70% of skin melanomas

Kit mutations seen in non-sun exposed melanomas

Mutations seen in both dysplastic nevus and melanoma familial syndromes

P16 inhibition is inhibited by CDKN2A mutations

CDK4 mutations block p16 inhibition

(- p16 normally inhibits cell metastases, but mutations in CDK4 will lead to inability of p16 to act on it and inhibit cell metastases)

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9
Q

What is the ABCD checklist for melanoma?

A

A = Asymmetry

Melanoma if lesion bisected & halves not identical

B = Border irregularity

Melanoma if the border is uneven or ragged (border can indicate sideway invasion)

C = Color variation

Melanoma if more than one shade of pigment (indicates clonality)

D = Diameter
Melanoma if diameter greater than 6 mm

(some use E = evolution, new appearance or change in lesion over time)

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10
Q

What is the morbidity/mortality of malignant melanoma?

A

Morbidity/Mortality (Survival) AJCC: Melanoma survival depends on stage: Melanoma metastatic to lymph node(s) represents regional disease (II/III); any distant metastasis is stage IV.

  • Mortality (Survival) malignant melanoma by thickness of melanoma: Breslow level (thickness from epidermal granular layer to deepest dermal penetration)
  • Clark level also indicates invasion based on histologic anatomy, not as useful
  • 10 year survival: 92% for melanoma < 1.00 mm thick; 80% if 1.01 to 2.00 mm thick; 63% if 2.01 to 4.00 mm thick; 50% if > 4.00 mm thick
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11
Q

What are some types of chronic actinic skin damage? What is process for each one?

A

•Solar lentigo

–Focal autonomous overproduction of melanosomes

–Resultant sustained increase in melanin in keratinocytes

•Solar elastosis

–Permanent, incremental damage to reticular collagen (elastosis)

–Loss of normal skin texture (leathery and wrinkled)

•Actinic keratosis

–Neoplastic proliferation of keratinocytes

•Does not involve full epidermal thickness

–Increased keratin production (scaling)

–Dermal increase in vascularity (redness)

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12
Q

What is actinic keratosis? Other names for it, where it occurs, and appearance.

A

•Also known as solar keratosis, senile keratosis, keratinocytic intraepidermal neoplasia

•Precancerous skin condition on sun-exposed areas

•Middle-aged and elderly individuals

–Face, particularly forehead

–Neck

–Dorsum of arms and hands

–Lips (actinic cheilitis)

  • Erythematous, reddish-brown macules or minimally elevated papules with overlying scale
  • Size of lesions varies - from scales to horns
  • Usually asymptomatic, may have mild tenderness
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13
Q

What is squamous cell carcinoma (SCC)?

A

•Malignant proliferation of epidermal keratinocytes with the potential for metastasis

–The malignant keratinocytes penetrate past the dermal-epidermal junction basement membrane.

–Exception: SCC in situ (e.g. Bowen disease, penile erythroplasia of Queyrat)

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14
Q

What is the epidemiology of SCC?

A

•Epidemiology

–Second most common cutaneous malignancy

•#1 is basal cell carcinoma

–Incidence of SCC increases with increasing age

–Male predominance

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15
Q

What is the primary etiology of SCC?

A

•Primary etiology in sun expose skin

–Long term sun exposure

  • UVB wavelengths (280 – 315 nm) are the most carcinogenic
  • Immunosuppression increases incidence of invasive SCC

–SCC of skin occurs in 40-70% in organ transplant recipient patients

–Increased incidence with HIV

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16
Q

In addition to sun exposure, what are some other etiologic agents for SCC?

A

Other etiologic agents (can be synergistic with sunlight)

  • Human papillomavirus (HPV)
  • Chronic skin inflammation, ulcers and draining fistulous tracts (osteomyelitis)
  • Some dermatoses
  • Burns
  • Ionizing radiation
  • Chemical exposures

–Tars → scrotal cancer in chimney sweeps

–Arsenic ingestion

–Tobacco and betel nut usage

•Genetic syndromes

–Epidermodysplasia verruciformis (predisposition to HPV infections and HPV subtypes 5 and 8 can lead to SCC)

–Xeroderma pigmentosa (nucleotide excision repair pathway defects)

–Other syndromes

17
Q

What are some genetic syndromes that are etiologic agents for SCC?

A

•Genetic syndromes

–Epidermodysplasia verruciformis (predisposition to HPV infections and HPV subtypes 5 and 8 can lead to SCC)

–Xeroderma pigmentosa (nucleotide excision repair pathway defects)

–Other syndromes

18
Q

What are the major clinical characteristics of SCC?

A
  • Areas of greatest cumulative sun exposure
  • Early invasive SCC is usually a small, firm, skin-colored or erythematous nodule with indistinct margins
  • Surface may be smooth, verrucous, ulcerated, papillomatous or granular and may bleed easily
  • Older SCCs are larger, invasive, and may be ulcerated
  • Mortality is low for SCC of skin
19
Q

What is a keratoacanthoma?

A
  • Better term “Squamous cell carcinoma, Keratoacanthoma type”
  • Variant of invasive SCC
  • Occurs on sun-exposed area
  • M>F

•Rapidly growing (days-weeks)

•Often involutes and clears spontaneously within 3 to 4 months

20
Q

What is basal cell carcinoma? What are the subtypes?

A
  • Previously known as “basal cell epithelioma”
  • Malignant neoplasm of the basal regenerative epithelium of the epidermis
  • Almost never metastasizes
  • Has numerous subtypes
  • Nodular and sclerosing types
  • Have local invasion and destruction of adjacent dermis
  • Tend to occur in hair-bearing skin subjected to sun exposure

•

–Sclerosing and multifocal superficial spreading types

  • Have difficult to identify margins
  • Have high incidence of post resection recurrences
21
Q

What is the primary etiology of basal cell carcinoma?

A

Etiology

•Increased sunlight exposure in childhood and adolescence, and chronic exposure during adulthood

22
Q

What is the epidemiology of basal cell carcinoma?

A
  • Most common cutaneous neoplasm (but is ignored in cancer data statistics)
  • 98% occur after age 40
  • After age 50, 1% of population develops BCC each year
  • M ~ F
  • Almost all individuals with a significant history of face/neck sun exposure will develop one or more BCCs
23
Q

What are the major clinical characteristics of basal cell carcinoma?

A
  • 85% occur on head and neck
  • Remainder predominantly on trunk/limbs

•Clinical appearance related to histologic type

–Rodent Ulcer = advanced presentation

24
Q

What is Gorlin syndrome?

A

Nevoid Basal Cell Carcinoma Syndrome

•Multiple basal cell carcinomas before age 20

•Pits of the palms and soles

  • Odontogenic keratocysts
  • Medulloblastomas
  • Ovarian fibromas
  • Autosomal dominant disorder with PATCH1 gene mutations
  • SMO is normally inactive via PATCH1 function
  • When hh (sonic, Indian and Desert) proteins bind to PATCH1, SMO is activated leading to production of transcription factors (GLI1) that drive gene activation
  • PATCH1 mutations in Gorlin syndrome bypass the hh protein needed for SMO activation and SMO is active in the absence of hh proteins
25
Q

What is nodular BCC?

A
  • Traditional or “classic” appearance of BCC
  • Dome-shaped, pearly papule or nodule
  • Prominent surface dilated dermal vessels (telangiectasia)
  • May become quite large if neglected
  • Easily treated by excision if not large
26
Q

What is sclerosing BCC?

A

AKA Morpheaform BCC

  • Typically waxy yellowish-white or pearly white, indurated plaque that may retract below plane of skin surface
  • Occurs predominately on face
  • Poorly defined margins (edge of lesion)

–Difficult to excise, high recurrence rate and may disfigure

–Mohs surgery can be used during excision to determine complete excision

27
Q

What is superficial BCC?

A
  • Multifocal erythematous, scaly plaque; elevated rolled edges.
  • Occurs non-sun exposed skin sites on proximal limbs or trunk
  • Multifocal growth pattern localized to dermal-epidermal junction
  • Do not become locally invasive or metastasize
  • Part of a “field defect” and therefore can recur after excision
  • If pigmented may be confused clinically with melanoma
28
Q

What is dermatofibrosarcoma protuberans?

A

–Malignant superficial fibroblastic neoplasm (fibrosarcoma of skin)

–Locally aggressive but rarely metastasizes

–Bednar tumor is pigmented variant

–Translocation of COL1A1 and PDGFB → ↑PDGFB

(AKA a bump

  • has malignant, low grade proliferation of spindle cells/fibroblasts
  • rapidly growing
  • pigmented, sometimes mimics growth of melanoma
  • malignant fibroblasts can sometimes produce pigment
  • can use Gleevec for these)
29
Q

How do cutaneous lymphomas penetrate skin?

A

Leukemias and lymphomas can penetrate skin

30
Q

What is mycosis fungoides?

A

Mycosis Fungoides

CD4+ T-cell lymphoma of the skin (CLA, CCR4 & CCR10)

Aggressive neoplasm with median survival 8-9 years (M>F)

Phases:

–Inflammatory erythrodermic pre-mycotic patch

–Plaque

–Tumor

31
Q

What is Sezary syndrome?

A

Sezary syndrome is a variant of mycosis fungoides in which skin involvement is manifest as a generalized exfoliative erythroderma

Leukemic phase with Sezary cell (cerebriform nuclei) seen in Sezary syndrome and 25% of plaque and tumor phases with survival <3 years

Lutzner cells are similar to Sezary cells but smaller in size

32
Q

What is a mastocytosis/mastocytoma?

A

mast cell tumor - generally pretty rare

Darier sign - stroking of the skin leads to histamine release which causes swelling, erythema and edema

Mast cell granules can be highlighted with toluidine blue or Wright-Giemsa stains

33
Q
A

MSK II Exam 1 (4 decks)

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