Dermatologic Neoplasms Flashcards
Seborrheic keratoses
Common epidermal tumors that occur most frequently in middle-aged people
- are round flat coin-like plaques that are TA in-dark brown
Arise on the trunk and extremities from mutations in the fibroblast growth factor receptor-3 (FGFR3)***
- can produce leser-trelat sign where large numbers arise very quickly as part of a paraneoplastic syndrome for GI cancer
**leser trelat is caused by TGF-a stimulation by tumor cells which are primarily carcinomas of the GI tract
Acanthosis nigricans
Thickened hyperpigmented skin with a “velvet-like” texture.
- most commonly occurs in flexure regions of the body
Two subtypes based on what it is caused by:
1) non malignancy reasons (AD genetics, obesity endocrine abnormalities and congenital syndrome) = (80%)
2) GI adenocarcinomas (20%)
Pathogenesis = increased growth factor receptor signaling on the skin
- nonmaliangncy and DM = FGFR3
(Most common)
- Insulin-like growth factor receptor-1 (IGFR1) is seen in diabetic patients
- paraneoplastic = TGF-a/EGFR
Fibroepithelial polyp
“Skin-tags”
Most common cutaneous lesion
Usually in middle aged and elderly people on the trunk/face/intertriginous areas
Very rarely can show up with Birt-Hogg-Dube syndrome, but vast majority are sporadic**
consist of a slender stalk and can undergo spontaneous torsion around themselves and produce ischemia
Epithelial or follicular inclusion cysts (“Wen”)
Common lesions formed by invagination and cystic expansion of the epidermis or hair follicles
*can induce spontaneous traumatic ruptures which spill keratin into the dermis and leads to extensive and often painful granulomatous inflammation responses
Types of adnexal appendage tumors
Cylindroma: scalp/hairline ductal growth
Eccrine poroma: palms and soles of eccrine glands
Syringomas: lesions of eccrine glands in the lower eyelids
Trichoepithelioma: proliferation of basaloid cells that look like hair follicles
Sebaceous adenoma: lobular proliferation fo sebocytes
Pilomatrixomas: basalaloid cells in normal hair bulbs
Actinic keratosis
Premalignant lesion caused by UV-induced DNA damage
Associated with TP53 mutations and SCCA of the skin
- rate of progression to SCCA is 0.1-2.6% a year
Majority regress or remain stable**
Usually less than 1cm in diameter and are tan-brown and sandpaper like to the touch
- histology shows blue-gray elastic fibers with thickened stratum corneum and parakeratosis
- rarely may show full-thickness of stratum corneum layer
Treatment = usually benign but to play it safe use topical agents or cryotherapy to remove
Squamous cell carcinoma (SCC)
Common tumor that arises on sun-exposed sites in older adults
- especially high risk people = xeroderma pigmentosum patients, immunosupression patients (HPV infections) and industrial carcinogen exposure
Caused by UV light damage. Chronic sun exposure also induces this.
Common mutations:
- TP53
- RAS gain of function
- NOTCH loss of function
Two subtypes:
- in situ: sharply defined red scaling plaques with atypical cells in all levels of epidermis
- invasive: nodular and scaly lesions that may undergo ulceration
Metastatic rates on average = 1%
- increases with relation to thickness of the lesion and degree of invasion
Basal cell carcinoma
Slow growing cancer that is rarely metastatic
Occurs due to chronic sun exposure
- this is the #1 risk factor
- also being closer tot he equator increases risk
Associated mutations:
- *PTCH1 loss of function
(This gene negatively regulates hedgehog signaling)
- TP53
**can be tied to goblin syndrome which is an autosomal dominant disorder caused by inherited defects in PTCH1
While metastasis is super rare, reoccurrence occurs in 40% of patients within 5yrs
2 types of BCC morphology patterns
1) multi focal: superficial and originates in the epidermis
2) nodular lesions: deeper and originates in the dermis with hyperchromatic nuclei and basophilic cells
Treatment of BCC
Hedgehog inhibitors are #1
- also surgical resection
Benign fibrous histocytoma
“Dermatofibroma”
Group of morphological and histologically benign dermal neoplasms
Most common in young and middle aged women
Lesions are asymptomatic or tender at worst with an indolent behavior pattern
- lesions are tan papules
- causes are unknown but believed to be trauma related
- most are less than 1 cm in diameter and consist of spindle-shaped cells arranged in a Well-defined nonencapsulated mass in the mid dermis
Dermatofibrosarcoma protuberans (DFSP)
Well-differentiated primary fibrosarcoma of the skin
Are slow growth and locally aggressive recurrent tumors
- however rarely metastasis
- show as protuberant nodules on the trunk that may also show plaques or ulcerations
- histologically = storiform “pinwheel” pattern
Melanocytic nevi
Common benign neoplasms with various subtypes
- acquired/congenital are the most common type
Are all derived from melanocytes
Caused by somatic gain-of-function BRAF/RAS mutations
- unknown exact pathogenesis however
Nevus cells differentiation
Superficial nevus
- larger and produce melanin pigments
- grow in nests
Deep nevus
- smaller and produce almost no pigment
- grow in single cells
Deepest nevus
- are fusiform and grow in fascicles
Dysplastic nevus
Can be sporadic or familial
- **familial form = increased risk of developing melanoma (almost 100% lifetime)
- sporadic form = increased risk of development melanoma only if 10 or more are seen at one time (which case = 50% lifetime)
Also still show BRAF/RAS mutations
Are much larger and show in tens-hundreds at one time usually
- flat macules with slightly raised plaques “pebble-like” surface
- show variable pigmentation and irregular borders
Histology
- grows in nests which enlarge and look abnormal
- also shows “lentiginous hyperplasia” which is replacement of the normal basal cell layer along the dermoepidermal junction ‘
- *often show on areas NOT sun exposed
- because they are at high risk for melanoma development, dysplastic nevus can be used as a marker for melanoma development
