Flashcards in NMSC Dan Deck (89)
What are high risk features of SCC?
Breslow thickness >2mm (esp >6mm) OR goes to fat
PNI (in nerve >0.1mm diameter)
Site; ear or nonhair-bearing lip
Poorly differentiated or undifferentiated
SCC arising in burn, XRT field or chronic dermatosis
Immunosuppression - esp solid organ Tx or CLL
Non-sun exposed site (e.g. sole of foot)
Aggressive subtypes (e.g. acantholytic, adenosquamous, spindle or especially desmoplastic)
What are the guidelines for treating SCC by C+C?
Can be used for low-risk tumours with three caveats:
- Not on terminal hair baring areas
- If subcutaneous layer is reached then surgical excision should be performed instead
- Histology of the C+C should be performed to determine if still low-risk and if not then should be excised
96% 5 year cure rate if these adhered to
What are the recommended excision argins for NMSC?
IEC - 3-5mm
BCC - 4mm; 5-10mm if morphoeic or recurrent but Mohs preferred for these
SCC - 4-6mm if low risk, 6-10mm or Mohs if high risk
KA - 3-5mm margin
Merkel Cell - 3cm (Robinson); others say 1-2cm
AFX - 1-2cm; Mohs if large or on head/neck
DFSP - 1.5-2cm if 2cm diameter (Rob/Rook); 2-4cm if >2cm diameter or Mohs
MAC - Mohs recommended, adjuvant XRT if exc incomplete
Sebaceous carcinoma- 1-2cm; Mohs if large or on head/neck
EMPD - Mohs first line, WLE with 5cm margin +/- mapping biopsies or preop efudix to delienate
When may SLNB be considered for SCC?
Not clear if of benefit or not
If AJCC-7 stage T2;
over 2cm diameter OR any size with ≥2 specific high risk features;
- Breslow thickness >2mm OR goes to fat (Clark ≥4)
- PNI (in nerve >0.1mm diameter)
- Site; ear or nonhair-bearing lip (vermillion)
- Poorly differentiated or undifferentiated
What is risk of skin cancer from PUVA?
14x increased risk of cutaneous SCC in patients who have received >200 PUVA treatments or >2000J /cm2
Also evidence of increased risk for melanoma in these PUVA patients
PUVA lentigines indicate higher risk of PUVA-related skin cancers
>200 phototherapy treatments (of any kind) is PBS contraindication for phototherapy in Biologics work up
No evidence that UVB phototherapy increases skin cancer but probably does
What are treatments for individual AKs?
spot treat peel e.g. TCA 35-50%
What are treatments for widespread AKs/field change?
5% fluorouracil cream (Efudix); max 23x23cm area or 5-FU chemowraps for legs (as per AJD, 2013)
5% Immiquimod cream (Aldara); max 5x5cm area
-3x/wk 4 wks on, 4 wks off +/- further 4 wks on Or;
-3x/wk for 4-16 wks
3% Diclofenac gel (Solaraze); 0.5g per 5x5cm area, max 8g per day
0.05% Treinoin cream (ReTrieve)
Ingenol Mebutate gel (Picato); max 5x5cm area
- Face and scalp: 0.015% gel once daily for 2-3 consecutive days
- Body: 0.05% gel once daily for 2 consecutive days
Superficial chemical peels (need a course)
Medium depth chemical peel
- TCA 35%-50%
- Jessner’s solution + 35% TCA
- 70% glycolic acid + 35% TCA
PDT - single session per region
Daylight PDT (not if hyperkeratotic; may rpt in 3 months)
What methods are available for prevention of AKs and skin cancers?
0.05% Treinoin cream (ReTrieve) nocte
Acitretin at least 20-30mg daily or 0.2mg/kg
Nicotinamide 500mg BD
Nicotinamide 500mg BD reduces the incidence of new BCCs
reduced AK, SCC and BCC
see effect from 2 mnths, further increased effectiveness until at least 12 mnths
When do SCCs metastasize?
Highest risk is in first 2 years
For high risk SCCs;
- consider 6 monthly FSE for 1st 2 years
- annual FSE thereafter
palmoplantar and periungual SCC associated with HPV 5
HPV 5 is associated with SCC in Epidermodysplasia verruciformis
What is the risk of IEC progressing to SCC?
3-5% for normal skin IEC
10% for Erythroplasia of Queyrat
Very low risk for Bowenoid papulosis
It may be reasonable to not treat IEC
Elderly patients with slowly progressive thin lesions esp on lower legs
Use emollient containing LA/SA or urea to reduce scaling and make less obvious
How long do you use efudix cream for IECs?
OD-BD for 4 wks face, 6wks limbs
for IEC, efudix is less effective than PDT
also less than immiquimod which is similar to PDT for IEC
Efudix similar efficacy to cryo
for sfBCC efudix is less effective than PDT
Immiquimod is non-surgical Rx of choice for sfBCC
for IEC, imiquimod is more effective than PDT
the same or slightly less than PDT
But for sfBCC, imiquimod is more effective than PDT
PDT is an effective and suitable choice for IEC anywhere
Limited by availability, cost and pain
excison of IEC should be avoided on the digits
good Rx choice on digits
How is IEC of nailbed treated?
Mohs is 1st line
PDT reasonable choice
Can try aldara, laser or XRT
arsenic exposure can cause a corn-like PPK
can turn into SCC
Rx with keratolytics and chemoprevention
monitor for skin Ca and visceral malignancy
DSAP is inherited in a recessive fasion
DSAP1 gene on chr 12
What are treatments for DSAP?
• 5-FU (also chemo wraps)
• topical retinoids
• Oral retinoids
• Ablative lasers
Keratoacathomas are less common in darker skin
Which syndromes get KAs?
Muir-Torre (KA w/ sebaceous apearance)
Multiple spontaneously regressing epitheliomas of Ferguson-Smith
Generalised eruptive keratoacanthomas of Grzybowski
What are the features of
Multiple spontaneously regressing epitheliomas of Ferguson-Smith?
multiple KAs in sun exposed areas in 20s
regress over weeks to months
What are the features of
Generalised eruptive keratoacanthomas of Grzybowski?
Thousands of papules resembling milia or early eruptive xanthomas; develop rapidly and persist indefinitely
Lesions inside oral mucosa
Mask like facies from skin thickening described
Lesion benign but persist indefinitely
Whats the natural Hx of KA?
reaches full size
What are variants of KA?
Solitary/craterfiorm (normal type)
Erruptive/Syndromic - Muir-Torre, F-S, Gryzbowski
locally destructive types;
- Mutilating KA
- Aggregated KA
- KA centrigugum marginatum
What are treatment options for KA?
Cryo - if small
Ablative laser - if small
Acitretin if numerous
Low dose XRT
What are associations of Verrucous Carcinoma?
LS if genital (Giant condyloma of Buschke-Lowenstein)
leukoplakia, smoking if oral
strong assoc w HPV infection; 6 and 11
XRT should be used for verrucous carcinoma
Do not treat with XRT – triggers anaplastic change and rapid growth and invasion
Oral retinoids may be useful
What is Epithelioma cuniculatum?
Rare tumour on sole of foot – variant of SCC
Discharges foul smelling keratin debris
Comprised of sinus-like tracts
Often infiltrate bone and overlyng nailbed
Histo looks like pseudoepitheliomatous hyperplasia but lesion is progressive and destructive
Other than treating BCCs what is the management of Gorlin's syndrome?
Strict sun protection
Baseline MRI brain and repeat yearly till 8y for medualloblastoma (ave age to develop is 2yrs; Mx by neurologist)
6 monthly skin exams
digital panorex of jaw at 3-4y and repeat yearly till 21y (Mx by Maxfax surgeon)
pelvic USS of female at menarche (paeds)
scoliosis assessment (ortho)
developmental screening (paeds)
prenatal counselling (genetics)
How are BCCs maanged in Gorlin's?
Strict sun protection + avoid XRT
6 monthly skin exams
BCC ‘s on central face - excision best
use non surgical methods to Rx BCC’s elsewhere;
C+C’s/ Cryo/ PDT/ aldara/ 5 FU
role of retinoids unclear (isotretinoin)
Smoothened receptor inhibitor
Off label use for Gorlins; NEJM 2012 study
93% reduction in new BCCs over 8 months, but 50% had to discontinue due to AEs (muscle spasms, alopecia, dysgeusia (altered taste), decreased appetite, wt loss, fatigue, nausea/vomiting, diarrhoea, constipation)
chronic occupational sun exposure is the main environmental risk factor for BCCs
intermittent intense esxposure more important for BCCs
What are the high risk subtypes of BCC?
What is Basisquamous (or Basosquamous) BCC?
Features of both BCC and SCC on histo
aggressive subtype of BCC
5% risk of mets
must completely excise
Which BCCs are not suitable for curretage (unless as palliative procedure)?
Large tumours (≥2 cm diameter)
Tumours at sites where curettage produces a poor cosmetic result, is technically
difficult or is associated with a high risk of recurrence (most of face and scalp off limits except mid cheek)
Morphoeic, infiltrating or basisquamous BCCs
Tumours penetrating muscle, fat, bone, etc.
Tumours where an incisional biopsy has been performed
What are the indications for Mohs surgery on BCCs?
high risk sites = mask area on face / scalp/ anatomic fusion planes/ periorbital or eyelid
tumour > 2cm
aggressive histological subtypes
incompletely exc BCC
Previously RXT Rx area
situations requiring conservation of normal tissue or highest probability of cure
some SCCs can be treated by C+C
If well-differentiated, primary, slowgrowing SCC arising on sun-exposed sites and no high risk factors in tumour or patient
>95% cure rate
esp good for older patients
How does tumour thickness impact on SCC risk?
less than 2mm virtually no risk of mets
2-4mm some risk
6mm thick or more = highest risk of mets
Which dermatoses predispose to NMSC?
Occulocutaneous albinism - SCC
XP - those SCC
Chronic non-healing wounds (Morjolin ulcer)
Lichen planus (erosive)
Skin fistulae or discharging sinuses
HS esp perianal
What is the risk of SCC arising from AK?
less than 0.1% per lesion per year
What are the drawbacks of treating BCC with LN2?
histology not possible
fibrous scar tissue may obscure recurrence
But 99% cure rate for DFTC
BCCs with involved margins always need re-excision
If low rsik type in low risk site and involved lateral margin on direct side-to-side closure can observe
In other cases Mohs best
Photodynamic therapy has a 14% better chance of complete lesion clearance at 3 months after treatment than cryotherapy for thin AKs on the face and scalp
JAMA Derm meta-analysis 2015
HPV 16 is the most common type found in
patients with penile cancer, followed by HPV types 18,
6, and 11
HPV found in 50-63% of penile SCC
JAAD CME 2015
75% of penile cancers are SCC
JAAD CME 2015
QLD has highest incidence of both SCC and BCC in Aus
and Aus has highest rates in the world
Perineural invasion occurs is seen in 10% of NMSC
What is incidental PNI?
When there are no clinical signs or symptoms or radiological evidence of PNI or perineural spread
What are the histological high risk factors in PNI?
Multifocal: >1 focus of PNI seen
Involves nerve of diameter >1mm (1mm and under is lower risk)
Extratumoral PNI (implies possible perineural spread)
When can clinical perineural invasion be diagnosed?
defined as one of the following;
Dysaesthesia (formication) and positive imaging for PNI
Facial nerve palsy in setting of a cutaneous tumour w/ or w/out evidence of PNI on histo
Cranial or spinal nerve involved on histo
Consider recurrence due to PNI if formication occurs at or near site of skin cancer excision
Can do MRNeurography to assess
What are complications of SLNB?
allergic reactions to the blue dye used intraoperatively
cutaneous lymphatic fistula
What stain differentiates merkel cell carcinoma from metastatic deposit of small cell lung carcinoma?
- positive in MCC, negative if SSLC
What IHC stains are posiitve in Merkel cell carcinoma?
Merkel Cell Carcinoma is a rare highly aggressive primary cutaneous carcinoma of skin with epithelial and endocrine features
derived from skin mechanorceptor Merkel cells
neuroendocrine in origin
What are risk factors for Merkel Cell Carcinoma?
solar damage esp in fiar skin
Older age (>50)
What are clues to the diagnosis of Merkel Cell Carcinoma?
Asymptomatic/lack of tenderness
Over 50 years
Ultraviolet-exposed site on a person with fair skin
Most Merkel Cell Carcinomas occur on the trunk
Most on head and neck - 53%
extremities - 35%
Trunk, oral and genital mucosa
5-yr survival of Merkel Cell Carcinoma is approximately 50%
10-yr survival of Merkel Cell Carcinoma is approximately 50%
What are poor prognostic histo features of Merkel Cell Carcinoma?
Dense mononuclear inflammatory cell infiltrate
Deep extension (esp into subcutis)
Diffuse growth pattern including lymphovascular invasion
What are poor prognostic clinical features of Merkel Cell Carcinoma?
head and neck site
tumour Diameter over 5cm (stage T3)
Lymph node status is the most important independent predictor
How are Merkel Cell Carcinomas staged?
should always stage tumour
5 yr survival 80% if stage 1A (tumour up to 2cm max diameter)
How is Merkel Cell Carcinoma managed?
Diagnosis of MCC should prompt FSE and clinical palpation of regional LNs for nodal involvement
Usually referred to plastic/soft tissue surgeon
SLNB for all lesions at time of WLE
- margin recommendations vary; 3cm (Robinson); others say 1-2cm
- LN dissection if SLNB +ve
PET CT for staging
Offer Adjuvant XRT to tumour region – reduced local relapse but not improved mortality
Consider adjuvant chemo if LN +ve or metastatic – but no proven benefit and signif morbidity
Close folow up and consider PET-CT every year for 5yrs
How is DFSP managed?
WLE - 1.5-2cm if 2cm diameter (Rob/Rook); 2-4cm if >2cm diameter or Mohs
Staged excision with margin control (Slow Moh’s) is an option
Post op radiotherapy may reduce recurrence
Can use imatinib (Gleevac) if unresectable/metastatic – some data to support use as adjuvant
DFSP has local recurrence rate of 15-60%
Mets to LNs or organs rare
except for fibrosarcomatous variant (herring bone pattern); Presence and amount of fibrosarcomatous areas relates directly to recurrence rate and metastatic potential
AFX only occurs in sun damaged skin of older people
AFX is a diagnosis of exclusion
Stains should be done in all cases;
sarcomatous SCC (pan-keratin; MNF116 or AE1/AE3)
leimyosarcoma (desmin, SMA)
CD10 and CD99 usually +ve in AFX
Also +ve for Vimentin, CD31, CD34, CD68
Dermatofibroma is always negative for CD34
May be focally positive for CD34 esp at periphery
Which subtypes of Dermatofibroma are classes as high risk?
Cellular(25%), Atypical(14%) and Aneurysmal(19%)
Cellular and Atypical
the 4th main variant is Epitheloid fibrous histiocytoma
What are treatment options for Kaposis Sarcoma?
If HIV/AIDS-related best treated with HAART
Organ transplant KS – Reduce immunosuppression, substitute sirolimus for CsA can lead to improvement
EOL, XRT, LN cryo, CO2 or PDLaser, PDT, 5FU, aldara, topical alitretinoin
For individual lesions - intralesional vincristine, cisplatin or bleomycin +/- prior diathermy
XRT for multifocal disease
Chemotherapy (doxorubicin, vincristine, etoposide, bleomycin) or IFN alpha indicated if; Rapidly progressive/ pulmonary KS/ symptomatic visceral involvement/ lymphoedema
Systemic IL-2 or Bexarotene also reported
Angiogenesis inhibitors; thalidomide, COL3, antiVEGF
Angiosarcoma can arise as a complication of lymphoedema
T - classical presentation
Known as Stewart-Treves syndrome esp if arises after radical mastectomy or XRT for Ca breast
4 types of Angiosarcoma - PILL;
- Post XRT
- Idiopathic (esp face of old men)
- Lymphoedema associated
- arising in Lymphatic or vascular malformation
What is the management of Angiosarcoma?
WLE + adjuvant XRT
high risk of both recurrence and mets
Doxorubicin chemo for palliation if unresectable mets
What is an AFX if it extends into fat?
Undifferentiated pleomorphic sarcoma
connective tissue lesion that needs to be dealt with by specialist surgeon/oncologist; worse prognosis
What is Gryzbowski syndrome?
generalised eruptive keratoacanthomas
sudden onset acquired condition cause unknown
young-mid aged adults, M=F
small widespread KAs - benign behaviour
B/g widespread erythematous rash
scleroderma and ectropion of face
white papules in mouth and nodules on larynx causing hoarseness
Resolves in months if treated;Acitretin, isotretinoin
what is the risk of mets from an SCC?
what is the risk of recurrence of an SCC?
overall risk 3%
Efudix has the best evidence of all topicals for field AK treatment
Immiquimod has good long term clearance rates as thought to cause induction of specific memory T cells that maintain immune surveillance against AKs
Efudix, immiquimod, picato and solaraze all have similar efficacy
But elsewhere JAAD rw states solaraze may have lower efficacy than other agents
What non surgical options are available for sfBCC?
Which is best?
XRT - good cure rates but risk of aggressive recurrence
Aldara has 80% CR confirmed in long term studies
aldara and efudix are effective for erythroplasia of Queyrat
Both have shown some effect in case reports but complete excsion is treatment of choice
If topicals used need close follow up as high rates of recurrence
What is the genetic aberration responsible for DFSP?
Chr 17;22 translocation
results in ring chromasome on FISH (can also identify on PCR)
Involved genes are collagen type 1 alpha 1 (COL1A1) gene on chromosome 17 and platelet derived growth factor B (PDGFB) gene on chr 22
Basis for Imatinib Rx (PDGF receptor inhibitor)
AFX recurs in 25%
What pts are at risk of multiple DFSPs?
pts with SCID due to adenosine deaminase deficiency