Fwd: Skin Cancer (Cormac Joyce)
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Transcript of Fwd: Skin Cancer (Cormac Joyce)
Skin Cancer
September 17th 2008Cormac Joyce
Basal Cell Carcinoma
BCC
Most common cutaneous malignancy Almost NEVER metastasizes• Often leads to local destruction Usually arise from epidermis or outer
root sheath of hair follicle
Epidemiology
Most common in fair skin• Fitzpatrick types : I and II Males > Females Rarely found before age 40
Fitzpatrick Skin Types
Type 1• Pale skin• Blond, red hair• Never tans
Fitzpatrick Skin Types
Type 2• Fair skin, blue eyes• Burns easily• Tans poorly
. .
Fitzpatrick Skin Types
Type 3• Darker white skin• Tans after burning first
Fitzpatrick Skin Types
Type 4• Light brown skin• Burns minimally• Tans easily
Fitzpatrick Skin Types
Type 5• Brown skin• Tans easily• Rarely burns
Fitzpatrick Skin Types
Type 6• Black skin• Never burns
Aetiology
Sunlight: mainly UVB Artificial UVB: Tanning salons Ionizing radiation• For acne treatment Immunosuppression• Renal transplants etc
Aetiology
Xeroderma Pigmentosa• Autosomal recessive: inability to repair UV
damaged DNA,increased risk of all skin Ca.• Other features: corneal deposits, blindness Gorlin syndrome• Autosomal Dominant• Odontogenic keratocysts, palmoplantar
pitting, intracranial calcs, rib anomalies
Aetiology
Bazex Syndrome• Features:
-follicular atrophoderma : “ice pick hands”
-local anhydrosis
-multiple BCCs Hx of previous non-melanoma skin Ca
Types of BCC
Nodular-Ulcerative Cystic Pigmented Sclerosing Superficial
Types of BCC
Nodular-ulcerative• Most common type• Raised, round pearly lesion• As it enlarges : telangiectasia and
central ulceration• Mainly on face
Nodular BCC
Types of BCC
Cystic• Uncommon variant of nodular• Polypoid appearance• Typically blue-grey cyst
Types of BCC
Pigmented• Brown - black macules in some areas• Difficult to distinguish from MM
Types of BCC
Sclerosing• White-yellow, waxy sclerotic plaque• Increased collagen deposit from
fibroblasts- thus resembling a scar• Margins are difficult to see
Types of BCC
Superficial• Erythematous patch or plaque• Multicentric
-normal skin interspersed with malignant patches
Investigations
Biopsy• Punch• Shave• Incisional• Excisional• Deep-wedge
Investigations
Imaging• Not required as very little risk of
metastasis < 0.01%
Treatment
Medical• 5-FU cream (Efudex)
-T bd x 2/52
-cure in 93% in some trials
-surgery is preferred
Treatment
Surgery• Excision
-direct closure
-local flap
-FTSG ie PAWG (Wolf)• Mohs Micrographically controlled
surgery
Mohs Surgery
Tumour excised and 1mm of surrounding tissue is examined under microscope
Additional pieces of tumour are removed in the persisting area
Highest cure rate: 99% Time consuming, LA top ups required
Recurrence
Risk factors:• BCC in NL fold• Recurrent tumours• Large tumours >2cm• Deeply infiltrating tumours• Young females
Squamous Cell Carcinoma
Squamous Cell Carcinoma
2nd most common skin Ca Malignant tumour of epidermal
keratinocytes Can Metastasize Strongly related to sun exposure 70% occur on head and neck
Epidemiology
Age > 50 Fitzpatrick I and II Males Closer to equator
Aetiology
Sunlight: UVB Sunbeds Ionizing Radiation Arsenic Xeroderma
Pigmentosa Transplants:
greatest in heart
HPV: 5,6,8,11,16 Chronic Ulcers:
Marjolins Burns Necrobiotic
Lipoidica Hidradenitis Actinic Keratosis
SCC
Bowens Disease
Intra-epidermal form of SCC SCC in situ: BM not invaded Well demarcated erythematous plaque• Irregular border• Surface crusting or scaling Rx: Photodynamic therapy, Cryotherapy
or topical 5-FU.
Bowens Disease
SCC Types
Typical: most common Periungual Perioral Marjolins Anogenital Verrucous
Typical SCC
A raised, firm, pink-to-flesh–coloured keratotic papule or plaque arising on sun-exposed skin
70% occur on head and neck Surface changes may include: Scaling Ulceration Crusting
SCC Pathophysiology
malignant tumour of epidermal keratinocytes
De novo or from actinic keratoses Capable of: Local infiltration Spread to regional nodes Distant mets
Investigations
Biopsy Incisional Excisional Punch Must reach level of mid dermis to see if
invasion has occurred
Investigations
If a patient has lymphadenopathy:• Imaging studies: CT• LN biopsy or FNA• May require lympadenectomy of the
draining basin
Staging: AJCC
Use TNM guidelines Most SCC are not metastatic at time of
presentation
Staging: AJCC
Classification of primary tumour:• T0: no evidence of primary• Tis: Ca in situ• T1: <2cm in greatest diameter• T2: 2-5cm in greatest diameter• T3: >5cm in greatest diameter• T4: deep invasion; bone,cartilage, muscle
Medical Care
Topical therapy• For premalignant and in-situ lesions• Efudex (5 FU)Topical immune response modifier enhances cell-mediated immune
responses via the induction of proinflammatory cytokines
e.g. imidazoquinoline (Imiquimod)
Medical Care
Radiotherapy• Indications:
-patients refusing/not fit for surgery
-metastatic disease
Medical Care
Radiotherapy problems:• Expensive and time consuming• Irritation at site: erythema, erosions• Pain: requiring narcotic analgesia• Poor long term cosmesis: cutaneous atrophy,
dyspigmentation, telangiectasia• Increased risk of further cutaneous
malignancy
Surgery
Cryotherapy• Liquid nitrogen• For selective SCCs: AKs or Cis• Complications:
-transient pain
-oedema
-blistering
Surgery
Electrodessication and Curettage• Indications; AK and Cis• Tumour margins are delineated with a
curette and scraped out: tumour is far more friable than normal tissue
• Main disadvantage is loss of margin• Cure rates of 96-99% have been quoted
Surgery
Excision with conventional margins• 4mm margin for low risk lesions:
<2cm, well differentiated, without fat invasion
• 6mm margin for higher risk lesions:
>2cm, fat invasion, high risk areas- central face, ears, genitalia
Surgery
Mohs Micrographic Surgery • Excellent option if tissue preservation is
required• Almost 100% of histologic margin is
examined (compared to 1% in conventional excision)
Surgery
Mohs Micrographic Surgery• Best cure rates for SCC (94-99%)• Local recurrences are fewer
Chemotherapy
Useful for metastatic disease Capecitabine (Xeloda) and IFN α
Prognosis
Variable:• Tumor- and patient-related risk
factors associated with higher rates of recurrence and metastasis are as follows:
Prognosis
Tumor-related factors in high-risk SCC:
• Location: lips, ears, scar• Tumour size > 2cm• Poorly diff tumour• Recurrent tumour• Perineural involvement
Prognosis
Patient-related factors in high-risk SCC
• Organ transplant recipient• Haematological malignancy ie CLL• Chronic immunosuppression• HIV infection
Prognosis: Overall
The 3-year disease-specific survival rate is 85%
Almost 100% if none of previous risk factors
70% if 1 risk factor present
The Future?
NSAIDS:• May protect against SCC development• COX 2 often overexpressed in SCC• Studies are ongoing
Malignant Melanoma
MM
A malignancy of pigment producing melanocytes
Predominantly skin Also: eyes, ears, GI tract, and oral and
genital mucous membranes
MM
Accounts for 4% of skin cancers Responsible for 74% of all skin cancer
deaths
Frequency
6th most common cancer in U.S. 1 in 60 lifetime risk of developing
melanoma in Caucasians Highest incidence in Australia and NZ Incidence increasing worldwide.
Epidemiology
Primarily disease of whites• Whites: African-Americans = 20:1• MR far higher in darker skin types Incidence greatest in females Mortality highest in males Median age at Dx = 53
Aetiology/Risk factors
Changing mole Atypical naevus Large numbers of
common naevi >100 Naevus >20cm Previous melanoma Sun exposure 1st degree relative
BCC/SCC Male >50 XP Fitzpatrick I and II Immunosuppression
Pathophysiology
Tumour progression: 5 stages
1. Benign melanocytic naevus
2. Dysplastic naevus: cytolological atypia
3. Primary MM: radial growth phase
4. Primary MM: vertical growth phase
5. Metastatic MM
Classification
1. Superficial Spreading Melanoma
2. Nodular Melanoma
3. Lentigo Maligna Melanoma
4. Acral Lentiginous Melanoma
5. Amelanocytic Melanoma
6. Rare sub-types
Superficial Spreading Melanoma
Most common, accounts for 70% Usually > 6mm in diameter Occurs most commonly:• On trunk in men• On legs in women
Superficial Spreading Melanoma
Irregular, asymmetric borders are characteristic
Histologically, characterized by “buckshot scatter “(pagetoid) of atypical melanocytes within the epidermis
Superficial Spreading Melanoma
Nodular Melanoma
Second most common : 25% Legs and trunk are most common sites Raised dark brown-black papule or
nodule Usually lacks the ABCDE warning signs Lacks radial growth phase
Nodular Melanoma
Nodular Melanoma
Lentigo Maligna Melanoma
Accounts for 4-10% Most common on head, neck and arms Precursor lesion = lentigo maligna• Usually present for 10-15yrs• Dark brown macule or patch Dermal invasion characterized by raised
blue-black lesions within precursor
Lentigo Maligna Melanoma
In Australia: on the face..• More common in men on RHS• More common in women on LHS
Lentigo Maligna Melanoma
Acral Lentiginous Melanoma
Accounts for 2-4% Accounts for 55% in dark skinned
individuals Usually occurs in glabrous skin or beneath
the nail plate (subungual variant) Pigment spread to the proximal or lateral
nail folds is termed the “Hutchinson sign”
Acral Lentiginous Melanoma
Characteristic features:• Irregular pigmentation• Large size > 3cm• Plantar location
Acral Lentiginous Melanoma
Amelanotic Melanoma
Non pigmented Pink or flesh coloured – often mimicking
BCC or SCC
Rare Sub-Types
Desmoplastic Melanoma Mucosal Melanoma Malignant Blue Naevus Melanoma of Soft Parts (clear cell
sarcoma)
Assessment
History Exam• Inspection alone can diagnose 65%• Nodes: axillary, cervical and groin
Assessment
MacKies 7 point checklist Major (2 points each)• Change in size• Irregular pigmentation• Irregular outline• Diameter > 6mm
Assessment
MacKies 7 point checklist Minor (1 point each)• Inflammation• Oozing• Itch or altered sensation
Assessment
MacKies 7 point checklist Needs further evaluation in presence of
one major or if score = 3
Assessment
American ABCDE• A: asymmetry• B: border is irregular• C: colour variation• D: diameter >6mm• E: examine other lesions
ABCDE
Biopsy
Incisional Excisional Punch
NB not shave
Biopsy
Information gained from biopsy:• Tumour depth• Anatomical level• Ulceration• Presence of mitoses• LVI• Host response (tumour infiltrating
lymphocytes)
Biopsy
Information gained from biopsy: ctd• Regression• Immunohistochemical staining for
lineage: (S-100) or for proliferation markers (Ki67)
Biopsy
Excisional biopsy• 1-3mm of normal skin should be
removed with the lesion as more than this could disrupt lymphatic drainage and compromise subsequent LN mapping
Clarkes Level
Classifies level of invasion Level 1: only epidermis involved Level 2: invades part of papillary dermis Level 3: invasion fills papillary dermis Level 4: invades reticular dermis Level 5: invades subcutaneous tissue
Breslows Thickness
Most important histological determinant of prognosis
Measured vertically in mm• From top of granular layer (base of
superficial ulceration)• To deepest point of tumour invasion
Breslows Thickness
5yr survival
1. </= 0.75mm 90%
2. 0.76mm – 1.5mm 80%
3. 1.5mm – 4mm 65%
4. >/= 4mm 35%
Breslows Thickness
Gives better indication of prognosis• As depth (Clarkes) of papillary and
reticular dermis vary throughout the body
Staging
AJCC• Incorporates TNM with Clarkes and
Breslow
Spread
Locally, in LN basins or distally:• Remote skin• Remote nodes• Viscera• Skeleton• CNS
Surgery
Excision margins;• 0.5 cm for melanoma in situ• 1cm with Breslow thickness <2mm• 2cm with Breslow thickness >/= 2mm
Surgery
Melanomas near vital structures may require a reduced margin
Aggressive histological features may necessitate a wider margin
Mohs surgery may have certain "niche" indications- MM of face, neck or hands
Sentinel Node Mapping
Growing in popularity Isosulfan blue dye and
lymphoscintigraphy Is it as useful as mapping in breast Ca?
Sentinel Node Mapping
Advantages• If node –ve, no need for nodal
clearance• More thorough pathological assessment
of nodes• Psychological relief to patient if node
negative
Sentinel Node Mapping
Disadvantages• Poor mapping in head and neck
tumours• Tumour may skip SN
Sentinel Node Mapping
Indications: controversial• Patients in whom the estimated risk of
LN metastasis is at least 10%• Clinically node –ve patients with
tumours >/= 1mm Not indicated in tumours <0.75mm 0.76-0.9mm: nebulous area
Elective LN Dissection
Lymphadenectomy when nodes are clinically negative
Rationale is that MM spreads to nodal basin first – so clearing the LNs reduces risk of spread
Controversial: studies have conflicting results
Nodal Dissection
Patients with palpable, clinically +ve nodes should undergo complete nodal dissection
Adjuvant Therapy
Interferon α 2b• For high risk resected MM: >4mm depth Regional nodal metastases• Diminishes occurrence of mets• Prolongs disease free survival
Chemotherapy
For unresectable regional mets or distant mets
Dacarbazine is the most active chemotherapeutic agent
Biological Therapy
Interleukin 2• Useful for metastatic melanoma• In one study, 7% had complete
response with patients remaining disease free for up to 8yrs
Biological Therapy
Monoclonal antibody therapy• Experimental but very promising Vaccines • Undergoing trials currently
Perfusion Chemo
Isolated Limb Perfusion (ILP)• Tourniquet applied• Artery and vein cannulated• Agent infused and removed from
circulation• Most effective method of Rx for local
recurrence or in-transit metastases• Agents used: TNFα, melphalan
Radiotherapy
For palliation Specific indications:• Brain metastases• Pain with bony mets• Superficial subcutaneous mets
Prevention
Public education• Australia: “slip, slop, slap” campaign Adequate clothing Avoid UV rays Systemic carotenoids : retinol• Useful in preventing malignant
transformation
Thank You
Will be on Blackboard tomorrow!!