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Scc
- 2.
- 5. Incidence • 2nd mostcommon skin cancer – Behind BCC, accounting for 20% skin cancers • Due to propensity to metastasise, makes them responsible for majority of NMSC deaths
- 6. Pathogenesis • UV – Incidence doubles with 8-10 degrees decrease in latitude – Induces formation of pyrimidine dimers resulting in DNA point mutations – Causes mutations in p53 tumour suppressor gene
- 7. • Skin pigmentation •Age • Primary dermatoses – xeroderma pigmentosa, oculocutaneous albinism
- 8. • Immunosuppression –due to immunosuppressive drugs, UVR, viral infection esp HPV – Reversed ratio of BCC:SCC, SCC being 3x more common in transplant patients – Higher rates – cumulative risk of SCC/ BCC in heart transplant recipient is 3% at one year, 21% at 5 years, 35% at 10 years
- 9. Histological subtypes • Pleomorphic • Adenoid/Acantholytic • Simplex • Small cell • Verrucous • Keratoacanthoma • Actinic keratosis • Bowenoid/Erythoplasia of Queyrat
- 10. Simplex • Majority ofSCCs • Atypical keratinocytes develop within epidermis and invade the dermis • Tumour cells are enlarged, hyperchromatic, variably pleomorphic nuclei, prominent mitotic activity • Keratin pearls
- 11. Actinic Keratosis • AlsoSCC in situ, micro invasive SCC, as there is considerable overlap in the histology • Atypical keratinocytes that have not breached the dermal barrier – SCCIS is typically full thickness keratinocyte atypia
- 12. • Rate ofmalignant transformation is 0.1% per lesion per year – About 16% will eventually transform – Can progress to other skin cancers such as sebaceous carcinoma
- 13. Pleomorphic • AKA spindle/ sarcomatoid, RARE • Associated with previous trauma or RTX • Most commonly found on face or sun exposed areas of elderly • Commonly ulcerate, but may present as an exophytic mass
- 14. • Microscopically whorlsof atypical squamous cells co- mingle with collagen fibres • Pleomorphic giant/spindle cells may be present • Neoplastic keratinocytes have hyperchromatic eosinophilic cytoplasm, elongated, pleomorphic and veiscular nuclei with multiple nucleoli
- 15. Small cell • Mayresemble metastatic small cell neuroendocrine carcinoma or Merkel cell carcinoma • Invades in cohesive nests with adjacent intense inflammatory and desmoplastic host response • Stains for cytokeratin, but may stain for neuron specific enolase (NSE), a neuroendocrine marker
- 16. Verrucous • Exophytic orendophytic masses growing at sites of chronic irritation • Slowly locally invasive, little or no propensity to metastasise • Morphologically appear well differentiated with little atypia • Thickened papillae composed with well differentiated squamous cells invading into dermis
- 17. Verrucous • 3 distinct clinicopathologic subtypes – Oral • Associated with tobacco chewing, betel nut chewing, HPV, poor oral hygiene • Typically wart like white/gray lesion • Well differentiated – Plantar • Many crypt like openings • Slowly enlarging, fleshy pink exophytic mass • Verrucous hyper/para keratotic component, epithelial crypts with keratinaceous debris – Buschke-Loewenstein • Anogenital type, described by B-L in 1925 • Occur most commonly in uncircumcised men under 50, associated with HPV 6 & 11 • Present as caulflower like lesions most commonly on glans penis • Extensive verrucous acanthosis with dermal extension, keratinocyte atypia minimal, hypergranulosis and crypt/sinus formation
- 18. Keratoacanthoma • Period ofrapid growth lasts 4-8 weeks • Potential for spontaneous involution usually within 4-6 months, sometimes with considerable scarring • Clinically tend to be rapid growing smooth, firm nodule with central keratin plug
- 19. • Histologically difficultto distinguish between benign KA and SCC KA type, so being amalgamated by histopathologists • Atypical squamous proliferation with intradermal invasion • Typically crateriform architecture with keratin plug and well developed collarette
- 20. Adenoid / Acantholytic •Form a pseudoglandular appearance • Cells arranged in cords and nests with clefts produced by acantholysis of cells leaving spaces that superficially resemble glands
- 21. • Enlarged freefloating dysplastic keratinocytes found in lumina • Clinically appear as ulcer on head & neck of men in 5th to 6th decade • High incidence of recurrence after radiation therapy • Tend to be more locally aggressive but metastasise less
- 22. Bowenoid • Considered tobe SCC in situ • Most common site is head and neck, followed by limbs and then trunk • Well demarcated, slow growing, erythematous scaly patch, usually small in size
- 23. • Histologically shows hyperkeratosis, acanthosis, psoriasiform hyperplasia, full thickness atypia, loss of polarity reflecting cessation of maturation • When neoplastic keratinocytes invade the dermis, this lesion is termed Bowenoid SCC • Especially associated with HPV – HPV2 with extragenital lesions, HPV16 with genital lesions
- 24. Metastasis • Overall riskis 2 – 6%, not 0.5% • Recurrent SCC has metastatic rate of 30%, and metastatic cases had a survival rate of 1/3 • Metastases tend to be to regional lymph nodes • Most mets (and local recurrences) are found within first 2 years, and 95% within first 5 years
- 25. Risk factors formetastasis and recurrence • Recurrence rate doubled and tripled metastatic rate – Size > 2cm – Grade 3 & 4 vs. Grade 1 & 2 tumours • Well differentiated has recurrence 7%, mod well diff 23%, poor diff 28% • Tumour thickness – 3 year recurrence free survival is 98% for <3.5mm, 84% for > 3.5mm (Breslow thickness) • Rapid growth rate
- 26. • Sun exposed areas tend to metastasise and recur less than mucosal SCC • Scar SCC are very aggressive • Lip and ear SCC have higher metastatic rate than other head and neck sites (16 & 10%) – Probably due to decreased subcutaneous fat – Nose and scalp, anogenital are intermediate risk – Periungal SCC has high recurrence rate but almost never metastasises • Previous treatment – recurrent cancers have a metastatic rate of 25% – Location – ear 45%, lip 32% metastatic rate
- 27. • Histopathology – Isolated strands, infiltrative pattern, haphazard growth vs. broad pushing borders – Perineural invasion (occurs in 2-14% SCC, most commonly H&N in elderly men) • Has been quoted as local recurrence 47%, regional mets 35%, distant nodes 15%; so post op RTX commonly offered – NO good evidence that any subtype has greater risk recurrence or metastasis
- 28. Immunosuppression – Biologically moreaggressive, with higher rates of lymph node metastases and deaths secondary to skin cancer
- 29. Tumour size Size (cm) Metastatic 5 yr disease free rate survival T <2 1.4% 95-99% 1 T 2–4 9.2% 85-60% 2 T >4 > 13% 75-60% 3 T Invading deep < 40% 4 structures
- 30. Tumour depth andmetastatic rate Depth Metastatic rate < 2mm 0 2 – 6mm 4.5% > 6mm 15%
- 31. Grades Broder’s Grade Undifferentiated Ratio of cells differentiated cells I – Well < 25% 3:1 differentiated II – Moderately 25 – 50% 1:1 well differentiated III – Poorly 50 – 75% 1:3 differentiated IV – Anaplastic or > 75% Nil pleomorphic
- 32. Surgical Management • Tumours< 2cm diameter are successfully excised 95% of the time with a margin of 4mm, 6mm for high risk cases (Brodland & Zitelli) • Tumours > 2cm diameter require margin of 10mm for equivalent local control rates • Moh’s surgery
- 33. Other modalities • Dessicationand curettage – Lesions less than 2cm diameter have cure rates of 97-98.8% • Cryosurgery – Well localised, superficial lesions on trunk or limbs • 5FU & Imiquimod & Photodynamic therapy – Useful for actinic keratoses
- 34. Radiation Therapy – <2cm tumours have a cure rate of 95% – Adjunctive RTX must be given within 8 weeks for greatest efficiency – (Late) changes include : – atrophy, fibrosis, hypopigmentation, telangiectasia, ulceration – “As late results of RTX can be poor, it is not recommended for patients under 60 yo with uncomplicated primary SCC” – May hasten natural history of KA