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CLASSIFICATION OF CUTANEOUS MALIGNANCIES PowerPoint Presentation
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CLASSIFICATION OF CUTANEOUS MALIGNANCIES

CLASSIFICATION OF CUTANEOUS MALIGNANCIES

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CLASSIFICATION OF CUTANEOUS MALIGNANCIES

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  1. CLASSIFICATION OF CUTANEOUS MALIGNANCIES

  2. Actinic keratosis Bowen’s disease Lentigo maligna Keratinocyte Keratinocyte Melanocyte 1- PREMALİGNANCİES (in situ)

  3. Basal cell carcinoma Squamous cell carcinoma Keratoacanthoma Debatable ( follicular keratinocyte, basal keratinocyte, primary germ cell ) Keratinocyte Follicular keratinocyte 2- COMMON CUTANEOUS MALİGNANCİES

  4. Malignant melanoma Lentigo maligna melanoma Melanocyte Melanocyte 3- MELANOMAS

  5. Sweat gland carcinomas Follicular carcinomas Extramammary Paget’s disease Merkel cell carcinoma Atypical fibroxanthoma Dermatofibrosarcoma protuberans Fibrosarcoma Angiosarcoma Kaposi’s sarcoma Hemangiopericytoma Malignant peripheral nerve sheath tms Liposarcoma Apocrine or eccrine sweat gland / duct Follicular epithelial cells Unknown- apocrine Fibroblast or dermal dendrocyte Fibroblast Fibroblast Fibroblast Endothelial cell Endothelial cell Pericyte Schwann cells Lipocyte 4- UNCOMMON CUTANEOUS MALİGNANCİES

  6. COMMON CUTANEOUS MALİGNANCİES Primary cutaneous cancers are classified on the basis of their cell of origin within the skin. They originate most commonly in the epidermal germinative keratinocytes or adnexal structures (e.g.,sweat apparatus, hair follicle).The two principal cutaneous epithelial cancers(nonmelanoma skin cancers- NMSC-) are basal cell carcinoma (BCC) and squamous cell carcinoma (SCC).

  7. SQUAMOUS CELL CARCINOMA (SCC) • Malignant tumour of keratinocytes, arising in the epidermis, skin appendages, and other stratified squamous mucosa. • SCC usually arises in epidermal precancerous lesions • The majority of UVR-induced lesions have a low rate of distant metastasis in otherwise healty individuals. • More aggressive SCC occur in immunosuppressed individuals with a greater incidence of metastasis.

  8. SCC (2) • Etiology: Ultraviolet radiation (sunlight, phototherapy), Human Papillomavirus (HPV), Immunosuppression, Chronic inflammation ( DLE, chronic ulcers, burn scars, chronic radiation dermatitis, lichen planus of oral mucosa), Industrial Carcinogens (Pitch, tar, crude paraffin oil, fuel oil, creosote, nitrosureas), Inorganic arsenic. • Differential diagnosis: Any persistent nodule, plaque, or ulcer, but especially when these occur in sun-damaged skin, on the lower lips, in areas of radiodermatitis, in old burn scars, or on the genitalia. Keratoacanthoma may be clinically indistinguishable from differentiated SCC. • Course and prognosis: Significant potential for metastasis; metastases are directed to regional lymph nodes. SCC in the skin has an overall metastatic rate of 3 to 4%. Cancers arising in chronic osteomyelitis sinus tracts, in burn scars, and in sites of radiation dermatitis have a metastatic rate of 31, 20, and 18 %, respectively. • High-risk SCCs: Diameter > 2 cm, depth > 4 mm, inolvement of bone, muscle, and nerve, location on ear, lip and genitalia, tumors arising in a scar or following ionizing radiation, highly dedifferentiated tumours, in immunosuppressed patients. • Management: Surgery, radiotherapy

  9. SCC IN SITU (SCCIS) • SCCIS is most common caused by UVR or HPV infection, presenting as solitary or multiple macules, papules, or plaques, which may be scaling or hyperkeratotic. • SCCIS commonly arises in epithelial dysplastic lesions such as solar keratoses or HPV-induced squamous intraepithelial lesions (SIL) • Bowen’s disease • Erythroplasia of Queyrat (glans penis, labia minora) • Bowenoid papulosis (anogenital) • Differential diagnosis: Nummuler eczema, psoriasis, seborrheic keratosis, solar keratosis, verruca vulgaris, condyloma acuminatum, superficial BCC, amelanotic melanoma, Paget’s disease • Course and prognosis: Untreated SCCIS will progress to invasive SCC. Lymph node metastasis can occur without demonstrable invasion. • Management: Topical 5-FU, imiquimod, cryosurgery, photodynamic therapy, surgical excision

  10. BASAL CELL CARCINOMA (BCC) • Most common type of skin cancer. • Locally invasive, destructive, but there is very limited capacity to metastasize. • SPT I and II with prolonged sun exposure • Five clinical types: NodularBCC, Ulcerating BCC, Sclerosing BCC, Superficial spreading BCC, Pigmented BCC • Distribution: Isolated single lesion, >90% occur in the face. Superficial spreading (multicentric) BCCs occur on the trunk. • Course and prognosis: BCC does not metastasize.

  11. BCC (2) • Differential diagnosis: All smooth papules like dermal nevus, trichoepitelioma, dermatofibroma, and others; if pigmented, superficial spreading and nodular melanoma; if ulceratedall nonpainful firm ulcers including SCC and a (extragenital) primary chancre of syphilis. • Management: Excision with primary closure, skin flaps or grafts, cryosurgery or electrosurgery, Mohs surgery, radiation therapy, topical 5-FU, imiquimod cream, photodynamic therapy.

  12. KERATOACANTHOMA (KA) • KA is a special lesion, a pseudocancer, occurring as an isolated nodule, usually on the face, and mimicking SCC. • Rapid growth! Achieving a size of 2.5 cm within a few weeks. • Etiology: HPV, UVR, chemical carcinogens (pitch, tar). • Differential diagnosis: SCC, hypertrophic actinic keratosis, verruca vulgaris. • Spontaneous regression in 2 to 6 months or sometimes > 1 year. • Management: Surgery

  13. CUTANEOUS T CELL LYMPHOMA (CTCL) • CTCL is a term that applies to T cell lymphoma first manifested in the skin. • The lymph nodes and internal organs become involved in the course of the disease. • CTCL is a malignancy of helper T cells (CD4+). • All Mycosis Fungoides (MF) is CTCL, not all CTCLs are MF. • Differential diagnosis: Atypical or refractory “ psoriasis”, “eczema”, and poikiloderma. • Management: Phototherapy (PUVA, UVB), isotretinoin, s.c interferon, topical nitrogen mustard, topical potent steroid (early patch stage), electron-beam therapy, chemotherapy.