Skin Malignancies BCC SCC MM

Skin Malignancies Basal Cell Carcinoms Squamous Cell Carcinoma Malignant Melanoma

1. Skin Malignancies;
BCC,SCC,MM
DrOkoye
29/04/2019

2. Outline
Introduction
–Epidemiology
–Skin Histology
Etiologic / risk factors
Pathology
Classification
Diagnosis
–History
–Examination
–Investigations

3. Outline
•Treatment
–Surgical
–Non Surgical
•Prevention
•Follow up
•Conclusion
•References

4. Introduction
•Skin malignancies/cancers are cancers that arise
from the skin
•They are due to the development of abnormal cells
that have the ability to invade or spread to other
parts of the body.
•There are three main types of skin cancers: Basal
Cell Carcinoma(BCC), Squamous-Cell Carcinoma
(SCC) and Malignant Melanoma(MM).

5. •Basal-cell carcinoma grows slowly and can
damage the tissue around it but is unlikely to
spread to distant areas or result in death.
•Squamous-cell skin carcinoma is more likely to
spread.It usually presents as a hard lump with a
scaly top but may also form an ulcer.
•Melanomas are the most aggressive. Signs include
a mole that has changed in size, shape, color, has
irregular edges, has more than one color, is itchy
or bleeds.

6. Epidemiology
•800,000 cases per year
•Incidence is increasing
•Mortality is decreasing
•Most occur in patients over 60 years

7. BCC
•Common in caucasiansof northern Europe
descent & rare in Africans.
•90% occur in the face above the corner of
the mouth to the ear lobe, can also occur
anywhere in the body.
•Incidence is the same for both sexes.

8. SCC
•5% is found in Africans
•Head & Neck region in caucasians
•Commoner in males –lifetime risk 9–14%;
4–9% in women.
•Can also be seen in vulva region, scrotum,
anal canal & uncircumcised penis.

9. MM
•Common in 3
rd
–6
th
decade of life.
•Male dominance (2:1)
•Incidence is increasing over the years with a
worldwide incidence of 2-4/100,000.
•Australia & Queensland has the highest
incidence of 40/100,000.

10. Normal Skin Histology
•Stratum Corneum
•Stratum Lucidum
•Stratum Granulosum
•Stratum Spinosum
•Stratum Basale

12. Etiology/Risk Factors
•Ultraviolet light
–Sun Exposure–Ionizing radiation causes
mutation of tumor suppressor genes
–UV B light: 280-320nm, UV A light 320-
400nm–Amount of UV B radiation is inversely
proportional to ozone
•Amount of UV B exposure during childhood and
adolescence is directly proportional to risk for
BCC

13. Etiology/Risk Factors
The following groups have the least melanin and are
at greatest risk for BCC
•fair complexion
•light hair
•inability to tan
•history of multiple or severe sunburns
•celticancestry

14. Etiology/Risk Factors
•Arsenic
•Radiation Therapy
•Burns, Scars, Ulcers
•Immunosuppression
•Albinism

15. Basal Cell Carcinoma
•Slowly growing malignancy of the epidermis
•Rarely metastasizes (.028-.55%)
•Cells appear histologically similar to basal cells of
epidermis

16. Pathogenesis
•Most cases are sporadic.
∘Associated with sun exposure, particularly UVB.
•UV radiation induces gene mutations, notably in
p53 and PTCH1.
•UV-induced inflammation of the skin is also
thought to contribute to pathogenesis.

17. Pathology
Clinical subtypes
•Nodular
•Superficial
•Pigmented
•Morpheaform

18. Pathology
•Nodular
–Discrete, raised, circular
–Central ulceration
–Pink, waxy rolled borders
–Relatively non-aggressive

19. Pathology
•Superficial
–Threadlike, waxy border
–Red, scaling patches
–Spread by radial extension

20. Pathology
•Pigmented
–Resemble nevus or melanoma
–Behave the same as nodular variant

21. Pathology
•Morpheaform
–Macular, whitish, or yellowish plaque
–Indistinct clinical margins

22. •Histology
–Large oval nuclei with little cytoplasm
–Nuclei are uniform
–Connective tissue stromacauses palisading

23. •Histologic Subtypes
–Solid
–Cystic
–Adenoid
–Keratotic(Basosquamous)

24. Clinically;
•Lesion has pearly translucent edges which may
become erythematous or pigmented, and can also
ulcerate and invade underlying structures.
•Talengiectasiais present

25. Squamous Cell Carcinoma
•More aggressive in terms of local invasion and
rate of metastasis than BCC (2-5%)
•Often a progression from sun-damaged areas
•Actinic Keratoses
•Bowen’s disease

26. Histology
•Irregular masses of epidermal cells proliferating
into dermis
•Keratinization in well-differentiated tumors
(Broders)
•Subtypes of Verrucous, Adenoid squamous, and
Spindle Pleomorphic

27. Histology
•Verrucous
–Minimal atypia
–Individual cell keratinization
–White, cauliflower lesions
–Uncommon in Head and Neck

28. Histology
•Spindle-Pleomorphic
–Anaplastic
–Little keratinization

29. Histology
•Adenoid Squamous
–Anaplasia
–Acantholysis
–Tubular and adenoid appearance

30. •Clinically
–SCC presents as a crusting, erythematous,
ulcerated lesion with a granular friable base.

31. Indicators of Metastatic Potential
–Invasion of muscle, bone, or cartilage
–Anatomic site: Ear, lip; locally recurrent
–Size > 2cm
–Poorly differentiated (Broders3 or 4)
–Thickness > 2mm
–Perineuralinvasion
–Invasion of reticular dermis or subcutaneous tissue
–Immunosuppression

33. Malignant Melanoma
•It’s a melanoblastic tumour of the skin. Can arise
de-novo or follows a naevus
•Commoner in caucasians who inhabit countries
near the equator. Uncommon in blacks and
Asians.
•Common in 3
rd
–6
th
decade of life.
•Male dominance (2:1)
•Incidence is increasing over the years with a
worldwide incidence of 2-4/100,000.
•Australia & Queensland has the highest incidence
of 40/100,000.

34. Etiology/Risk Factors
•Exposure to sunburn
•Albinism and fair skin
•Freckles
•Xerodermapigmentosa
•Immunosuppression

35. Classification
•This is based on macroscopic and microscopic
appearance of the tumour. Four morphologic types
are recognized viz;-
1.Superficial spreading
2.Nodular malignant
3.Acrallentiginous
4.Lentigomaligna

36. SUPERFICIALSPREADING MELANOMA
•Commonest in caucasians(55-70%)
•Arises from a mole, characterized by a long
radial growth phase prior to deep invasion
•May be of varied color
•Edge is irregular or notched
•Good prognosis

37. NODULAR MELANOMA
•25%, Blue-black in color
•Elevated plaque with irregular edges
•Arises from dermal-epidermal junction &
can become ulcerated
•Spreads vertically
•Poor prognosis

38. ACRAL LENTIGINOUS
•Commonest form in Negroes(60%), 10% in
caucasians
•Occurs in glabrous skin of sole & palm, nail
bed(subungual), mucosal surfaces.
•Lesions are black & can be amelanotic
•Prognosis depends on depth of invasion,
usually b/w superficial spreading and nodular
melanoma.

39. LENTIGO MALIGNA
•Also called “melanotic freckles of
Hutchinsons”
•Seen in 6
th
-7
th
decade of life
•Lesion are brown-black or varigated
•Common in exposed area of the body
•Prognosis is excellent

40. STAGING
•This could be ;
•CLINICAL
•PATHOLOGICAL

41. CLINICAL STAGING

42. PATHOLOGIC
•This includes
•CLARKE’S which asseses the level of
invasion
•BRESLOW which asseses the depth of
invasion or thickness of the lesion using the
Breslow scale. Its an important indicator for
survival.

44. CLARK’S
•I-;Tumour confined to the epidermis
•II-;Extends into papillary dermis
•III-;Invades papillary dermis and impinge
on reticular dermis
•IV-;Invades reticular dermis
•V-;Invades subcutaneous tissue

45. BRESLOW
•Tumour <0.75mm; Never metastasize
•Tumour >1.5mm; Increase likelihood to
metastasize
•Tumour >3.5mm; > tendency to metastasize

46. TNM CLASSIFICATION
•Tis ; Melanoma insitu, Clark’s level 1
•T1 ; Tumour <0.75mm, Clark’s level 2
•T2 ; Tumour >0.75mm but <1.5mm, Clark’s
level 3
•T3 ; Tumour >1.5mm but <3.5mm, Clark’s
level 4
•T4 ; Tumour >3.5mm, Clark’s level 5

47. TNM CLASSIFICATION CON’T
•N0 ; No nodal involvement
•N1 ; Involve LN <3cm in dimension
•N2 ; Involve LN >3cm & contralateral
•M0 ; No distance metastasis
•M1 ; Distance metastasis present

48. MANAGEMENT
•History & Examination
•Investigations
•Staging / TNM classification
•Treatment

49. INVESTIGATIONS
•HISTOLOGIC
•RADIOLOGIC & IMAGING
•HAEMATOLOGIC
•BLOOD CHEMISTRY

50. TREATMENT
•SURGICAL
•NON SURGICAL

51. TREATMENT
•Excision of lesion & lymph node
•Mohsmicrographic surgery
•Amputation of digit

52. TumorthicknessExcisionmarginRegional lymph
node treatment
In situ 0.5cm None
Lessthan 1mm1cm None
1mm-4mm 2cm Sentinel lymph
node biopsy
>4mm 3cm Sentinel lymph
node biopsy

53. Non Surgical
1.Chemotherapy
2.Immunotherapy
3.Radiotherapy
4.Gene therapy
5.Curettage and cautery
6.Cryotherapy
7.Photodynamic therapy
8.CO2 laser

54. Prevention
•Sun Protection
•Clothing
•Education

55. Follow up
•The greatest hope for controlling this
disease lies in careful surveillance and early
detection of atypical pigmented lesions.
•Follow-up visits are scheduled 3 months
after therapy and every 6 months to 1 year
thereafter for the life of the patient.

56. Conclusion
•Skin cancers are the most common cancers in the
western world, comprising fully 50% of all the
cancers diagnosed every year.
•Their biologic behavior is also quite variable,
some following a relatively benign course and
others progressing to extreme morbidity,
mutilation, metastasis, and death.

57. •THANK YOU

58. References
•Daniel J.C and Keith M.B. Dermatology for Plastic Surgeons II-
Cutaneous Malignancies. Grabb and Smith’s Plastic Surgery. 7
th
edition. China. Lippincott Williams & Wilkins. 2014: 115-124
•Lo JS, Snow SN, Reizner GT, Mohs FE, Larson PO, Hruza GJ.
Metastatic basal cell carcinoma: report of twelve cases with a review
of the literature. J Am Acad Dermatol 1991;24: 715-9.
•Sassmannshausen, MD et al“Pilmatrix carcinoma: A report of a case
arising from a previously excised pilomatrixoma and a review of the
literature,” J Am Acad Dermatol2001;44:358-61.
•Geh JL et al“Unusual multiple pilomatrixomata: case report and
review of the literature,” British Journal of Plastic Surgery. 1999;
52(4):320-1
•Swanson, NA, “Mohs surgery: technique, indications, applications,
and the future.”Arch Dermatol1983; 1, 19:761.