11. • UV induced mutation of the p53 tumor
suppressor gene
• 56 % mutation occurs in both p53 alleles
• Aggressiveness of the tumor relates to the
presence of p53 protein
• Mutation in the patched gene PTCH is
responsible for BCC in Gorlin's, XP
12. Carcinogenesis
Initiation - Genetic mutation , DNA changes
Promotion – Changes in cellular environment
Progression – Further genetic alteration.
If erroneous sequences are not repaired propagation
continues during DNA replication.
13. • UV induced immunosuppression – depletion
of Langerhans cells and stimulation of
suppressor T cells – hindering the detection
and destruction of the tumor cells.
14. Non UV
• < 1%
• Arsenic
• Non ionizing radiation
• Immunosuppression
• Tobacco
• Human papilloma virus
• Scars
15. Spread
• BCC’s are stromal
dependant
• Do not survive
transplantation
• Rarely metastasize –
0.1 %
16. Spread
• Aggressive local growth - following the path of
least resistance
• Spreads along:
• periosteum
• Perichondrium
• Fascia
• tarsal plate
17. Spread
• Can spread deeply
between nasal
cartilages
• Embryonic fusion
planes
19. Xeroderma Pigmentosum
• Autosomal recessive defect
• DNA repair – skin intolerant of
UV light
• Skin normal as infant- becomes
dry,pigmented,cutaneous,
s/c atrophy
• Xerodermic idiocy – progressive
neurological deterioration
• BCC,SCC,Melanomas
• Usually die in second decade
20. Gorlin’s Syndrome
• Basal cell nevus syndrome
• Autosomal dominant with low penetrance
• Mutation in tumor suppressor gene located
on 9q23-q31
Multiple Nevi Reddish Brown, Papular
and
Variously sized
Appear after puberty several to
thousands
76% become invasive BCCs
24. Papulonodular Bcc
• Commonest - 45%
• PN Solid 38% Smooth, raised,
waxy Translucent, NODULE, thin
epithelial cover,Minute vessels in the
periphery, surface shows fine venules,
Pearly edge, central depression
• PN Cystic 6.9% Pale, pearly pink
Lucid gray with a well defined margin
Acid mucopolysaccharide gel
25. Multifocal Bcc
• 35%
• Multifocal Superficial
Often merely red areas with a patchily adherent
Parakeratotic scales
Pattern with small areas of epithelial discontinuity
Margin ill defined Pearly edge defined on stretch
• Superficial
Early stage of MFS – small red patch with a localized
superficial cluster of BCC cells
• Cicatrizing, Field Fire
Red irregular scaly rim round a whitish healing centre
26. Morphoeic / Sclerosing
• 8.9%
• Flat whitish plaques
• Fine pearly edge
Noticed on stretching the skin at the edge of the
Plaque
• Central regression- skin pit
On stretching the skin the white plaque becomes
Evident may be localized or infiltrating
Synthesize type IV collagenase
Discontinuous basement membrane
27. Infiltrating Bcc
• Primary Infiltrating 8%
No characteristic clinical appearance
Red or gray scaling area
Induration, Ulceration, Whitish plaque
Microscopic examination diagnostic
• Secondary Infiltrating
Parts of the lesion of bcc develops an
Infiltrative character
• Recurrent Infiltrating
Recurrent bcc develops into an
infiltrative
type
D/D Solar Keratoses
Squamous cell ca.
28. Metatypical
• Irregular mammilated pale
pink flesh colored lesion
• Without marginal light reflex
• Without any superficial vv.
• May stay like this for years
• Ulceration
29. Pigmented Type
• Variation in pigment
• Scant flecks to deeper pig.
• Edge - pearly translucence
• Fine superficial venules
• Stromal melanophages
• Central regression
• D/D Melanoma
30. HISTOLOGY
• Cutaneous epithelial tumors
• Nests and sheets of basal
type cells with a large oval
nucleus
• Intercellular bridges not seen
• Peripheral layer is arranged
like a palisade
• Central haphazard arrangement
• Abundant connective tissue
stroma rich in acid
mucopolysaccharides mucinuous
appearance
• Amyloid in 65% bccs
32. Solid, Micronodular
• 70% • Smaller nests
• Islands of Cells • Palisading less
• Peripheral palisading • Infiltration into dermis
• Central haphazard and subcutis
• Retraction spaces • Increased rec.
33. Cystic, Keratotic
• Similar to solid • Similar to solid
• Cystic spaces present • Keratinization towards
towards the centre dt the centre
degeneration of tumor • Very little stroma
cells
34. Infiltrating, Multifocal
• Elongated strands of • Discreet nests of tumor cells
basiloid cells between apparently interconnected
collagen bundles • Multiple small islands of
basiloid cells attached to
• Fibroblasts the extending to the
• Focal infiltration in rec. papillary dermis
Solid in scar
35. Sclerosing, Metatypical
• Thin strands and nests • Plump squamous cells
of cells embedded in a with loss of peripheral
dense fibrous stroma palisading
• Eosinophillic areas - • Represents basiloid and
Morphoeic squamous features
36. Invasive Histological Features
• Microfilaments located on the periphery of the
individual cells with the highest density at the tumor
borders
• Increased type IV collagenase
• Focal gaps in the basement membrane
• Loss of intercellular bridges
• Increased cytokines which stimulate fibroblast
glycosamineglycans synthesis
• Increased peri tumor stroma
43. • Cryosurgery
• lesions up to 2 cm 97% high morbidity
• lack of microscopic evaluation
• Edema
• hypo pigmentation
• atrophic scars
• Neuropathy
• sub clinical spread
• unpredictable cosmesis
44. • Surgical Excision
• 90% overall success rate
• Nodular lesions <1cm - 2mm margin
• Lesions < 2cm 3-4 mm
• Lesions > 2cm, subclinical spread, aggressive
histology, multifocal - may require margins up
to 10mm
45. • Mohs micrographic surgery:
recurrent bccs, morphoeaform or arising from
scar, anatomic sites with relatively high rates
of treatment failure, critical locations – eyelid
99% primary, 95% recurrent
• Frozen Sections
• Delayed primary repair temporary grafting
46. ADJUNCTS
• Topical Chemotherapy
5 FU with retinoids
Imiquimod – immune response modifier that induces
cytokines including interferons
Radiation Therapy - older patients, adjuvant therapy
where negative margins are difficult to obtain –
nasal, periorbital, periauricular
92%
47. Others
• Alpha-interferon Therapy
• Laser excisions
• Photodynamic Therapy
includes the administration of Dihaematoporphyrine or its
derivative followed by exposure to 630 nm light with a
tunable dye laser .It localizes to the tumor cells and
absorption of light by dihaematoporphyrin ether has a
cytotoxic effect
48. Follow up
• Follow up for 5 yrs
• Recurrence is defined as the reappearance
of a bcc within or contiguous to a scar
resulting from an initial attempt at definitive
treatment
49. Increased Risk
• Long time presence of the lesion
• Location in a high risk area
• Aggressive clinical and histological features
50. • 20% will develop a new lesion within 1 yr of having
been treated
• 36% will develop another lesion by 5 years
• Overall recurrence rate of 2.9 % - 9 %
• 82% recurrence occurs in first 5 years ,18% in 6-10
yrs
51. Incomplete Resection
• 35% recurrence if one margin is involved
• 12% recurrence when tumor within one high
power field of margin