BCC and SCC

1. BASAL CELL CARCINOMA
DR.ARCHANA VAISHNAV

2. INTRODUCTION
BCC is slow progressing NMSC that aises from basal cells ,most deeper layer of epidermis.
SYNONYMS- Rodent ulcer
Basiloma
non melanoma skin cancer (NMSC),
‐ to distinguish them from ‘melanomas’ which have a much higher
malignant potential.
 BCC represent approximately 74% of NMSC whilst SCC are less common at 23%.
 BCC is the most common skin cancer in immunocompetent individuals where as SCC is most common skin
cancer in immunosuppressed organ transplantation recipients.

3. BASAL CELL CARCINOMA
EPIDEMIOLOGY
 Increases as age advances-80% of cases occur in people aged 60yrs and over.
 The life time risk of developing BCC is 28%-33%.
 Male > female.
 Risk is higher in individuals with markers of UV susceptibility.
 Markers of chronic photodamage are positively associated with BCC.

4. PATHOPHYSIOLOGY
RISK FACTORS
 Solar UV radiation – intermittent ,intense & infrequent sun exposer .
 Genetic predisposition
 Immunosuppression
 Phototherapy
 Photosensitizing drugs( doxycycline, FQs, triazole antifungals.)
 Ionizing radiation
 Occupational factors, Arsenic exposure
 Previous history of basal cell carcinomas

5. ENVIRONMENTAL FACTORS
 Both UVA and UVB radiation are mutagenic.
UVB-Radiation
Damages both DNA&RNA
UVA-Radiation
Generation of mutagenic photoadducts
Induces covalent bond formation b/w
adjacent pyrimidines
ROS by a photo oxidative stress
Interact with lipids,proteins&DNA
Generates intermediates that combine with
DNA to form adducts
Interact with lipids,proteins&DNA

6. GENETICS
 PTCH1 , a segment polarity gene (9q22.3) with tumour suppressor functions encodes a
transmembrane protein, Patched 1 which acts like the receptor for SHH.
‐
 Ptch 1 acts as a tumour suppressor, repressing the G protein coupled receptor smoothened (Smo).
‐ ‐
Loss of function mutations of PTCH1
‐ ‐
Reduced suppression of Smo
activation of the Gli family of transcription factors
resulting in sustained activation of target genes.
 50% of BCCs – TP53 tumour suppressor gene mutations.

8. SYNDROMES ASSOCIATED WITH BCC
 A. XERODERMA PIGMENTOSA - Defect in DNA repair pathway,
Clinical Features- Photosensitivity, Freckles, Multiple skin cancer at
early age.
 B. ALBINISM - AR disorder, defective melanogenesis, lightly or non
pigmented skin, silvery-white hair, reduced visual acuity, ocular
nystagmus predisposition to skin cancer.
 . ROMBO SYNDROME: C/F- Atrophoderma Vermiculata, Milia,
Hypotrichosis, Trichoepithelioma,
 BCC, And Peripheral Vasodilatation With Cyanosis.

9. BASAL CELL NEVUS SYNDROME/ GORLIN SYNDROME
 BCNS is an AD disorder due to an inactivating mutation in PTCH1 or rarely PTCH2.
Manifestations-
Multiple Or Early-onset Bccs
Odontogenic Keratocysts Of The Jaw
Palmoplantar Pits
Calcification Of The Falx Cerebri
Skeletal Anomalies .
 Affected individuals may develop specific neoplasms such as medulloblastomas,
meningiomas , ovarian fibromas, and cardiac fibromas.

11. BAZEX–DUPRÉ–CHRISTOL SYNDROME
 A rare X linked dominant genodermatosis that predisposes affected individuals to multiple BCCs.
‐
 Syndrome is characterized by hypotrichosis,
follicular atrophoderma of the cheeks,
milia cysts and
BCCs.
 BCCs usually appear after the first decade of life.
 Only females are affected.

12. Occupational risk factors
 Persons with outdoor occupations have a higher risk of developing skin cancer.
 Agricultural workers, sailors, locomotive engineers, and textile workers.
Chemical exposures
 Occupational chemical exposures which can lead to skin cancer most commonly involve
pesticides, coal tar, and polycyclic aromatic hydrocarbons.
 BCC has been reported following extensive arsenic exposure. The typical latency period
from exposure to tumor development is 20–40 years.

13. CLINICAL FEATURES
 BCC usually develops on sun exposed area of head & neck but can
occur any where on the body.
 The typical BCC runs a slow progressive course of peripheral
extension, which produces the thread like margin
‐ .
 Early BCCs are usually small, translucent or pearly, with raised
telangiectatic edges.
 However, the presentation may be varied and small lesions can be
lichenoid or keratotic, excoriated or ulcerated.
 More advanced lesions can present as classical rodent ulcer with
an indurated edge.

14. Clinical variants
 Superficial BCC
 Nodular BCC
 Pigmented BCC
 Morphoeic BCC
 Ulcerated BCC
 Fibroepithelial BCC
 Advanced and metastatic BCC

15. HISTOPATHOLOGY
Tumour masses are connected to epidermis and
composed of uniform cells that appear like basal
cells with elongated,dark nucleus and scant
cytoplasm.
 The cells lie side by side –palisading
arrangement.
 The cell masses are always surrounded by dermal
stroma,which may be separated by the tumour
mass by a clear space called retraction space.

17. HISTOPATHOLOGICAL VARIANTS
 Superficial BCC
 Nodular BCC
 Infiltrative BCC
 Micronodular BCC
 Morpheaform BCC
 Basosquamous or metatypical BCC

18. NODULAR BCC
 It is the commonest subtype of BCC and usually presents on head & neck.
 Red or pink translucent papule or nodule with telangiectasis .
 Nodules may have cystic centres, which add to the translucent appearance.
HISTOLOGY
 As nests of basaloid cells in either the papillary or reticular dermis.
 The nests are separated from the stroma by a slit like retraction.
‐
 The surrounding stroma shows myxoid change, and calcification may be
seen in discrete islands of tumour or in adjacent stroma.

19. SUPERFICIAL BCC
 Less common and predominantly present on the trunk.
 These are bounded by a slightly raised thread like margin or a ‘whipcord’ edge which is
‐
irregular in outline.
 The epidermis covering the central zone is usually atrophic and may be scaly.
HISTOLOGY
 Proliferating atypical basaloid cells usually confined to papillary dermis.
 A band like lymphoid infiltrate may be present .
‐

20. PIGMENTED BCC
Sub type of nodular bcc that exhibits increased melanization.
 It appears as translucent , hyperpigmented papule.
 Clinically mistaken for nodular melanoma.
HISTOLOGY
 Large solid islands of basaloid cells with central pigmentation.
 Peripheral palisade is a prominent feature.
 Melanocytes are interspersd in b/w tumour cells and contain
numerous melanin granules.

21. MORPHOEIC BCC
 Also k/a sclerodermiform, because dense fibrosis of the stroma
produces a thickened plaque rather than a tumour.
 It is yellow in colour with ill defined borders.
‐
 The surface is smooth and may be slightly raised above or slightly depressed
below, the normal level.
 Ulceration is uncommon and only very superficial when it does occur.
HISTOLOGY
 One to two cells thick columns of basaloid cells enmeshed
in a dense collagenous stroma.
 Stromal fibroplasia and fibrosis of the tumour cords is commonly seen.
 Invasion of the deep dermis and subcutis is another feature of morphoeaform BCC.

22. ULCERATED BCC
 Start as a small macule or papule but with expansion of the thread like
‐
margins, the attenuated surface ulcerates with an indurated and raised
edge.
 Atypical ulcerated BCC also has an indurated edge and base but no
thread like margin.
‐
 The floor of the ulcer is depressed, fleshy in appearance and not very
vascular.
 If left, the tumour and its following ulcer may spread deeply and cause
great destruction,especially around the eye, nose or ear.
 Wide extension in the periorbital tissues,bones of the face, skull;
and even the meninges -‘ulcus terebrans’.

23. MICRONODULAR BCC
 The tumour nests are smaller than those in nodular BCC and
more widely and asymmetrically dispersed in the dermis
and/or subcutis.
 The retraction spaces are uncommon and the surrounding
stroma shows either a myxoid or collagenized morphology.

24. INFILTRATIVE BCC
 Typically show elongated tumour cell strands, five to eight
cells in thickness,
 present histologically as irregularly sized and shaped
nests which are poorly circumscribed.
 show invasion of the subcutis and adjacent muscular
structures.

25. ADVANCED AND METASTATIC BCC
 1–2%.
 Mutilation of the face or scalp, with destruction of the nose or eye and exposure of the
paranasal sinuses or the skull, dura or brain may eventually result in death .
 bloodstream metastasis - deposits in the viscera or spinal column have caused the
symptoms of the terminal illness.
 Tumour cells spread via the lymphatics to the regional lymph nodes before disseminating.

26. FEATURES OF METASTATIC BCC
 Large size >3cm and locally aggressive
 Recurrent
 Younger age onset
 Morpheaform MC
 Median time to metastasise is 9years
 10% survival rate.

27. DIFFERENTIAL DIAGNOSIS
Nodular BCC -Melanocytic naevus ,
Molluscum contagiosum
Sebaceous hyperplasia,
Warts, keratoacanthoma, SCC.
Superficial BCC - patches of eczema, psoriasis or
bowen disease

28. DIFFERENTIAL DIAGNOSIS

29. INVESTIGATIONS
 The diagnosis of BCC is primarily clinical.
 In clinically challenging cases, a biopsy is required.
 Nodular BCC- shave biopsy
 Morphoeic BCC - punch biopsy
Non invasive techniques for the diagnosis of BCC include
‐
 Dermoscopy
 High frequency ultrasound,
‐
 Optical coherence tomography and
 In vivo confocal microscopy.

30. DERMOSCOPY
 white and grey brown structureless areas
‐
 blue grey globules
‐
 spoke wheel areas
‐
 concentric structures
 maple leaf like areas
Vasculature includes –
 Atypical red , arborizing, comma and
telangiectactic vessels.

34. MANAGEMENT
 Clinical and histological nature, size and site of tumour & patient factors determine the choice of treatment
of BCC.
AIM OF TREATMENT-
 Complete removal or destruction of the BCC.
 Achieving a good and acceptable cosmetic outcome.
MEDICAL MANAGEMENT SURGICAL MANAGEMENT
Imiquimod Excision
5FU MMS
PDT C&C
Intralesional INFA-2B Cryotherapy
HH INHIBITORS Lasers
RT

35. MEDICAL MANAGEMENT
IMIQUIMOD
Stimulates toll like receptor 7 and 8 expressed on dendritic cells and monocytes,
‐
Leading to increased production of cytokines and chemokines.
Promote both th1 innate and adaptive cell mediated immune responses
‐
Recognition and destruction of the tumour cells.
 use in superficial BCC, with a maximum tumour diameter of 2 cm.
 Topical 5% imiquimod cream, applied five times per week over 6 weeks is effective in clearing 69–100%
of superficial BCC and 42–76% of nodular BCC.
 S/E- Erythema, pruritus, erosion, ulceration, dyspigmentation and scabbing.
 Patients may experience flu like symptoms.
‐

36. 5 FLUOROURACIL
‐
 5 FU used to treat superficial BCCs , not recommended for the treatment of large, nodular
and high risk BCC.
 5 FU disrupts DNA and RNA synthesis by inhibiting the enzyme
‐ Thymidylate synthetase.
 Local irritation and skin reaction resulting in erythema, swelling, desquamation and
tenderness are common post treatment.
 Requires prolonged course,twice daily for 6-12 weeks.

37. PHOTODYNAMIC THERAPY
 PDT involves the activation of a photosensitizing drug by visible
light to produce activated oxygen species that destroy the
cancer cells.
 Complete response rates for superficial BCCs from 85% to
93% at 3 months.
 Topical photosensitisers ALA or Methyl
aminolevulinic acid is used.
 Used for small small low risk superficial BCC.
 Treatment is repeated every 7 days.
 Cosmetic results is excellent.

38. INTRALESIONAL INFΑ 2B
‐
 High cure rates
 1.5 million U IL inj ,3times/week for 3 weeks.
Limitations
 High cost
 Multiple sessions.
HEDGEHOG PATHWAY INHIBITORS
 Vismodegib is an inhibitor of SMO used in the treatment of metastatic and locally advanced BCCs
 DOSE-150 mg orally daily for 9-10 month.
Adverse reactions - fatigue, weight loss and dyspnoea, muscle spasm , aspiration, back pain, corneal
abrasion, dehydration, hyponatraemia , lymphopenia , pneumonia,

39. SURGICAL METHODS
Surgical excision –
 complete clearance can be achieved in approximately 95% of the well defined small BCC with a 4–5 mm surgical
‐
margin ,
 recurrence rates are low
 cosmetic outcomes are good.
 may not be appropriate for recurrent, morphoeic or large BCC
Mohs micrographic surgery
 MMS offers superior histologic analysis of tumor margins while permitting maximal conservation of tissue
 It is the treatment of first choice for primary & recurrent facial BCCs.
 MMS is the treatment of choice for morpheaform, poorly delineated, incompletely removed BCCs.

41. Curretage and electrodessication –
 Growth is scraped of with currete with a sharp ring
shaped tip ,then tumour is desiccated(burned) with the
electrocautery.
 Leaves white round whitish scar.
Low risk non facial BCCs best treated with C&C.
 Not employed for- recurrent, illdefined, high risk BCCs.

42. CRYOTHERAPY
 Cryotherapy is treatment of superficial lesion by freezing it,usually
with liquid nitrogen .
 Suitable for BCC present in covered site like trunk ,limb as it
leaves permanent white mark.
 Two freeze–thaw cycles with a tissue temperature of −50°C are
required to destroy BCC.

 A margin of clinically normal tissue must be destroyed to eradicate
subclinical extension.

43. RADIATION THERAPY
 Superficial and electron beam radiotherapy or brachytherapy are effective in primary or surgically recurrent ,
high risk BCC.
‐
 RT may be used as a palliative modality in improving the quality of life in patients with advanced disease
 Given in fractionated dose of 10-16 fractions for <5cm & 15-30 divided doses for >5cm tumours
 RT advantages – effective in troublesome areas nose, ear and eyelid.
 useful in elderly patient where surgery can not be performed.
Recurrent tumours,
Disadvantage- Radiation necrosis of skin
Expensive and time consuming as many session needed.
Tumours with poorly defined clinical margins
 Incomplete clearance and recurrences after radiotherapy are higher and cosmosis is poor when compared
with surgical excision.

45. 
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