The document discusses various types of squamous cell carcinoma (SCC) and their precursor lesions, including actinic keratosis, cutaneous horn, arsenical keratosis, and Bowen's disease. It provides details on their clinical features, risk factors, potential for malignant transformation, and management options. The document emphasizes the importance of early diagnosis and treatment, as well as the differing risks associated with various clinical presentations.

2. SQUAMOUS CELL
CARCINOMA
&
ITS PRECURSORS

3. PRECUROR
LESIONS

4. PREMALIGNANT / PRECURSOR LESIONS
 Actinic keratosis
 Cutaneous horn
 Arsenical keratosis
 Post ioninzing radiation keratosis
 Disseminated superficial actinic porokeratosis
 Bowen’s disease / carcinoma in situ

5. ACTINIC
KERATOSIS

6. ACTINIC KERATOSIS
 UV-induced precancerous skin lesion that may progress to
skin cancer on chronically sun exposed areas affecting
elderly males & females
 More common in white population & those with red hair &
blue eyes.
 Relapsing-remitting lesions.

7.  Initially: small lesion
(macules or papules)
with rough surface
→ coarse sandpaper-
like texture
 Usually asymptomatic
 Better appreciated by
palpation
 May pass unnoticed by
patient

8.  Later: lesions grow and
become erythematous and
adherent hyperkeratotic
scale -removed with difficulty
and pain , revealing punctate
bleeding points
 Presence of tenderness,
induration , or a raised
shoulder beyond
disorganized scaling-
malignant transformation.

9. 4
Clinical
Variants
Of
Actinic
Keratosis
1.Flat
2.Atrophic
3.Lichenoid
4.Pigmented

10.  H/P
-solar elastosis ,
-epithelial dysplasia
restricted to basal layer
-hyperkeratosis
-parakeratosis
-absent granular layer

11. HIGH RISK CLINICAL FEATURES OF AK --EARLY
INVASIVE SCC
 Multiple thick Aks
 Past history of NMSC
 Extensive actinic damage
 Immunocompromised state
 Tenderness, induration & enlarging lesion

13. T
TREATMENT

15. Other Rx options
 Topical & oral retinoids
 Dermabrasions & chemical peels with trichloracetic acid
 Non ablative fractional resurfacing

16. CUTANEOUS HORN

17. CUTANEOUS HORN
• Benign curved, hard, yellow-to-
brown outgrowths composed
of keratin - resembles a horn & may
develop from preexisting actinic
and seborrheic keratosis or warts
• UVR-induced on light exposed areas
• May progress to squamous cell
carcinoma (SCC) ~ 40%

18.  Keratotic lesion with a height of at least half the widest
diameter of its base
 Dysplastic epidermal changes similar to AK
 Inflammation, induration & pain at the base suggests
malignant transformation
clinically – wide base or low height-to-weight ratio
H/P – budding from basal layers in long established lesions

19. DIFFERENTIAL DIAGNOSIS
 Viral warts
 Actinic keratosis
 Seborrheic keratosis
 Keratoacanthoma
 Invasive SCC

20. MANAGEMENT
 Clinical appearance
 H/P of base to rule out malignancy
 Surgical excision – to obtain pathology & rule out
malignany

21. ARSENICAL
KERATOSIS

22. ARSENICAL KERATOSIS
 A corn like punctate keratosis caused
by arsenic / a few years after
exposure, mainly affecting the palms &
soles.
 Hyperpigmentation –raindrop pattern ,
accompanied by hypopigmenated
areas, and progression to generalized
thickness of palms and soles .
 Smoking , nutritional deficiencies
(retinol, Ca, iron, folate ,vitamin
A,E,C)

23.  H/P – epithelial dysplasia or hyperplasia. No typical
microscopic feature.
 May progress to BCC, SCC or Bowen’s disease – induration ,
inflammation and ulceration become apparent.
DIFFERNTIAL DIAGNOSIS
 Disseminated puntate keratoderma
 Darier’s disease
 Lichen planus
 Planter warts

24. MANAGEMENT
 Reduce arsenic exposure
 Well balanced diet
1st line
 Solitary / few lesions – cryotherapy ,cautery or curettage.
 Multiple keratosis – oral retinoid in combination with
keratolytics
2nd line
 Imiquimod cream 5% OD for 6weeks or OD 3-5times per
week

25. BOWEN’S DISEASE

26. BOWEN’S DISEASE
 Squamous cell carcinoma in situ
(SCCIS) of the skin.
 UVR-induced damage in sun-exposed
areas & non exposed areas, often
associated with HPV
 Single, large, persistently non-elevated,
well demarcated, erythematous plaque,
with white-to-yellow scale – moist ,
reddened, granular surface on
detachment with no bleeding point.

27.  ~10-20% multiple lesions , either
widely spread or sometimes close
together.
 Slower growth rate and spontaneous
partial regression at times.
 Can occur on perianal skin,
subungal region, palms & soles -
higher risk of invasion & recurrence.
 May progress to invasive squamous
cell carcinoma. ~3-5% risk

28. Clinical
Variants
OF
Bowen’s
Disease
1.Psoriasiform
2.Atrophic
3.Verrocous
4.Papillated
5.Irregular

29. Histopathology
 Full thickness epidermal dysplasia
& disordered differentiation with
loss of epithelial polarity.
 Parakeratosis & acanthosis.
 Large hyperchromatic nuclei
 Atypical mitosis and gaint cells.

30. DIFFERENTIAL
DIAGNOSIS

32. MANAGEMENT

34. POST –IONIZING
RADIATION
KERATOSIS

35. POST –IONIZING RADIATION
KERATOSIS
 An area of scarring following accidental exposure to radiation
or after therapeutic radiotherapy or excessive fluoroscopy
 Relatively uncommon –after months to years following
exposure
 On limbs mostly or covered body sites.
 Changes similar to AK, telangiectasia, vasculitis, radiation
ulcers, hemangiomas, subcutaneous sclerosis of connective
tissue.

36. D/D – Actinic Keratosis
H/P – epidermal changes similar to
AK.
Dermis – much extensive
replacement of collagen by scar and
elastotic material
MANAGEMENT
 Skin biopsy to confirm the
diagnosis
 Immediate reduction to exposure
 Cryotherapy for individual lesions.

37. DISSEMINATED
SUPERFICIAL
ACTINIC
POROKERATOSIS

38. DISSEMINATED SUPERFICIAL
ACTINIC POROKERATOSIS
 Multiple enlarging rough hyperkeratotic
papules surrounded by a thread like
elevated border , on distal extermeties
– usually around a follicle
 Skin within the ring is atrophic ,
erythematous or hyperpigmented.
 Hypopigmented ring just inside the
ridge.

39.  Prominent in summer &
improve in winter.
 Very low chances of
malignant transformation.
 H/P
-cornoid lamella at the
margins.
- narrow column of altered
keratin
- dyskeratotic & vacuolated
epidermal cells

40. Clinical
varaints
of
Porokeratosis
1. Porokeratosis of Mibelli
2. linear porokeratosis
3. DSAK
4.Porokeratosis palmaris &
plantaris diffusa
5. Punctate porokeratosis

41. DIFFERENTIAL DIAGNOSIS
 Actinic keratosis
– esp if on face , but present on other sun exposed sites as
well
 Bowen’s disease
– on legs
 Superficial BCC

42. MANAGEMENT
 Good use of emollient & high factor broad spectrum sunscreen
 Cryotherapy with liquid nitrogen
 Topical diclofenac gel , vit D3 analogues, 5% 5-FU cream, 5%
imiquimod cream
 Photodynamic therapy
 Erbium , CO2, Q-switch ruby laser, Nd:YAG –under successful
trials.

45. SCC
 Older males
 Common type of Non Melanoma Skin Cancer
( NMSC )
 It is derived from keratinocytes
 May develop de novo or from precursor AK or SCC in situ
 Mainly on sun exposed sites
(hairless scalp, upper part of face, lips (Lowerlip), ears
(helices), dorsa of hands, forearms, lower legs)
 Size
few milimeters to centimeters in diameter.

48. PATHOPHYSIOLOGY
 Common mutations (tumor suppressor genes )
p53 – UVB induced
p16 – UVR induced
 Chromosomal abnormalities ( Genome-wide expression & SNP
analysis)
3p, 8q, 9p, 11p, 13q, 17p and 18p

50. RISK FACTORS
 UVR –Major risk factor ( UVB > UVA, sunlight & artificial
tanning lamps)
 Fair-skinned individuals (Fitzpatrick skin type 1 and 2)
 Premalignant conditions
 Inherited predisposition
 Smoking (lower lip SCC)

51. ...cont
 Viral Infections (HPV-16,-18) – viral warts,genital warts, many
mucosal SCCs.
B-type of HPV > excess risk of SCC.
 Longstanding dermatosis
longstanding leg ulcer, fistula tracts, chronic injury site,
inflammation sec to Hidradenitis supparativa.Thermal scars –
Marjolin’s ulcer that occurs on chronic wound or scar including
scars from burn.
 Immunosuppression ( ciclosposrin , azathioprine , organ
transplant recipients , haematological malignancies , HIV )

53.  1st clinical sign – induration.
 Firm , tender , erythematous nodule or plaque with keratotic
crust , verrucous, tumid
 Eroded fungating mass – that shows easy bleeding
 Lesions that fail to heal – develop ulcers
with everted edge , indurated base & necrotic floor
 Outline – mostly irregular , sometimes rounded.

55.  Mobile structures like lip & Genitalia
show early fissuring or small erosions or ulcers that fail to
heal and bleeds recurrently.
 May be associated with other features of photodamage or
premalignant lesions.
 Parestheisa , anesthesia, tenderness, pain particularly in
perineural invasion
 Regional LN enlargement (later –hard & fixed)

69.  Proliferation of Atypical
Keratinocytes
 Typical SCC has nests of
squamous epithelial cells
arising from epidermis
and invading into dermis

70.  Malignant cell – large,
abundant eosinophilic
cytoplasm & large
vesicular or
hyperchromatic
nucleus with
pleomorphism &
mitosis.

71.  Variable keratinaization
squamous eddies ,
keratin pearls
(concentric layers of
squamous cells with
increasing keratinization
towards the center)
 Inflammatory infiltrates –
varies considerably in
intensity
primarily lymphocytes &
plasma cells

72. Grading of SCC
 Depends on how easy it is to recognize the characteristics
of squamous epithelium (e.g, intracellular bridges ,
keratinization ) , pleomorphism & mitotic activity
 The greater the degree of keratinization – the better
differentiated tumor.

73. Well differentiated Poorly differentiated
SCC SCC

75. METASTATIC SCC
 Upto 5% RISK OF METASTASIS
 Invasive SCC rarely metastasize and prove fetal.
that refers to growth into deeper layers of skin , the
dermis.
 More difficult to treat than the original skin lesions.
 In 80% cases metastases develops from draining LN.

79. DIFFERENTIAL
DIAGNOSIS

80. DIAGNOSIS DIFFERENTIATING POINTS
Keratoacanthoma (KA ) Faster growth rate, involute to leave a scar.
Classified as well differentiated SCC.
No precursor lesion unlike SCC.
Presents (initially) as firm, rounded flesh coloured papule
(like MC) , (later) if keratotic > like a viral wart.
More hyperkeratotic than AK
Spontaneous resolution ~ 3months
Actinic keratosis ( AK ) Sun exposed area. Multiple. Macules or papules with
rough scaly surface & lack of dermal component on
palpation. Asymptomatic. 10% chances of SCC
Bowen’s disease / carcinoma in situ Solitary, larger, persistently non elevated, erythematous
scaly plaque, with no bleeding on detachment. Slower
growth rate and spont partial regression at times.
Asymptoamtic

81. … cont
Cutaneous horns Curved , hard, yellow to brown keratotic outgro
circumferential ridges.Mostly single. Inflammati
induration & pain at the base suggests malignan
transformation. ~40%/usually SCC
Warty leasion ( viral warts , seborrheic keratosis) Multiple , not indurated.
SK have darker, raised & greasy warty surface.
Basal cell carcinoma ( BCC ) Single , less hyperkeratotic than AK, irregular
erythematous base.
Arsenical keratosis Corn like , punctate keratosis caused by arsenic
after exposure), mainly on palms and soles.
Presents as hyperpigmentation of skin ,accompa
hypopigmented areas.
Progress over time with increase in numbers. Hi
developing BCC, SCC/ bowen’s disease.

82. INVESTIGATIONS

83.  Skin biopsy - to confirm diagnosis
 MRI (in case of head and neck tumors and higher chances of
mets)
 CT scan(in case of nerve involvement )
 USG combined with a guided fine needle aspiration or core
biopsy (in case of LN involvement )
 High resolution micro oil MRI / SPECT / PET – role in future.
 Reflectance confocal microscopy & high resolution optical
coherence tomography – under trials.

85. Aim
 Remove primary tumor & prevent recurrence
Rx
 Depends on clinical (size, location, number) & pathological
features of tumor.
 Long term prognosis for adequately treated SCC is excellent.
 Larger / aggressive lesions need imaging before starting the
treatment.

87.  High Risk Clinical Features (HRCP)
- diameter >20mm
- immunosuppressive
- site: ear, lip, scalp,eyelid
- SCC arising in burns, scars, chronic
ulceration , radiation damage.
Bowen’s disease in non sun exposed
skin , inflammatory conditions.
 High Risk Pathological Features (HRPF)
- depth >4mm & diameter >20mm
-poorly differentiated
- perineural invasion
-lymphovascular invasion
-subtypes: desmoplastic , spindle cell,
acantholytic, arising in Bowen’s
disease in non-sun-exposed skin

88. Rx Low Risk lesions Rx High risk lesions