This document discusses cutaneous malignancies including benign and malignant skin tumors. It provides classifications of skin tumors and describes various types of non-melanoma skin cancers like basal cell carcinoma, squamous cell carcinoma, and malignant adnexal tumors. It discusses the pathophysiology of skin cancer in relation to ultraviolet and ionizing radiation damage. Risk factors, presentations, investigations and treatments are summarized for different non-melanoma skin cancers and malignant melanoma.

1. Cutaneous Malignancies
-Dr. Harish Kumar Kabilan

4. ❖ Benign
Classification of skin tumours
❖ o Squamous cell carcinoma.
o Basal cell carcinoma.
o Melanoma.
o Malignant skin adnexal tumour.
o Secondaries in the skin..
❖Malignant
o Seborrhoeic keratosis.
o Trichilemmal tumour.
o Sebaceous adenoma.
o Sebaceous epithelioma.
o Hydrocystoma, syringoma, spiradenoma.
•Melanoma
•Non melanoma cutaneous
malignancies

5. PATHOPHYSIOLOGY OF THE SKIN AND
SUBCUTANEOUS TISSUES
RADIATION DAMAGE:
Ultraviolet radiation (UVR) and ionising radiation (IR) damage cellular DNA via
the tumour suppressor gene p53.
UV RADIATION:
UVR is divisible into A, B and C according to wavelength. UVR is the principal
cause of skin cancer in all skin types
IONISING RADIATION:
it is dose and time dependent.

6. Ultraviolet light
UV A – 320nm-400nm
B – 290nm-320nm
C – 100nm-280 nm

7. .UVA contributes to skin cancer via
indirect DNA damage (free radicals
such as reactive oxygen species).
UVB photons can cause direct DNA
damage.
As a defense against UV radiation,
the amount of melanin in the skin
increases when exposed to moderate
levels of radiation.

9. Benign lesions
1.Basal cell papilloma (seborrhoeic keratosis, senile
keratosis, verruca Senilis)
2.Papillary wart (verruca vulgaris)
SKIN LESIONS
3.Freckle (ephilis)

10. 4.Lentigo
5.Moles/naevi
6.Junctional naevus

11. 7.Spitz naevus
8.Spindle cell naevus
9.Halo naevus
10.Café-au-lait spots

12. 11.Mongolian spot
12.Blue naevus
13.Naevi of Ota and Ito

13. Premalignant lesions
1.Actinic/solar keratosis
3.Keratoacanthoma
4.Bowen’s disease
.
2.Cutaneous horn

14. 5.Extramammary Paget’s disease
6.Giant congenital pigmented naevus or giant hairy
naevus
7.Dysplastic (atypical) naevus

15. CHARACTERISTICS OF A
DYSPLASTIC NAEVUS
❖ Asymmetry
❖ Border- Irregular/ poorly defined
❖ Colour - Variable. Tan brown/black. Red
❖ Blue, white
❖ Diameter - >6mm
❖ Evolving in color/size/ shape

16. CONGENITAL/ GENETIC SYNDROMES
Naevoid basal cell carcinoma (Gorlin’s) syndrome
Xeroderma pigmentosum
.

17. Gardner’s syndrome Ferguson-Smith syndrome

18. ❖ Malignant melanoma (MM) accounts for 3 per cent of all
malignancy worldwide. It is the most common cancer in young
adults (20–39 years) and the most likely cause of cancer-related
death.
MALIGNANT LESIONS
CUTANEOUS MELANOMA

19. Pathophysiology
Clark’s concept—Two phases of growth: Initial radial growth phase occurs horizontally, later vertical growth phase occurs with invasion.
UV exposure is the major causal factor for developing MM.

20. Risk Factors
o Exposure to sunlight (exposure to UV light; more common in white-skinned—20 times).
o Ethnic factors,socioeconomic status(highsociety),lifestyle, climate.
o Albinism.
o Xeroderma pigmentosa
o Junctional naevus.
o Familial dysplastic naevus syndrome.
o Sporadic dysplastic naevi. 10% risk.
o Large congenital naevi (larger than 20 cm).
o Family history of melanoma
o History of earlier skin cancers other than melanoma.
o Patients who are on immunosuppressive drugs or after renal
transplantation or NHL

21. Examination• History
• high-risk skin type a history of severe
blistering sunburns,
• intense intermittent sun exposure,
• upper socioeconomic status,
• family history of melanoma,
• large number of nevi,
• giant congenital nevi,
• presence of dysplastic nevi,
• immunosuppression,
• history of prior melanoma or other skin
cancers
• xeroderma pigmentosum.

22. • Non painful, itchy lesion, in sun exposed sites, with a recent change in
colour/ size, sometimes with ulcer formation often covered with a crust.
• Bleeding and sub acute infection is common.
• Firm in consistency. The ulcer may need easily on touch
• The regional lymph nodes are involved quite early and these are almost
always enlarged when the patient presents to the surgeon. Nodes are also
hard to firm in consistency
• Satellite nodules may be seen in the skin and subcutaneous tissue
between the primary tumour and the nearest regional lymph nodes.
Typical Presentation

23. Physical examination
Asymmetry
Border- Irregular/ poorly defined
Colour - Variable. Tan brown/black. Red
Blue, white
Diameter - >6mm
Evolving in color/size/ shape

24. Glasgow criteria:Major signs: Change in size (diameter more than 6 mm), shape and colour
• Other changes:
Inflammation, crusting, bleeding, itching
Nodularity, ulceration, halo around a mole
Satellite lesions
Doppler positive pigmented lesions using hand held
Doppler ( > 1 mm thick lesion)

25. 3. Lentigo maligna melanoma:
TYPES
2. Nodular melanoma: 12-25%.
4. Acral lentiginous melanoma:
6. Desmoplastic melanoma5. Amelanotic melanoma:

26. Familial Melanoma
There may also be a family history of other malignancies, especially pancreatic
cancer.
They require detailed dermatologic evaluation several times annually, with
periodic biopsies of the most suspicious lesions.
Mutations in the gene CDKN2A in the 9p21 region
CDK4

27. o No incision biopsy. It can cause early blood spread.
o Excision biopsy of primary.
It is done with 2 mm margin with deeper fatty tissue. o FNAC of lymph
node.
o U/S abdomen to look for liver secondaries (usually huge
hepatomegaly occurs).
o Chest X-ray to look for secondaries in lung (“cannon ball”
appearance). HRCT of chest is ideal.
o Relevant other methods depending on site and spread, e.g.
CT scan of head, chest, abdomen, pelvis.
o Urine for melanuria signifies advanced disease.
o Sentinel lymph node biopsy (SLNB).
Investigations

30. Classifications
Clark’s levels
Level 1: Only in epidermis
Level 2: Extension into papillary dermis
Level 3: Filling of papillary dermis completely
Level 4: Extension into reticular dermis
Level 5: Extension into subcutaneous tissue
Relation of Tumour Thickness to Nodal Spread— Based on AJCC Classification

31. Breslow’s classification (1970): Based on thickness of invasion
measured by optical micrometer—most important prognostic indicator
until nodal spread
I: Less than 0.75 mm
II: Between0.76to1.5mm
III: 1.51 mm to 4 mm
IV: more than 4 mm

32. Treatment
For Primary:
a. Handley’s wide local excision (WLE) is wide excision with clearance of margin as well as
depth.
b. Primary closure or SSG or local flaps are used to cover the defect.
b. In fingers and toes, disarticulation is required. 1 joint above.
c. Melanoma in anal canal may require abdominoperineal resection.
d. Enucleation in case of melanoma in eye.

35. For lymph node secondaries:
1.In a clinically palpable lymph node, FNAC of lymph node is done.
2.In a fixed lymph node, only chemotherapy is the treatment because it is inoperable.
3.Lymphatic mapping and sentinel node biopsy
SLNB is useful for melanoma with thickness more than 1 mm depth.
4.Prophylactic regional block dissection - not done anymore.
5. Management in unknown primary (2%) presenting as nodal secondaries is by nodal radical
dissection at the region with adjuvant chemotherapy. T

36. A vital blue dye (e.g., isosulfan blue) is injected into the dermis around the
melanoma site.
It is combined lymphatic mapping technique allows for the identification
of the sentinel nodes in 99% of patients
It is injected just before the operation. it is best to inject it within the
margins of the planned WLE. A hand-held gamma probe is used to
identify the location of the sentinel node(s), and dissection is performed to
identify blue lymphatic channels entering into a blue, radioactive lymph
node, which is removed
SLN biopsy

37. The only adjuvant therapy approved by the U.S. Food and Drug Administration (FDA) is high-dose inte
Interferon alfa-2b is administered at a dose near the maximally tolerated dose, with 1 month of IV thera
Adjuvant Therapy
Systemic therapy

38. Radiation therapy

39. Stage 0, I, and IIA - followed by history and physical examination at least every 6 months for the first 3
For stage IIB, IIC, and III melanoma patients, history and physical examination every 3 or 4 months fo
For patients with stage IIB, IIC, or III melanoma, use of laboratory tests and imaging tests such as CT,
Patients with stage IV melanoma will have regular clinical, laboratory, and radiologic evalu- ations to mo
Follow-Up After Treatment of Melanom

40. Treatment of Recurrent or Metastatic Dis
Local recurrence is one which recurs within 5 cm radius of the primary tumour in skin or subcutaneous tis
For Distant Spread:
o Brain, lung and liver are the most common sites; skin, bone, GI are less common sites. But melano
o Distant spread when found or suspected, CT scan of head, chest, abdomen and pelvis are needed. PET sc

41. Isolated limb perfusion

42. In-transit Disease• In-transit recurrence represents endolymphatic disease manifested by cutaneous or subcutaneous
tumor nodules between the primary tumour site and regional nodal basin.
• Local injection of refractory in-transit disease with agents such as Bacille Calmette-Guérin (BCG),
interferon, and interleukin-2 may, in some cases, result in complete response.
• Laser and other ablative therapies may be considered.
• When confined to the upper or lower extremity, may be treated by hyperthermic isolated limb
perfusion (HILP) with L-phenylalanine mustard (melphalan).
• Repeat perfusion can be performed in patients who recur, but should only be attempted in patients
who responded well to the initial perfusion.
• Percutaneous catheters are placed into the major artery and vein supplying the extremity, followed by
pneumatic tourniquet isolation. Perfusion with ILI is accomplished by manual circulation using a
syringe.

43. Examples of in-transit melanoma of the arm (left) and leg (right). Note the distribution and extent of
disease, making these presentations very poor candidates for surgical excision. On the left, there is
evidence of in-transit metastases both within the area of previous skin flap, as well as extending more
proximally along its course of lymphatic drainage. On the right, there is extensive disease extending
up to the inguinal crease.

44. Immunotherapy/Biological Therapy
o It is done using specific tumour antibodies, BCG, levamisole, Corynebacterium parvum, alpha interf
o Biochemotherapy is combination of CVD with interferon α and interleukin 2.
o GM2 ganglioside based vaccine (stimulates production of IgM antibodies), Melacine (contains mela

45. Unknown Primary Melanoma
Occurs in less than 2% of all melanoma cases and less than 5% of all patients who present with metastatic melanoma. Occult melanomas (primary unknown) are common in :
— Anus
— Scalp
— External auditory canal — Nail bed
— Genitalia
— Eye
— Adrenal medulla
Melanoma During Pregnancy
The prognosis is same patients treated during pregnancy is no different from non pregnant patients of a similar stage.
Noncutaneous Melanomas
the eye, mucosal surfaces, and unknown primary sites.
MRI of the liver is a more sensitive test, which will often demonstrate hundreds of small metastases.
The most common sites of origin for melanomas arising on the mucous membranes are the head and neck, anal canal, rectum, and female genitalia.
Compared with melanomas arising on the skin, mucosal melanomas are more advanced and have a uniformly poor prognosis. these tumors should be excised to negative margins.
Special Situations and Non-cutaneous Melanoma
Ocular melanoma is the most common malignancy arising in the eye. Ocular melanoma rarely metastasizes to lymph nodes because the uveal tract has no lymphatic vessels. Ocular mela

47. Prevention
Much excessive UV radiation exposure, in the form sunbathing and tanning bed use, is
intentional and completely preventable. Recommendations for reducing UV radiation exposure
include avoiding these activities, use of protective clothing, and use of sunscreens. Although
most experts believe that the use of sun- screens will reduce the risk of melanoma, this topic is
controversial, because some have suggested that sunscreens may provide a false sense of security
and allow persons at risk to experience more prolonged sun exposure. However, a meta- analysis
of 18 studies has found no evidence that use of sun- screens increased the incidence of
melanoma.

48. Cutaneous squamous cell carcinoma/ Epithelioma/ Khangri Cancer) (Chimney Cancer/
Epidermoid carcinoma
• SCC is a malignant tumour of keratinising cells of the epidermis or its appendages. It arises from the
stratum germinatum of the epidermis and expresses cytokeratins 1 and 10.
Epidemiology
• SCC is the second most common form of skin cancer.
• The time taken to develop an SCC after radiation exposure is proportional to the wavelength
of the radiation.
• SCC is also caused by chemical carcinogens (arsenicals, tar), and infection with human
papilloma virus 5 and 16.
• There is also evidence that current and previous tobacco use doubles the relative risk of SCC.Exposure to UV B rays (ultraviolet rays are A,B,C types)
causes SCC by direct carcinogenic effects on keratinocytes, unrepaired mutations, decreased immune
surveillance response, inhibition of tumour rejection, mutation of p53 suppressor gene (seen in 90%
SCC).

49. It occurs in premalignant conditions like Bowen’s disease, Paget’s disease, leukoplakia, chronic scars,
chemically induced chronic irritation, radiodermatitis, senile keratosis, e.g. Khangri cancer in
Kashmir, Chimney scrotal cancer, Kang cancer of Tibetans.
Bowen's disease, also known as squamous cell carcinoma in situ[
Extramammary Paget’s disease (EMPD)

50. Examination
Squamous cell carcinoma
▪ Associated with chronic inflammation
▪ Invariably ulcerated lesion
▪ Metastasis in 2 per cent cases
Common Sites are:
o Dorsum of hand, limbs, face, and skin of
abdominal wall SCC can occur in external genitalia,
mucocutaneous junction, oral cavity, respiratory
system, oesophagus, gall- bladder, in urinary bladder
as metaplasia from transitional cell lining.

51. o An ulcerative or ulceroproliferative lesion.
o Raised and everted edge.
o Indurated base and edge.
o Bloody discharge from the lesion.
o Regional lymph nodes are commonly involved, which are hard, nodular, initially mobile but eventually f
o Usually blood spread does not occur.

52. Variants
o Marjolin’s ulcer which occurs in chronic scar is a type of squamous cell carcinoma without lymph node s
no lymphatics in scar tissue, it will not spread to lymph nodes.
o Verrucous carcinoma is a squamous cell carcinoma, commonly occurring in mucous membrane or muco

53. Histology
An invasive, epidermal keratinising tumour characterised by proliferation of atypical squamous cells with ‘horn pearls’

54. o Radiotherapy using radiation needles,moulds,etc.isgiven.
o Wide excision, 2 cm clearance followed by skin grafting or flaps.
Reconstruction is usually done by primary split
skin grafting (SSG/Thiersch).
Delayed skin grafting also can
be done once wound granulates well. Often flaps of different types may be needed depending on the site of lesion.
o Amputation with one joint above.
For lymph nodes, block dissection of the regional lymph nodes is done.
o Curative radiotherapy (RT) is also useful in tumours which are not adherent to deeper planes or cartilage as SCC is radiosensitive. o In adv
o Chemotherapy is given using methotrexate, vincristine, bleomycin.
o Field therapy using cryo probe or topical fluorouracil or electrodessication.
Treatment

58. In contrast to SCCs and actinic keratoses, there is no precursor skin lesion for BCCs.
Basal cell carcinoma/ Rodent ulcer/ Tear cancer
This tumour of low-grade malignancy is common in white-skinned people. It originates from th
skin.
It does not arise from mucosa.
It is the commonest (70%) malignant skin tumour.
o It is more common in white-skinned people than blacks.
o Common in places where exposure to UV light is more
(Australia).

59. ONGHREN’S LINE

60. Examination
It starts as a small brownish-red nodule with
translucent colour and shiny surface showing a net work
of capillaries. At this stage it is diagnosed due to its
hardness, painlessness and presence of capillaries. Later on the tumour becomes ulcerated with a well defined
hard and raised edge (but not everted as seen in ^ epithelioma) with a beaded appearance. There is a central
scab but the margin gradually spreads and infiltrates into the surrounding tissues as well as deeper tissues even up to the bone. This characteristic feature of eroding the
tissues, which come in contact with it, has given it the name ‘rodent’. At first it may itch, but at a later stage it may be painful if it has eroded any nerve.
Dissemination by lymphatic or blood vessels does not occur. So the regional lymph nodes are not enlarged and there will be no metastasis to the distant organs. There may
be squamous celled carcinomatous change, though very rare.

61. 1. Nodular.
2. Cystic/nodulocystic.
3. Ulcerative.
4. Multiple,oftenassociatedwithsyndromesandothermalig-
nancies.
5. Pigmented BCC—mimics melanoma.
6. Geographical or field fire or forest fire BCC is wide area
involvement with central scabbing and peripheral active
proliferating edge.
7. Basisquamous—behaves like squamous cell carcinoma
Clinicopathological Types
a. Superficial type—small buds of tumour masses.
b. Morpheic type—dense stroma with basal cells and type IV
collagen; spreads rapidly.
c. Fibroepithelioma type of Pinkus shows elongated cords of
basaloid cells with mesh work.
Types

62. • Radiosensitive.
• Radiotherapy is not given, if it erodes cartilage or bone.
• RT is not given to BCC of ear and close to lacrimal canaliculi.
Surgery:
 Wide excision (1 cm clearance) with skin grafting, primary suturing or flap (Z
plasty, rhomboid flap, rotation flap) is the procedure of choice.
 Laser surgery.
 Cryosurgery.
• MOHS (Microscopically Oriented Histographic Surgery) is useful to get a
clearance margin and in conditions like BCC close to eyes, nose or ear, to preserve
Treatment

63. MOHS (Microscopically Oriented Histographic
Surgery)

66. Ninety-five per cent of local recurrence and regional metas- tases occur within five years, thus follow up b
Prognosis is excellent if the appropriate method of treatment is used in early primary basal-cell c

67. Uncommon Cutaneous Malignancies
Cutaneous angiosarcoma
is a rare, aggressive, soft
tissue sarcoma derived
from blood or lymphatic
vessel endothelium.
Dermato brosarcoma protuberans is
a low-grade sarcoma arising from
dermal fibroblasts.

68. Extramammary Paget’s disease (EMPD)
Kaposi’s sarcoma
Merkel cell carcinoma

70. “Destructive treatment options are generally reserved for low-risk basal cell
tumors and use a variety of methods to destroy neoplastic tissue including
electrosurgery, cryosurgery, topical 5-fluorouracil, topical imiquimod,
intralesional interferon, radiation, and photodynamic therapy. ”

71. Primary closure

72. Skin grafting

73. Tissue expander

74. Local flap

75. Local flap

76. Local flap

77. Free flap

78. Free flap

79. Conclusion
The important principles in the management of these entities are the same as those reviewed earlier:
1. Clinicians must have a low threshold for biopsy of new or changing skin lesions.
2. The diagnosis is made by biopsy and histologic analysis.
3. If appropriate, surgical excision is performed, with histo-
logically de ned negative margins.
4. Further treatment and follow-up schedules will be deter-
mined by the speci c diagnosis.

80. Any questions?

81. Bibliography
❖ Sabiston Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 19th Edition
❖ Bailey & Love's Short Practice of Surgery 26E
❖ https://www.nccn.org
❖ Grabb & Smith's Plastic Surgery
❖ Das’ manual of clinical surgery