Page 84 - The Netter Collection of Medical Illustrations - Integumentary System_ Volume 4 ( PDFDrive )
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Plate 3-19 Integumentary System
CLINICAL AND HISTOLOGICAL EVALUATION OF SUN-INDUCED SQUAMUS CELL CARCINOMA
SQUAMOUS CELL CARCINOMA
(Continued)
pyrimidine dimers and other DNA mutations. The
damaged DNA leads to errors in translation and tran-
scription and ultimately can lead to cancer. The p53
gene (TP53) is one of the most frequently mutated
genes. This gene encodes a protein that is important in
cell cycle arrest, which allows for DNA damage repair
and apoptosis of those cells that have been damaged. If Large ulcerative tumor destroying the ear.
the p53 gene is dysfunctional, this critical cell cycle Squamous cell carcinomas arising on the
arrest period is bypassed, and the cell is allowed to ear have a higher rate of metastasis.
replicate without the normal DNA repair mechanisms
acting on the damaged DNA. This ultimately leads to
unregulated cell division and cancer.
Histology: Actinic keratosis shows partial-thickness
atypia of the lower portions of the epidermis. The
adnexal structures are spared. SCC in situ shows full-
thickness atypia of the epidermis that also affects the
adnexal epithelium. Large nodule on the dorsal hand
SCC is derived from the keratinocytes. The patho-
logical findings are characterized by full-thickness
atypia of the epidermis and invasion of the abnormal
squamous epithelium into the dermis. Variable numbers
of mitoses are seen, as well as invasion into the underly-
ing subcutaneous tissue. Horn pearls are often seen
throughout the tumor. The tumors are often described
as being well, moderately, or poorly differentiated.
Many histological subtypes of SCC have been reported,
including clear cell, spindle cell, verrucous, basosqua-
mous, and adenosquamous cell carcinomas.
Treatment: Actinic keratoses can be treated in myriad
ways. Cryotherapy with liquid nitrogen is very effective
and can be used repeatedly. If this fails to clear the area,
or if the actinic keratoses are numerous, medical therapy
is often given with 5-fluorouracil (5-FU) or imiquimod.
These creams work, respectively, by directly killing the
affected cells or by causing the immune system to attack
and kill the affected cells. They are both highly effec-
tive. The disadvantage is that they cause an inflamma-
tory response that can be severe and cause erythema,
crusting, and weeping during the period of application,
usually 1 month or longer. Invasive SCC, low power. Atypical squamous epi- Invasive SCC, high power. Atypical keratinocytes,
The treatment for SCC in situ is often electrodessi- thelium invading the dermis. This tumor is poorly
cation and curettage or simple elliptical excision. 5-FU circumscribed. mitotic figures, and horn pearl formation
cream is also effective but leads to a higher rate of
recurrence than the traditional surgical methods. 5-FU
is appropriate as a first-line agent for bowenoid papu-
losis. If in follow-up any residual areas are left, surgical curettage. The metastatic rate for cutaneous SCC is higher risk for metastases; the reason is unknown but
removal is indicated. Occasionally, large areas of SCC low, but certain locations have a higher rate of metas- is thought to be related to the immunosuppression
in situ on the face are treated by the Mohs surgical tasis. These areas include the lip, the ear, and areas of resulting from their CLL. The most common areas for
technique. chronic scarring or ulceration in which the tumors metastasis are the local lymph nodes and lung.
Invasive SCC should be treated surgically, with Mohs develop. Recurrent SCCs, those larger than 2 cm in Metastatic SCC of the skin should be treated with
surgery for lesions on the face or recurrent lesions; diameter, and those developing in patients taking adjunctive radiotherapy and chemotherapy. However,
standard elliptical excision is adequate for most invasive chronic immunosuppressive medications pose a higher these therapies have not shown a clear survival benefit,
SCCs. Some small, well-differentiated SCCs have risk for the development of metastatic disease. Patients and the key to treatment ultimately lies in the preven-
been treated successfully with electrodessication and with chronic lymphocytic leukemia (CLL) are at much tion of metastasis.
70 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

