chapter 41 Pre- and Paraneoplastic Syndromes.........................
DEFINITION/OVERVIEW
Preneoplastic dermatoses: lesions with a malignant predisposition; atendencyto
become tumors (not consistent).
Paraneoplastic dermatoses: lesions resulting from the metabolic effects of internal
malignancy; often a marker for specific cancer.
Categorizing preneoplastic versus paraneoplastic dermatoses: difficult in some syn-
dromes – progression from a reactive pattern to overt neoplasia may be inconsistent.
ETIOLOGY/PATHOPHYSIOLOGY
Canine preneoplastic dermatoses:
Actinic keratoses: ultraviolet light (UVL) causes DNA damage directly and indi-
rectly by free radicals; specific UVL-induced mutations have been documented in
the tumor suppressor gene p53, leading to expansion of mutated keratinocytes;
may represent a premalignant condition; close association of and genetic simi-
larities between AK and squamous cell carcinoma (SCC); actinic carcinomain
situdenotes SCC that has not penetrated to the dermis (see relevant chapter)
Cutaneous lymphocytosis: expansion of T cells in response to persistent anti-
genic stimulation such as drugs or vaccines; clonal rearrangement may result in
overt lymphoma
Cutaneous mastocytosis: a specific mutation in mast cells leading to systemic
mastocytosis has not been identified; associated with mutations of thec-kitonco-
gene in human beings
Nodular fasciitis: benign reactive lesion, possibly due to trauma; occasionally
used to describe proliferative inflammatory processes, including reactive histio-
cytosis.
Canine paraneoplastic dermatoses:
Cutaneous (primary nodular) amyloidosis: increased production of amyloido-
genic immunoglobulin light chains by proliferating plasma cells; associated with
multiple myeloma and extramedullary plasmacytoma; associated with chronic
inflammatory conditions
Cutaneous mucinosis (secondary): excessive accumulation of mucin in the der-
mis rarely associated with mast cell tumors
Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Dermatology, Third Edition.
Karen Helton Rhodes and Alexander H. Werner.
©2018 John Wiley & Sons, Inc. Published 2018 by John Wiley & Sons, Inc.
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