Keratoacanthoma

To assess presence of virus DNA in skin lesions, swab samples from 82 squamous cell carcinomas of the skin (SCCs), 60 actinic keratoses (AKs), paraffin-embedded biopsies from 28 SCCs and 72 kerathoacanthomas (KAs) and fresh-frozen biopsies from 92 KAs, 85 SCCs and 92 AKs were analyzed by high throughput sequencing (HTS) using 454 or Ion Torrent technology. We found total of 4,284 viral reads, out of which 4,168 were Human Papillomavirus (HPV)-related, belonging to 15 known (HPV8, HPV12, HPV20, HPV36, HPV38, HPV45, HPV57, HPV59, HPV104, HPV105, HPV107, HPV109, HPV124, HPV138, HPV147), four previously described putative (HPV 915 F 06 007 FD1, FA73, FA101, SE42) and two putatively new HPV types (SE46, SE47). SE42 was cloned, sequenced, designated as HPV155 and found to have 76% similarity to the most closely related known HPV type. In conclusion, an unbiased approach for viral DNA detection in skin tumors has found that, although some new putative HPVs were found, known HPV types constituted most of the viral DNA.

Desmosomes are intercellular junctions that have been shown to be down-regulated in certain types of carcinoma and that may play a role in suppression of invasion and metastasis. This paper describes an immunohistochemical study of three types of epidermal neoplasms with monoclonal antibody to desmoglein in order to determine how desmosomal staining correlates with the clinical, biological and histopathological features of these neoplasms. Actinic keratosis (AK) is the most common keratinocytic premalignant neoplasm that was reported to have a 10-20% rate of malignant transformation into squamous cell carcinoma (SCC). Keratoacanthoma (KA) is a benign neoplasm that involutes spontaneously after a few months of rapid growth. SCC is a malignant tumour capable of metastasis. Electron microscope studies of KA and SCC showed significantly reduced staining for desmosomes in SCC but not in KA. We have examined staining for desmoglein using the monoclonal antibody 33-3D, a mouse IgM monoclonal antibody, that recognizes the cytoplasmic domains of desmoglein (Dsg)1 and Dsg2 on frozen sections. Immunohistochemical staining of normal skin with this antibody revealed strong pericellular localization of the antigen, outlining the cell membranes of the keratinocytes. A series of 30 AKs, 12 KAs and 24 SCCs was stained immunohistochemically with 33-3D monoclonal antibody. All examined KAs showed extensive pericellular staining for Dsg. By contrast, juxtanuclear staining for Dsg was noted in 12 SCCs, and completely negative staining in seven SCCs. The five remaining SCCs showed focal pericellular staining for the Dsg marker. The most common finding in AK was focal pericellular staining for Dsg, with complete absence of staining in dysplastic areas (25 cases). In five cases negative pericellular staining in dysplastic areas was associated with juxtanuclear accumulation of the Dsg marker. A strong negative correlation between Dsg staining and degree of dysplasia was obtained. The Dsg pattern in KA is similar to normal epidermis and shows a clear difference between KA and SCC. AK has a limited loss of Dsg expression in a SCC-like pattern that is congruent with its premalignant nature. As the stain works on frozen tissue, it may be helpful for rapid differentiation in selected cases in cutaneous oncology and Mohs micrographic surgery. This antibody may also have great potential for the detection of the effects of chemopreventive agents in skin cancer.

Keratoacanthomas (KAs) resemble squamous cell carcinomas (SCCs) except that, unlike SCCs, after a period of rapid growth over a few months they involute completely. The basis of their regressing natural history is not known. We have examined keratoacanthomas and another benign cutaneous tumour, the basal cell papilloma (BCP), for loss of heterozygosity (LOH) at a number of loci that are frequently lost in SCCs and other skin tumours. The frequency of LOH for both KAs and BCPs was low, with only isolated losses identified at 9p, 9q and 10q in KAs [fractional allelic loss (FAL) was 1.3%], and at 9p and 17p in BCPs (FAL was 0.4%). This contrasts with previous work showing a FAL of 32% in SCC and 46% in actinic keratoses. The results show a clear difference between KA and SCC and do not support the hypothesis that KAs are SCCs that regress as a result of external (host) influences but rather suggest that KAs and SCCs are different de novo. LOH around the locus implicated in the multiple self-healing epitheliomata of Ferguson-Smith (9q22-q31) was shown in only 1 of 11 KAs.

BackgroundTo systematically review the literature on clinicopathological features of keratoacanthomas (KA) in the oral and perioral region.Material and methodsThe review protocol as registered under the number CRD42022323274. Electronic searches were conducted in four databases with a specific search strategy using MeSH and free terms.Results60 studies reporting 73 cases of KA were included in this systematic review. KA affects more men with a mean age of 49.09 years old. Sun-exposed area of the lower lip was the most common anatomical location of the perioral lesions (38.35%) and the oral mucosa (9.58%) of the intra-oral ones. The most frequent clinical presentation of the perioral lesions was of an ulcerated nodule (36.23) and intra-orally of an papule (11.59) or nodule (11.59). Incisional biopsies were the commonest procedure for the diagnosis. The histological findings commonly presented a hyperplastic epithelial tissue forming a crater-like structure filled with keratin. Slightly atypia, keratin pearls and an inflammatory infiltrate in connective tissue could also be seen. Surgical excision was the treatment of choice in the majority of cases (45.71%). A low recurrence rate (6.89%) was seen in a mean follow-up time of 20.54 months.ConclusionsKA affects commonly sun-exposed areas of men in their sixth decade of life. Given the similarity of squamous cell carcinoma, it is important to study KA to help clinicians with the correct diagnosis and treatment.