Pathology and pathobiology of the actinic (solar) keratosis

Cockerell, Clay J.

doi:10.1046/j.0366-077x.2003.05625.x

Cited by 70 publications

(51 citation statements)

References 12 publications

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“…The morphology of atypical cells in both actinic keratosis and squamous cell carcinoma (SCC) is indistinguishable. The risk of rapid progression to squamous cell carcinoma is minimal, but up to 60% of squamous cell carcinoma cases arise on actinic keratosis (1). Thus, actinic keratosis requires careful diagnosis and follow-up.…”

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confidence: 99%

“…Early treatment of these lesions is important because 20% ofAK lesions evolve into squamous carcinoma; usually the first sign of progression is the presence of inflammation which is associated to a loss of differentiation leading to malignancy (4). Other well-known risk factors towards cancer progression include chronic UVB exposure, skin phototype, painful sunburns before the age of 20 years, immunosuppression and genetic predisposition (1). Many studies suggest a role of infection by human papillomaviruses (HPV) in NMSC development (5).…”

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confidence: 99%

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Cutaneous Human Papillomaviruses as Recurrence Factor in Actinic Keratoses

Dianzani

Pierangeli

Chiricozzi

et al. 2008

Int J Immunopathol Pharmacol

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Actinic keratoses (AK) are common, premalignant lesions cause mainly by UV DNA damage. Progression into squamous cell carcinoma may be influenced by other several factors such as chronic chemical exposure or viral infection. A carcinogenic role of Human Papillomaviruses (HPV) in early steps of skin tumour development was recently hypothesized; moreover the presence of HPV DNA seems to be higher in cancer precursor lesions. The aim of this work is to identify the presence of HPV DNA in biopsies from Actinic Keratoses (AK) and from normal skin samples collected from dermatological healthy subjects in Italy, in order to evaluate the severity and the clinical evolution of the HPV positive lesions. The DNA test revealed 37% HPV positivity in AK patients versus 0% in the control group; many different genotypes and variants were identified by direct sequencing of peR product. The HPV positive AK were usually clinically indistinguishable from the HPV negative. All AK lesions were removed by laser treatment, but AK lesions recurred in all HPV positive patients after a period of 45-60 days whereas the same disappeared in the HPV negative ones. These data permit to hypothesize that the presence of HPV DNA could be an aggravating factor for AK lesion severity and recurrence.

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confidence: 99%

mentioning

confidence: 99%

Cutaneous Human Papillomaviruses as Recurrence Factor in Actinic Keratoses

Dianzani

Pierangeli

Chiricozzi

et al. 2008

Int J Immunopathol Pharmacol

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“…Histopathological changes detected in AC consist in squamous cell hyperplasia of the epithelium, with different degrees of keratinization, disordered maturation increased mitotic activity and cytologic atypia [7], inflammatory infiltration [8] and basophilic changes in the stroma [9]. The dysplastic feature of the disease can lead to the development of the LSSC [10].…”

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confidence: 99%

Immuno Expression of PAKs in Actinic Cheilitis and in Lip Squamous Cell Carcinoma

Nero¹,

Pinheiro²,

Martins³

et al. 2015

J Cytol Histol

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Lip squamous cell carcinoma (LSCC) may develop from a potentially malignant disorder known as Actinic cheilitis (AC). The p21-activated kinases (PAKs) are possible targets for cancer therapeutics. The LSSC and AC samples were analyzed by immunohistochemistry in order to detects endogenous levels PAKs group I (PAK1 and PAK2) and group II (PAK4, PAK5 and PAK6) only when they were in phosphorylated form (active). Keratinocytes of the basals stratum showed intense staining for phosphoPAKs 1/2, while the most superficial cells of the stratum spinosum and the surface layer showed moderate immunostaining for PAKs 4/5/6 phosphorylated in the epithelium adjacent to injured area. AC did not immunoexpress actives PAKs 1/2 and PAKs 4/5/6. LSSC did not immunoexpress phosphoPAKs 1/2, but some degenerating cells and cells in the necrotic area showed intense staining. Our results suggest that PAKs 1/2 not participate in the regulation of AC and LSCC pathogenesis, while PAKs 4/5/6 are involved in the regulation of cell death in LSCC.

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“…Ma azt gondoljuk, hogy a cheilitis actinica ezen módosult keratinociták expanzióját jelenti (11,44). Szövettani vizsgálatkor, emelkedett mitotikus ráta, nukleáris atípia (pl.…”

Section: Klinikumunclassified

The differential diagnosis of cheilitis

Németh¹

2012

BVSZ

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Pathology and pathobiology of the actinic (solar) keratosis

Cited by 70 publications

References 12 publications

Cutaneous Human Papillomaviruses as Recurrence Factor in Actinic Keratoses

Cutaneous Human Papillomaviruses as Recurrence Factor in Actinic Keratoses

Immuno Expression of PAKs in Actinic Cheilitis and in Lip Squamous Cell Carcinoma

The differential diagnosis of cheilitis

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