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Actinic Keratosis Pathology

  • Author: Neil M Coleman, MD; Chief Editor: Jon A Reed, MD, MS  more...
 
Updated: Sep 24, 2015
 

Overview

Actinic keratosis is an erythematous scaly papule or plaque that develops on sun-damaged skin as a result of chronic exposure to ultraviolet radiation, typically in elderly patients with lighter skin types. This condition is related to squamous cell carcinoma of the skin and is often described as a precursor or early form of squamous cell carcinoma in situ, although most actinic keratoses will not progress to invasive squamous cell carcinoma.

The primary histologic feature is atypia or dysplasia of the keratinocytes in the basal layers of the epidermis (see an example in the image below). This is often accompanied by parakeratosis, thinning of the granular layer, buds of atypical epidermis extending toward the papillary dermis, dermal solar elastosis, and inflammation.

The epidermis show mild hyperkeratosis with dyspla The epidermis show mild hyperkeratosis with dysplasia of the basal keratinocytes and formation of small buds extending into the papillary dermis. There is prominent solar elastosis in the superficial dermis. The dysplastic changes primarily affect the epidermis between follicles. (Hematoxylin & eosin, 5× magnification.)

Actinic keratoses are extremely common, and the populations most at risk are older individuals with chronic sun-exposure and light skin. Millions of office visits to dermatologists each year are related to actinic keratosis.[1] One early estimate of the prevalence of actinic keratosis in the United States was 39.5 million.[2] Factors leading to an increased incidence of actinic keratosis include cumulative ultraviolet radiation exposure, increasing age, childhood sun exposure, male sex, and residing in latitudes close to the equator.[3]

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Etiology

Chronic exposure to ultraviolet light (UV) or sunlight is one of the most important factors in the development of actinic keratoses. Both UVB (290-320 nm) and UVA (320-400 nm) likely play a role in the development of these conditions.[4, 5] UV radiation acts as an initiator and promoter of carcinogenesis in actinic keratosis and squamous cell carcinoma. Overexposure to UV in normal skin will induce p53-dependent apoptosis, which may serve to protect the skin from damaged cells. These individual apoptotic keratinocytes are often referred to as "sunburn" cells and are seen histologically in the epidermis of skin overexposed to sunlight or UV radiation.

UV-induced mutations of the tumor suppressor gene TP53 are of major importance in the development of actinic keratosis. Basal keratinocytes with mutated TP53 may not respond normally to UV-induced apoptosis, allowing further proliferation and development of new genetic abnormalities.[6, 7, 8, 9]

Immunosuppression can also contribute to the development of actinic keratosis. Solid organ transplant patients are at increased risk for actinic keratosis and squamous cell carcinoma. Some drugs may act as photosensitizers, increasing susceptibility to UV radiation, whereas others may increase the risk for squamous cell carcinoma regardless of exposure to UV radiation.[10] However, it has been proposed that some medications actually reduce the risk for actinic keratosis; regular users of nonsteroidal anti-inflammatory drugs (NSAIDs) may appear to have reduced counts of actinic keratosis.[11]

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Clinical Features

Areas of skin that are heavily exposed to ultraviolet (UV) light are the most common locations for actinic keratoses. These common areas include the upper limbs, face, forehead, ears, and neck. Actinic keratoses that develop on the lips are referred to as actinic cheilitis.[12]

The clinical appearance of an actinic keratosis is that of a small (several millimeters), red scaly papule or plaque, with induration and thickening of the epidermis. There may be associated erythema. Often, more than one actinic keratosis will be present, and the lesion may show signs of secondary trauma from excoriation or chronic rubbing. A cylindrical hyperkeratotic cutaneous horn may develop in some cases.[13]

Tumor staging does not apply to actinic keratosis. Squamous cell carcinomas that arise in association with actinic keratosis typically have a low risk for metastasis.[14, 15]

Differential diagnosis

Consider the following conditions when evaluating a patient with suspected actinic keratosis pathology:

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Gross and Microscopic Features

Hyperkeratosis may be apparent grossly in the typical shave biopsy specimen.

Histologically, actinic keratoses show dysplastic changes of the basilar layers of the epidermis, typically associated with parakeratosis, and some degree of dermal solar elastosis. The dysplastic changes may include nuclear enlargement and pleomorphism, nuclear hyperchromatism, increased or atypical mitoses, as well as cytoplasmic pallor. Buds of dysplastic epidermis may extend toward the papillary dermis. In some cases, these buds may be difficult to distinguish from superficially invasive squamous cell carcinoma, especially in a superficial shave biopsy. The dysplastic epidermal changes typically spare the cutaneous appendages. There may be hyperpigmentation of the epidermis, trauma-related changes (ulceration, lichen simplex chronicus), as well as an inflammatory response.[16, 17, 18] See the following images.

The epidermis show mild hyperkeratosis with dyspla The epidermis show mild hyperkeratosis with dysplasia of the basal keratinocytes and formation of small buds extending into the papillary dermis. There is prominent solar elastosis in the superficial dermis. The dysplastic changes primarily affect the epidermis between follicles. (Hematoxylin & eosin, 5× magnification.)
The basal keratinocytes show dysplastic changes, i The basal keratinocytes show dysplastic changes, including nuclear enlargement, hyperchromasia, increased cytoplasm, and form small buds that extend into the papillary dermis. There is subtle hyperkeratosis of the stratum corneum. (Hematoxylin & eosin, 10× magnification.)

Variants or subtypes of actinic keratosis that have been described include pigmented, hypertrophic, atrophic, lichenoid, proliferative, acantholytic, and Bowenoid.[16, 17, 18] Pigmented actinic keratosis may show heavy melanin pigmentation of the basal layer keratinocytes, and clinically and histologically these may mimic a melanocytic proliferation, as seen in the following image.[19]

Acantholysis is present in this actinic keratosis. Acantholysis is present in this actinic keratosis. The degree of acantholysis can vary. Such a lesion may show histologic overlap with Grover disease and Darier disease. (Hematoxylin & eosin, 10× magnification.)

The dorsal hand is a common place for hypertrophic actinic keratosis. Such lesions often show changes of lichen simplex chronicus due to chronic irritation and rubbing of the lesion (see the first image below).[20] Lichenoid actinic keratosis will show some degree of interface change with associated lymphocytic infiltrate within the superficial dermis (see the second image below). Changes of lichen simplex chronicus accompany many atypical squamoproliferative lesions, such as hypertrophic actinic keratosis and squamous cell carcinoma. Beware of a superficially sampled lesion, especially on sites such as the dorsal hand or forearm.

A hypertrophic/hyperplastic actinic keratosis from A hypertrophic/hyperplastic actinic keratosis from the dorsal hand. It is not uncommon to see changes of lichen simplex chronicus, in addition to the dysplastic epidermal changes. (Hematoxylin & eosin, 5× magnification.)
This lichenoid actinic keratosis showed interface This lichenoid actinic keratosis showed interface changes, including apoptotic basal keratinocytes and a bandlike infiltrate of lymphocytes in the superficial dermis. (Hematoxylin & eosin, 10× magnification.)

Acantholytic actinic keratosis may mimic other conditions associated with acantholysis, such as Grover disease, Darier disease, and warty dyskeratoma, as well as seborrheic keratosis with acantholysis (see the image below).

Acantholysis is present in this actinic keratosis. Acantholysis is present in this actinic keratosis. The degree of acantholysis can vary. Such a lesion may show histologic overlap with Grover disease and Darier disease. (Hematoxylin & eosin, 10× magnification.)

There is a histologic spectrum between actinic keratosis and squamous cell carcinoma, and the line between the actinic keratosis and squamous cell carcinoma in situ can sometimes be arbitrary. Some authors have proposed a revision in nomenclature to address this issue, suggesting the term keratinocytic intraepidermal neoplasia or keratinocytic intraepidermal malignant neoplasia (KIN), using a 3-tiered grading system.[21, 22] The term actinic keratosis, however, is still commonly used in clinical practice.

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Immunohistochemistry

Immunohistochemistry or special stains typically play a very limited role in the routine diagnosis of actinic keratosis. The histologic changes alone in most cases are sufficient to render the diagnosis.

With some pigmented actinic keratoses, especially on atrophic sun-damaged skin, melanocytic markers (S100, Melan-A/Mart-1, MiTF, tyrosinase) may be useful to rule out an atypical lentiginous melanocytic proliferation in cases in which it is difficult to sort out atypical keratinocytes from atypical melanocytes. Care should be taken in interpretation of these stains, as some pigmented actinic keratoses may show increased labeling with Melan-A/Mart-1 in keratinocytes, leading to an over diagnosis of melanoma in situ.[23] In addition, Melan-A-positive "pseudomelanocytic nests" have been described in a lichenoid dermatitis on sun-damaged skin, which may mimic melanoma in situ histologically; correlation with the clinical presentation (and perhaps additional biopsy) is often necessary.[24, 25, 26]

Different patterns of staining with MIB-1 and p53 have been shown with actinic keratosis and Bowen disease. P53 and MIB-1 stain the lower portions of the epidermis and the basal layer of the epidermis in actinic keratosis, whereas in Bowen lesions, the staining occurs throughout the epidermis, with lack of staining in the basal layer.[27, 28] Diffuse epidermal expression of p16INK4a may also help distinguish Bowen disease/squamous cell carcinoma in situ from actinic keratoses, in which staining is rare and typically limited to the basal layer.[29, 30]

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Molecular and Genetic Alterations

Ultraviolet (UV) radiation induces abnormalities that initiate and promote the development of actinic keratosis. Many of the same genetic alterations are found in cutaneous squamous cell carcinoma as well as other malignancies. The interplay of alterations in cell cycle regulators, signal transduction pathways, and other genetic alterations in the development and progression of actinic keratoses to squamous cell carcinoma is a subject of great interest and active research.

Mutations in TP53 appear to play a crucial role in the development of actinic keratosis.[7, 31] When exposed to UVB light, mice with severe combined immune deficiency (SCID) with transplanted human skin will develop actinic keratoses associated with specific TP53 mutations.[32] UVB light has also been shown to downregulate the tumor suppressor PTEN (phosphatase and tensin homologue deleted on chromosome 10) in actinic keratosis, via an ERK (extracellular signal-regulated kinase)/AKT–dependent mechanism.[33]

The immunosuppressive cyclosporin may also affect the PTEN/AKT pathway in the development of actinic keratosis.[34] Overexpression of matrix metalloproteinase-1 (MMP-1) is also associated with early development of actinic keratosis and metalloproteinases may also play a role in mediating the epidermal growth factor receptor (EGFR)/ERK/AKT/cyclin D1 pathways and cell cycle progression induced by UVB radiation.[35, 36]

Actinic keratosis has been shown to have higher frequency of loss of heterozygosity on several chromosome arms.[37] Upregulation of p53, bcl-2, and cyclin D protein expression as well as activated ras genes have been shown in actinic keratosis.[38, 39, 40, 41] MYC numeric aberrations have been detected in one third and EGFR to one half of actinic keratoses.[42, 43]

Other proteins identified as having overexpression in actinic keratoses include p63, survivin, and telomerase reverse transcriptase (TERT).[44] Gene expression profiling of actinic keratosis and squamous cell carcinoma have shown similar patterns of gene expression, when compared with non–sun-exposed and sun-exposed skin.[45]

A study indicated that the mitogen activated protein kinase pathway may be pivotal to the transition from actinic keratoses to cutaneous squamous cell carcinoma and that this may represent a potential target for cutaneous squamous cell carcinoma prevention.[46]

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Prognosis

Although the majority of cutaneous squamous cell carcinomas arise from or in association with actinic keratosis, the risk of progression of actinic keratosis to squamous cell carcinoma is low. No reliable histologic criteria have been established that predict which actinic keratoses will progress to squamous cell carcinoma in situ or invasive squamous cell carcinoma. Published estimates have ranged from 0.025% and 20% per year/per lesion, although few longitudinal studies have been performed.[3]

A longitudinal study that sought to quantify risk of progression in actinic keratoses of the face and ears in a high-risk, predominantly male population of patients in the United States found that the risk of progression from actinic keratosis to squamous cell carcinoma (either in situ or invasive) was 0.60% at 1 year and 2.57% at 4 years of follow-up.[47] For progression from actinic keratosis to primary invasive squamous cell carcinoma, the risk was 0.39% at 1 year and 1.97% at 4 years of follow-up.

This same study found that the majority of clinically diagnosed actinic keratoses were not found at 1-year (55%) and 5-year (70%) follow-up intervals.[47] An Australian study with longitudinal follow-up estimated the risk of progression from actinic keratosis to squamous cell carcinoma in 1 year at less than 1 in 1000.[48]

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Contributor Information and Disclosures
Author

Neil M Coleman, MD Clinical Assistant Professor, Department of Pathology, Graduate School of Medicine, University of Tennessee Medical Center at Knoxville; Dermatopathologist, Knoxville Dermatopathology Laboratory

Neil M Coleman, MD is a member of the following medical societies: American Society of Dermatopathology, College of American Pathologists, Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Jon A Reed, MD, MS Professor Emeritus of Pathology, Professor Emeritus of Dermatology, Baylor College of Medicine

Jon A Reed, MD, MS is a member of the following medical societies: American Society of Dermatopathology, College of American Pathologists, United States and Canadian Academy of Pathology, Society for Melanoma Research

Disclosure: Nothing to disclose.

References
  1. Feldman SR, Fleischer AB Jr, McConnell RC. Most common dermatologic problems identified by internists, 1990-1994. Arch Intern Med. 1998 Apr 13. 158(7):726-30. [Medline].

  2. Bickers DR, Lim HW, Margolis D, Weinstock MA, Goodman C, Faulkner E, et al. The burden of skin diseases: 2004 a joint project of the American Academy of Dermatology Association and the Society for Investigative Dermatology. J Am Acad Dermatol. 2006 Sep. 55(3):490-500. [Medline].

  3. Salasche SJ. Epidemiology of actinic keratoses and squamous cell carcinoma. J Am Acad Dermatol. 2000 Jan. 42(1 Pt 2):4-7. [Medline].

  4. Huang XX, Bernerd F, Halliday GM. Ultraviolet A within sunlight induces mutations in the epidermal basal layer of engineered human skin. Am J Pathol. 2009 Apr. 174(4):1534-43. [Medline]. [Full Text].

  5. Ibuki Y, Allanson M, Dixon KM, Reeve VE. Radiation sources providing increased UVA/UVB ratios attenuate the apoptotic effects of the UVB waveband UVA-dose-dependently in hairless mouse skin. J Invest Dermatol. 2007 Sep. 127(9):2236-44. [Medline].

  6. Brash DE, Rudolph JA, Simon JA, Lin A, McKenna GJ, Baden HP, et al. A role for sunlight in skin cancer: UV-induced p53 mutations in squamous cell carcinoma. Proc Natl Acad Sci U S A. 1991 Nov 15. 88(22):10124-8. [Medline]. [Full Text].

  7. Ziegler A, Jonason AS, Leffell DJ, Simon JA, Sharma HW, Kimmelman J, et al. Sunburn and p53 in the onset of skin cancer. Nature. 1994 Dec 22-29. 372(6508):773-6. [Medline].

  8. Brash DE, Ziegler A, Jonason AS, Simon JA, Kunala S, Leffell DJ. Sunlight and sunburn in human skin cancer: p53, apoptosis, and tumor promotion. J Investig Dermatol Symp Proc. 1996 Apr. 1(2):136-42. [Medline].

  9. Goldberg LH, Joseph AK, Tschen JA. Proliferative actinic keratosis. Int J Dermatol. 1994 May. 33(5):341-5. [Medline].

  10. Parrish JA. Immunosuppression, skin cancer, and ultraviolet A radiation. N Engl J Med. 2005 Dec 22. 353(25):2712-3. [Medline].

  11. Butler GJ, Neale R, Green AC, Pandeya N, Whiteman DC. Nonsteroidal anti-inflammatory drugs and the risk of actinic keratoses and squamous cell cancers of the skin. J Am Acad Dermatol. 2005 Dec. 53(6):966-72. [Medline].

  12. Frost CA, Green AC. Epidemiology of solar keratoses. Br J Dermatol. 1994 Oct. 131(4):455-64. [Medline].

  13. Moy RL. Clinical presentation of actinic keratoses and squamous cell carcinoma. J Am Acad Dermatol. 2000 Jan. 42(1 Pt 2):8-10. [Medline].

  14. Rowe DE, Carroll RJ, Day CL Jr. Prognostic factors for local recurrence, metastasis, and survival rates in squamous cell carcinoma of the skin, ear, and lip. Implications for treatment modality selection. J Am Acad Dermatol. 1992 Jun. 26(6):976-90. [Medline].

  15. Khanna M, Fortier-Riberdy G, Smoller B, Dinehart S. Reporting tumor thickness for cutaneous squamous cell carcinoma. J Cutan Pathol. 2002 Jul. 29(6):321-3. [Medline].

  16. Weedon D. Actinic keratosis. Weedon D. Weedon's Skin Pathology. 3rd ed. London, UK: Churchill Livingstone/Elsevier; 2010. 676-9.

  17. Brenn T, McKee PH. Tumors of surface epithelium. McKee PH, Calonje E, Granter SR, eds. Pathology of the Skin With Clinical Correlations. 3rd ed. Philadelphia, Pa: Elsevier Mosby; 2005. 22:

  18. LeBoit PE, Burg G, Weedon D, Sarasain A, eds. Actinic keratosis. World Health Organization Classification of Tumours. Pathology and Genetics of Skin Tumors. Lyon, France: IARC Press; 2006. 30-2.

  19. James MP, Wells GC, Whimster IW. Spreading pigmented actinic keratoses. Br J Dermatol. 1978 Apr. 98(4):373-9. [Medline].

  20. Billano RA, Little WP. Hypertrophic actinic keratosis. J Am Acad Dermatol. 1982 Oct. 7(4):484-9. [Medline].

  21. Cockerell CJ. Histopathology of incipient intraepidermal squamous cell carcinoma ("actinic keratosis"). J Am Acad Dermatol. 2000 Jan. 42(1 Pt 2):11-7. [Medline].

  22. Ramos-Ceballos FI, Ounpraseuth ST, Horn TD. Diagnostic concordance among dermatopathologists using a three-tiered keratinocytic intraepithelial neoplasia grading scheme. J Cutan Pathol. 2008 Apr. 35(4):386-91. [Medline].

  23. Wiltz KL, Qureshi H, Patterson JW, Mayes DC, Wick MR. Immunostaining for MART-1 in the interpretation of problematic intra-epidermal pigmented lesions. J Cutan Pathol. 2007 Aug. 34(8):601-5. [Medline].

  24. Helm K, Findeis-Hosey J. Immunohistochemistry of pigmented actinic keratoses, actinic keratoses, melanomas in situ and solar lentigines with Melan-A. J Cutan Pathol. 2008 Oct. 35(10):931-4. [Medline].

  25. Beltraminelli H, Shabrawi-Caelen LE, Kerl H, Cerroni L. Melan-a-positive "pseudomelanocytic nests": a pitfall in the histopathologic and immunohistochemical diagnosis of pigmented lesions on sun-damaged skin. Am J Dermatopathol. 2009 May. 31(3):305-8. [Medline].

  26. El Shabrawi-Caelen L, Kerl H, Cerroni L. Melan-A: not a helpful marker in distinction between melanoma in situ on sun-damaged skin and pigmented actinic keratosis. Am J Dermatopathol. 2004 Oct. 26(5):364-6. [Medline].

  27. Saglam O, Salama M, Meier F, Chaffins M, Ma C, Ormsby A, et al. Immunohistochemical staining of palisading basal cells in Bowen's disease and basal involvement in actinic keratosis: contrasting staining patterns suggest different cells of origin. Am J Dermatopathol. 2008 Apr. 30(2):123-6. [Medline].

  28. Sim CS, Slater S, McKee PH. Mutant p53 expression in solar keratosis: an immunohistochemical study. J Cutan Pathol. 1992 Aug. 19(4):302-8. [Medline].

  29. Salama ME, Mahmood MN, Qureshi HS, Ma C, Zarbo RJ, Ormsby AH. p16INK4a expression in actinic keratosis and Bowen's disease. Br J Dermatol. 2003 Nov. 149(5):1006-12. [Medline].

  30. Kanellou P, Zaravinos A, Zioga M, Stratigos A, Baritaki S, Soufla G, et al. Genomic instability, mutations and expression analysis of the tumour suppressor genes p14(ARF), p15(INK4b), p16(INK4a) and p53 in actinic keratosis. Cancer Lett. 2008 Jun 8. 264(1):145-61. [Medline].

  31. Park WS, Lee HK, Lee JY, Yoo NJ, Kim CS, Kim SH. p53 mutations in solar keratoses. Hum Pathol. 1996 Nov. 27(11):1180-4. [Medline].

  32. Nomura T, Nakajima H, Hongyo T, Taniguchi E, Fukuda K, Li LY, et al. Induction of cancer, actinic keratosis, and specific p53 mutations by UVB light in human skin maintained in severe combined immunodeficient mice. Cancer Res. 1997 Jun 1. 57(11):2081-4. [Medline].

  33. Ming M, Han W, Maddox J, Soltani K, Shea CR, Freeman DM, et al. UVB-induced ERK/AKT-dependent PTEN suppression promotes survival of epidermal keratinocytes. Oncogene. 2010 Jan 28. 29(4):492-502. [Medline]. [Full Text].

  34. Han W, Ming M, He TC, He YY. Immunosuppressive cyclosporin A activates AKT in keratinocytes through PTEN suppression: implications in skin carcinogenesis. J Biol Chem. 2010 Apr 9. 285(15):11369-77. [Medline]. [Full Text].

  35. Tsukifuji R, Tagawa K, Hatamochi A, Shinkai H. Expression of matrix metalloproteinase-1, -2 and -3 in squamous cell carcinoma and actinic keratosis. Br J Cancer. 1999 Jun. 80(7):1087-91. [Medline]. [Full Text].

  36. Han W, He YY. Requirement for metalloproteinase-dependent ERK and AKT activation in UVB-induced G1-S cell cycle progression of human keratinocytes. Photochem Photobiol. 2009 Jul-Aug. 85(4):997-1003. [Medline]. [Full Text].

  37. Rehman I, Quinn AG, Healy E, Rees JL. High frequency of loss of heterozygosity in actinic keratoses, a usually benign disease. Lancet. 1994 Sep 17. 344(8925):788-9. [Medline].

  38. Nelson MA, Einspahr JG, Alberts DS, Balfour CA, Wymer JA, Welch KL, et al. Analysis of the p53 gene in human precancerous actinic keratosis lesions and squamous cell cancers. Cancer Lett. 1994 Sep 30. 85(1):23-9. [Medline].

  39. Spencer JM, Kahn SM, Jiang W, DeLeo VA, Weinstein IB. Activated ras genes occur in human actinic keratoses, premalignant precursors to squamous cell carcinomas. Arch Dermatol. 1995 Jul. 131(7):796-800. [Medline].

  40. Bito T, Ueda M, Ahmed NU, Nagano T, Ichihashi M. Cyclin D and retinoblastoma gene product expression in actinic keratosis and cutaneous squamous cell carcinoma in relation to p53 expression. J Cutan Pathol. 1995 Oct. 22(5):427-34. [Medline].

  41. Hussein MR, Al-Badaiwy ZH, Guirguis MN. Analysis of p53 and bcl-2 protein expression in the non-tumorigenic, pretumorigenic, and tumorigenic keratinocytic hyperproliferative lesions. J Cutan Pathol. 2004 Nov. 31(10):643-51. [Medline].

  42. Toll A, Salgado R, Yébenes M, Martín-Ezquerra G, Gilaberte M, Baró T, et al. MYC gene numerical aberrations in actinic keratosis and cutaneous squamous cell carcinoma. Br J Dermatol. 2009 Nov. 161(5):1112-8. [Medline].

  43. Toll A, Salgado R, Yébenes M, Martín-Ezquerra G, Gilaberte M, Baró T, et al. Epidermal growth factor receptor gene numerical aberrations are frequent events in actinic keratoses and invasive cutaneous squamous cell carcinomas. Exp Dermatol. 2010 Feb. 19(2):151-3. [Medline].

  44. Park HR, Min SK, Cho HD, Kim KH, Shin HS, Park YE. Expression profiles of p63, p53, survivin, and hTERT in skin tumors. J Cutan Pathol. 2004 Sep. 31(8):544-9. [Medline].

  45. Padilla RS, Sebastian S, Jiang Z, Nindl I, Larson R. Gene expression patterns of normal human skin, actinic keratosis, and squamous cell carcinoma: a spectrum of disease progression. Arch Dermatol. 2010 Mar. 146(3):288-93. [Medline].

  46. Lambert SR, Mladkova N, Gulati A, Hamoudi R, Purdie K, Cerio R, et al. Key differences identified between actinic keratosis and cutaneous squamous cell carcinoma by transcriptome profiling. Br J Cancer. 2014 Jan 21. 110 (2):520-9. [Medline].

  47. Criscione VD, Weinstock MA, Naylor MF, Luque C, Eide MJ, Bingham SF. Actinic keratoses: Natural history and risk of malignant transformation in the Veterans Affairs Topical Tretinoin Chemoprevention Trial. Cancer. 2009 Jun 1. 115(11):2523-30. [Medline].

  48. Marks R, Rennie G, Selwood TS. Malignant transformation of solar keratoses to squamous cell carcinoma. Lancet. 1988 Apr 9. 1(8589):795-7. [Medline].

 
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The epidermis show mild hyperkeratosis with dysplasia of the basal keratinocytes and formation of small buds extending into the papillary dermis. There is prominent solar elastosis in the superficial dermis. The dysplastic changes primarily affect the epidermis between follicles. (Hematoxylin & eosin, 5× magnification.)
The basal keratinocytes show dysplastic changes, including nuclear enlargement, hyperchromasia, increased cytoplasm, and form small buds that extend into the papillary dermis. There is subtle hyperkeratosis of the stratum corneum. (Hematoxylin & eosin, 10× magnification.)
This lichenoid actinic keratosis showed interface changes, including apoptotic basal keratinocytes and a bandlike infiltrate of lymphocytes in the superficial dermis. (Hematoxylin & eosin, 10× magnification.)
A hypertrophic/hyperplastic actinic keratosis from the dorsal hand. It is not uncommon to see changes of lichen simplex chronicus, in addition to the dysplastic epidermal changes. (Hematoxylin & eosin, 5× magnification.)
Acantholysis is present in this actinic keratosis. The degree of acantholysis can vary. Such a lesion may show histologic overlap with Grover disease and Darier disease. (Hematoxylin & eosin, 10× magnification.)
Acantholysis is present in this actinic keratosis. The degree of acantholysis can vary. Such a lesion may show histologic overlap with Grover disease and Darier disease. (Hematoxylin & eosin, 10× magnification.)
 
 
 
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