Creation of psoriatic plaques: the ultimate tumor suppressor pathway.: A new model for an ancient T‐cell‐mediated skin disease. Viewpoint
Open accessAbstract
From an oncological and immunological perspective, the T‐cell‐mediated induction of psoriatic plaques should be prone to malignant transformation as the phenotype of psoriatic plaques includes: chronic inflammation, epidermal hyperplasia, prolonged survival and elevated telomerase levels in lesional keratinocytes, as well as angiogenesis, exposure to carcinogens and immunosuppressants. However, conversion of a psoriatic plaque to squamous cell carcinoma is exceedingly rare. This paper explores the possible molecular mechanism for the tumor suppressor pathway in psoriatic lesions, with an emphasis on a putative senescence‐switch involving p16.
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A TNF and IFNγ cocktail might provide dominant tumour suppressor activity through cytokine-induced senescence in psoriasis.
“Here also a TNF and IFNγ cocktail might provide a dominant tumour suppressor activity through cytokine-induced senescence.”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [135]
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Wolf, R., Mirmohammadsadegh, A., Walz, M., Lysa, B., Tartler, U., Remus, R., Hengge, U. R., Michel, G., & Ruzicka, T. (2003) · The FASEB Journal · doi:10.1096/fj.03-0148fje · Cited by 67 · see citing works
Nickoloff, B. J., Lingen, M. W., Chang, B.-D., Shen, M., Swift, M. E., Curry, J. L., Bacon, P. E., Bodner, B. K., & Roninson, I. B. (2004) · Cancer Research · doi:10.1158/0008-5472.can-03-2388 · Cited by 67 · see citing works
Self-citationKulski, J. K., Kenworthy, W. D., Bellgard, M., Taplin, R., Okamoto, K., Oka, A., Mabuchi, T., Ozawa, A., Tamiya, G., & Inoko, H. (2005) · Journal of Molecular Medicine · doi:10.1007/s00109-005-0721-x · Cited by 66 · see citing works
“This proliferative burst within the epidermis was postulated by Nickoloff [ 21 ] to be of sufficient intensity and duration to trigger keratinocytes in the suprabasal cell layers to undergo premature senescence and form the chronic, stable psoriatic plaques.”
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Portugal‐Cohen, M., Horev, L., Rüffer, C., Schlippe, G., Voss, W., Ma’or, Z., Oron, M., Soroka, Y., Frušić‐Zlotkin, M., Milner, Y., et al. (2012) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2011.12.009 · Cited by 52 · see citing works
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IL-21 in the pathogenesis and treatment of skin diseases
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Chaturvedi, V., Cesnjaj, M., Bacon, P., Panella, J., Choubey, D., Diaz, M., & Nickoloff, B. (2003) · American Journal of Pathology · doi:10.1016/s0002-9440(10)63807-2 · Cited by 44 · see citing works
Self-citationCCHCR1 Is Up-Regulated in Skin Cancer and Associated with EGFR Expression
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“Psoriasis lesions hardly ever progress to skin cancer despite chronic inflammation that often is a risk factor for cancer [6,7].”
BackgroundSquamous cell carcinoma in vitiligo lesion after long‐term PUVA therapy
Park, H., Lee, Y., & Chun, D. (2003) · Journal of the European Academy of Dermatology and Venereology · doi:10.1046/j.1468-3083.2003.00815.x · Cited by 36 · see citing works
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Psoriatic epidermis is associated with upregulation of CDK 2 and inhibition of CDK 4 activity
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Elomaa, O., Asumalahti, K., Kariniemi, A., Karvonen, S.-L., Peltonen, J. T. K., Kere, J., Suomela, S., & Saarialho‐Kere, U. (2003) · Journal of Investigative Dermatology · doi:10.1046/j.1523-1747.2003.12642.x · Cited by 32 · see citing works
“It is known that skin cancers hardly ever arise in psoriatic plaques, in contrast to lesions of many other skin diseases, due to the putative senescence of keratinocytes in the mid and upper levels of the psoriatic plaque”
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Expression of p53 protein in psoriasis.
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Balato, N., Costanzo, L. D., Balato, A., Patruno, C., Scalvenzi, M., & Ayala, F. (2011) · British Journal of Dermatology · doi:10.1111/j.1365-2133.2011.10271.x · Cited by 30 · see citing works
Amphiregulin Overexpression Results in Rapidly Growing Keratinocytic Tumors
Billings, S. D., Southall, M. D., Li, T., Cook, P. W., Baldridge, L., Moores, W. B., Spandau, D. F., Foley, J., & Travers, J. B. (2003) · American Journal Of Pathology · doi:10.1016/s0002-9440(10)63600-0 · Cited by 30 · see citing works
Imiquimod attenuates the growth of UVB ‐ I nduced SCC in mice through Th1/ T h17 cells
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Expression of genes involved in the regulation of p16 in psoriatic involved skin
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“Up-regulation of the tumour suppressor p16 in psoriatic involved skin has been suggested as an explanation for the relative resistance to malignant transformation [31, 32], and p16 immunostaining and gene expression have been reported in psoriatic plaques [6, 14, 31].”
InfluentialExpression of cyclin D1 and p16 in psoriasis before and after phototherapy
El-Ela, M. A., Nagui, N. A. R., Mahgoub, D. A., El‐Eishi, N. H., Fawzy, M. M., El-Tawdy, A., Hay, R. M. A., & Rashed, L. (2010) · Clinical and Experimental Dermatology · doi:10.1111/j.1365-2230.2009.03774.x · Cited by 24 · see citing works
The Skin Cancer Paradox of Psoriasis
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Self-citationAnti-thyroid thioureylenes in the treatment of psoriasis
Elias, A. N. (2004) · Medical Hypotheses · doi:10.1016/j.mehy.2003.12.003 · Cited by 22 · see citing works
Hussein, M. R., & Wood, G. S. (2002) · American Journal of Dermatopathology · doi:10.1097/00000372-200202000-00016 · Cited by 19 · see citing works
Animal models of psoriasis and pustular psoriasis
Mizutani, H., Yamanaka, K., Konishi, H., & Murakami, T. (2003) · Archives of Dermatological Research · doi:10.1007/s00403-002-0374-3 · Cited by 18 · see citing works
Koo, J. Y. M., Lee, E., Lee, C. S., & Lebwohl, M. (2004) · Journal of the American Academy of Dermatology · doi:10.1016/j.jaad.2003.11.046 · Cited by 18 · see citing works
Elias, A. N., Barr, R. J., & Nanda, V. S. (2004) · International Journal of Dermatology · doi:10.1111/j.1365-4632.2004.02260.x · Cited by 17 · see citing works
Are Patients With Psoriasis Susceptible to the Classic Risk Factors for Actinic Keratoses?
Paltiel, O., Adler, B., Hershko, K., Tsukrov, B., & David, M. (2004) · Archives of Dermatology · doi:10.1001/archderm.140.7.805 · Cited by 16 · see citing works
Kjellerup, R. B., Iversen, L., Kragballe, K., & Johansen, C. (2009) · British Journal of Dermatology · doi:10.1111/j.1365-2133.2009.09303.x · Cited by 16 · see citing works
Staniszewska, M., Kiełbowski, K., Rusińska, K., Bakinowska, E., Gromowska, E., & Pawlik, A. (2023) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2023.2285784 · Cited by 10 · see citing works
“However, psoriatic cells may undergo a senescence switch, which is associated with elevated p16 expression [158].”
BackgroundThe psoriasiform reaction pattern
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Potential therapeutic role of peroxisome proliferator activated receptor-γ agonists in psoriasis
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“(2005) 6(9) 1459 psoriasis is not uncommon, and these conditions may exist more often than predicted from the prevalence rate of either disorder alone [61].”
BackgroundMorisaka, H., Takaishi, M., Akira, S., & Sano, S. (2022) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2022.11.007 · Cited by 9 · see citing works
Serum TNF-α in psoriasis after treatment with propylthiouracil, an antithyroid thioureylene
Elias, A. N., Nanda, V. S., & Pandian, R. (2004) · BMC Dermatology · doi:10.1186/1471-5945-4-4 · Cited by 7 · see citing works
“The disease is presently believed to be a T cell disorder that leads to keratinocyte proliferation (6;10;11).”
BackgroundYim, J. H., Jeong, K., & Shin, M. K. (2016) · Skin Research and Technology · doi:10.1111/srt.12315 · Cited by 7 · see citing works
4 The psoriasiform reaction pattern
Weedon, D. D. (2010) · Elsevier eBooks · doi:10.1016/b978-0-7020-3485-5.00046-2 · Cited by 6 · see citing works
Hung, C., Huang, S., Cheng, H., Liu, S., Chang, Y., Liu, Y., & Wang, W. (2015) · Journal of Dermatological Science · doi:10.1016/j.jdermsci.2015.06.006 · Cited by 6 · see citing works
Epidermal Nbn deletion causes premature hair loss and a phenotype resembling psoriasiform dermatitis
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The role of telomerase activity in psoriatic skin lesions
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On the Immunopathogenesis of Psoriasis
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Atopic Dermatitis—More Than a Simple Skin Disorder
Anderson, M. L. (2005) · Journal of the American Academy of Nurse Practitioners · doi:10.1111/j.1745-7599.2005.0042.x · Cited by 4 · see citing works
“Eczema herpeticum (EH) is the most important disseminated viral infection because it occurs in many settings and requires immediate medical attention (Nickoloff, 2001).”
BackgroundThe Effect of TNF-α and INF-γ on the Telomerase Activity of Cultured Human Keratinocyte
Hong, K. K., Lew, B., Kim, Y., Lee, J. W., & Kim, N. (2007) · Annals of Dermatology · doi:10.5021/ad.2007.19.4.147 · Cited by 3 · see citing works
Molecular Dissection of Psoriasis: Integrating Genetics and
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NF-κB, IκB Kinase and Interacting Signal Networks in Squamous Cell Carcinomas
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Senescencia celular y envejecimiento
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Psoriasis-like disease prevents squamous skin tumor development by neutrophil-driven inflammation
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Perforin Expression in Plaque Psoriasis: An Immunohistochemical Study
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Maffezzoni, M. B. R., Moretti, F., Botti, E., Marinari, B., Rusin, M., Narcisi, A., Favaro, R., & Costanzo, A. (2026) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2026.07.004
- Authors
- Nickoloff, B. J.
- Affiliations
- Loyola University Medical Center (US)
- Corresponding author
- Nickoloff, Brian J.
- ORCID
- Nickoloff, Brian J.
- Venue
- Journal of Cutaneous Pathology
- Publisher
- Wiley
- Published
- 2001-02
- Volume
- 28
- Issue
- 2
- Pages
- 57-64
- ISSN
- 0303-6987 (ISSN-L)
- 1600-0560
- OpenAlex
- W1583462410
- Cited by
- 78
- References
- 78
- Citations by year
- 2026: 2 · 2023: 2 · 2022: 1 · 2020: 1 · 2019: 1 · 2016: 3 · 2015: 2 · 2014: 2 · 2012: 4
- FWCI
- 0.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Cutaneous Pathology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Epidemiology › Nonmelanoma Skin Cancer Studies
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- psoriasis, psoriatic plaques, tumor suppressor pathways, malignant transformation, squamous cell carcinoma, cellular senescence, p16, telomerase, chronic inflammation, epidermal hyperplasia, angiogenesis, carcinogen exposure, immunosuppressants, T cell-mediated inflammation, keratinocytes
- MeSH terms
- Carcinoma, Squamous Cell, Cell Transformation, Neoplastic, Humans, Models, Biological, Precancerous Conditions, Psoriasis, Skin Neoplasms, T-Lymphocytes, Keratinocytes, Genes, Tumor Suppressor
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