Altered expression of major histocompatibility complex (MHC) antigens by epidermal tumours

Markey, Andrew C.; Churchill, Linda J.; Macdonald, D.M.

doi:10.1111/j.1600-0560.1990.tb00058.x

Cited by 26 publications

(8 citation statements)

References 26 publications

(12 reference statements)

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“…Supporting this supposition are numerous studies demonstrating an increase of activated intratumoral CD4-positive T cells (34,35), fewer numbers of eosinophils (36), and increased Langerhans' cells (37) in KA compared with SCC, and a high incidence of KAs in patients who experience immunosuppression (20,38,39). In addition, KAs can exhibit expression of human leukocyte antigen DR (40). Despite these findings in support of immunologically mediated regression, nonimmunologic mechanisms have been postulated (41) and by chromosomal analysis, KAs seem to be distinct from SCCs de novo (42).…”

Section: Discussionmentioning

confidence: 98%

Comparison of Oncostatin M Expression in Keratoacanthoma and Squamous Cell Carcinoma

et al. 2000

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Oncostatin M (OSM) is a 28-kDa glycoprotein, produced by stimulated macrophages and T lymphocytes, that inhibits the proliferation and induces differentiation of a number of different cell lines derived from solid tumors. To determine whether keratoacanthoma (KA) is unique or a variant of squamous cell carcinoma (SCC), we compared the immunohistochemical expression of OSM in the tumor cells and peri-and intratumoral macrophages of 21 mature KAs, 7 regressing KAs, and 27 SCCs. An inverse correlation was identified between OSM tumor labeling and the density of OSM-labeled tumor-associated macrophages for KAs (r ‫؍‬ ؊.4; P ‫؍‬ .09). OSM tumor expression was significantly more frequent and more intense in KAs than in SCCs (95% versus 63%; P < .01). In contrast, the density of OSM-labeled macrophages was significantly higher in SCCs compared with mature KAs (7/3 high power fields versus 4/3 high power fields; P ‫؍‬ .02). These OSM-positive macrophages were predominantly located at the advancing, infiltrative margins of both neoplasms. Regressing KAs demonstrated a decreased level of OSM tumor expression compared with mature KAs (53% versus 95%; P ‫؍‬ .001), but there was no difference in density of OSMlabeled macrophages. Both the above differences and the overlapping patterns of OSM expression suggest that KAs are a variant of SCC where OSM, possibly as an autocrine factor, may mediate KA's overwhelming but not absolute tendency to involute.

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Section: Discussionmentioning

confidence: 98%

Comparison of Oncostatin M Expression in Keratoacanthoma and Squamous Cell Carcinoma

et al. 2000

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“…Associations between aberrant human leukocyte antigen (HLA) expression (75,76), or germline class-I and II allelic variations and keratinocyte carcinoma have been controversial (77)(78)(79)(80) and are affected by high UV exposure (81), immunosuppression (82), and HPV infection (83). Multiple variants in HLA-DRB1 ( Ã 01, Ã 07) have shown increased risk for BCC while HLA-DRB1 Ã 04 was protective (82).…”

Section: Germline Genetic Risk Factors and Risk Modelsmentioning

confidence: 99%

Keratinocyte Carcinomas: Current Concepts and Future Research Priorities

Nagarajan

Asgari

Green

et al. 2019

Clinical Cancer Research

103

123

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Cutaneous squamous cell carcinoma (cSCC) and basal cell carcinoma (BCC) are keratinocyte carcinomas, the most frequently diagnosed cancers in fair-skinned populations. Ultraviolet radiation (UVR) is the main driving carcinogen for these tumors, but immunosuppression, pigmentary factors, and aging are also risk factors. Scientific discoveries have improved the understanding of the role of human papillomaviruses (HPV) in cSCC as well as the skin microbiome and a compromised immune system in the development of both cSCC and BCC. Genomic analyses have uncovered genetic risk variants, high-risk susceptibility genes, and somatic events that underlie common pathways important in keratinocyte carcinoma tumorigenesis and tumor characteristics that have enabled development of prediction models for early identification of high-risk individuals. Advances in chemoprevention in high-risk individuals and progress in targeted and immune-based treatment approaches have the potential to decrease the morbidity and mortality associated with these tumors. As the incidence and prevalence of keratinocyte carcinoma continue to increase, strategies for prevention, including effective sun-protective behavior, educational interventions, and reduction of tanning bed access and usage, are essential. Gaps in our knowledge requiring additional research to reduce the high morbidity and costs associated with keratinocyte carcinoma include better understanding of factors leading to more aggressive tumors, the roles of microbiome and HPV infection, prediction of response to therapies including immune checkpoint blockade, and how to tailor both prevention and treatment to individual risk factors and needs.

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“…Multiple studies have shown that cSCC tumors also demonstrate high cell surface expression of class II HLA proteins [24–28]. Specifically, cSCC tumors most often express HLA-DR, though HLA-DP and DQ expression have also been reported [24,26]. Peripheral areas of cSCC tumors near inflammatory infiltrates show highest expression of class II HLA proteins [24–28].…”

Section: Resultsmentioning

confidence: 99%

Cutaneous squamous cell cancer (cSCC) risk and the human leukocyte antigen (HLA) system

et al. 2017

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Cutaneous squamous cell carcinoma (cSCC) is the second most common cancer among Caucasians in the United States, with rising incidence over the past decade. Treatment for non-melanoma skin cancer, including cSCC, in the United States was estimated to cost $4.8 billion in 2014. Thus, an understanding of cSCC pathogenesis could have important public health implications. Immune function impacts cSCC risk, given that cSCC incidence rates are substantially higher in patients with compromised immune systems. We report a systematic review of published associations between cSCC risk and the human leukocyte antigen (HLA) system. This review includes studies that analyze germline class I and class II HLA allelic variation as well as HLA cell-surface protein expression levels associated with cSCC risk. We propose biological mechanisms for these HLA-cSCC associations based on known mechanisms of HLA involvement in other diseases. The review suggests that immunity regulates the development of cSCC and that HLA-cSCC associations differ between immunocompetent and immunosuppressed patients. This difference may reflect the presence of viral co-factors that affect tumorigenesis in immunosuppressed patients. Finally, we highlight limitations in the literature on HLA-cSCC associations, and suggest directions for future research aimed at understanding, preventing and treating cSCC.

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Altered expression of major histocompatibility complex (MHC) antigens by epidermal tumours

Cited by 26 publications

References 26 publications

Comparison of Oncostatin M Expression in Keratoacanthoma and Squamous Cell Carcinoma

Comparison of Oncostatin M Expression in Keratoacanthoma and Squamous Cell Carcinoma

Keratinocyte Carcinomas: Current Concepts and Future Research Priorities

Cutaneous squamous cell cancer (cSCC) risk and the human leukocyte antigen (HLA) system

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