How Often Does Squamous Cell Carcinoma of the Skin Metastasize?

Lund, Herbert Z.

doi:10.1001/archderm.1965.01600180027004

Cited by 199 publications

(59 citation statements)

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“…7,42,43 The metastatic rate for cSCC is between 0.1 and 9.9% and represents the main cause of death for patients suffering from NMSC. [4][5][6][7] For tumors with a depth >6 mm, the metastatic rate rises to 16% and high-risk patients such as those on immunosuppression are at an increased risk of developing aggressive cSCC with a corresponding higher rate of metastasis. 3,7,44 For these patients in particular, a biomarker to distinguish primary tumors with an increased risk of metastasis would be a highly desirable clinical tool, enabling more efficient targeted management such as sentinel lymph node surveillance.…”

Section: Discussionmentioning

confidence: 99%

“…[4][5][6][7] Metastatic cSCC is currently treated by surgical intervention and/or chemotherapy or radiotherapy and is associated with a poor outcome.…”

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confidence: 99%

“…3 Risk factors for metastasis include poor differentiation of the tumor cells, large tumor size, tumor depth >5 mm, immunosuppression and localization on the ear and lip. [4][5][6][7] Metastatic cSCC is currently treated by surgical intervention and/or chemotherapy or radiotherapy and is associated with a poor outcome. 8 Despite the well-established role of ultraviolet radiation (UVR) in the etiology of cSCC, the molecular events underlying its development remain largely undefined.…”

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Metastatic cutaneous squamous cell carcinoma shows frequent deletion in the protein tyrosine phosphatase receptor Type D gene

Lambert

Harwood

Purdie

et al. 2011

Intl Journal of Cancer

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Cutaneous squamous cell carcinoma (cSCC) is the second most common form of nonmelanoma skin cancer (NMSC), and its incidence is increasing rapidly. Metastatic cSCC accounts for the majority of deaths associated with NMSC, but the genetic basis for cSCC progression remains poorly understood. A previous study identified small deletions (typically <1 Mb) in the protein tyrosine phosphatase receptor Type D (PTPRD) gene that segregated with more aggressive cSCC. To investigate the apparent association between deletion within PTPRD and cSCC metastasis, a series of 74 formalin-fixed paraffin-embedded tumors from 31 patients was analyzed using a custom Illumina 384 SNP microarray. Deletions were found in 37% of patients with metastatic cSCC and were strongly associated with metastatic tumors when compared to those that had not metastasized (p 5 0.007). Subsequent mutation analysis revealed a higher mutation rate for PTPRD than has been reported in any other cancer type, with 37% of tumors harboring a somatic mutation. Conversely, bisulfite sequencing showed that methylation was not a mechanism of PTPRD disruption in cSCC. This is the first report to observe an association between deletion within PTPRD and metastatic disease and highlights the potential use of these deletions as a diagnostic biomarker for tumor progression. Combined with the high mutation rate observed in our study, PTPRD is one of the most commonly altered genes in cSCC and warrants further investigation to determine its significance for metastasis in other tumor types.Nonmelanoma skin cancer (NMSC) has a predicted prevalence equal to that of all other cancers combined and its incidence is increasing.1 There are more than 81,500 new cases of NMSC diagnosed annually in the United Kingdom alone, placing a heavy burden on both patients and healthcare resources.2 Despite accounting for only 20% of total NMSC cases, cutaneous squamous cell carcinoma (cSCC) is responsible for the majority of NMSC deaths, largely as a result of metastatic disease. A subset of immunosuppressed individuals, such as organ transplant recipients on long-term immunosuppressive drugs, develop particularly aggressive tumors with an increased risk of metastasis.3 Risk factors for metastasis include poor differentiation of the tumor cells, large tumor size, tumor depth >5 mm, immunosuppression and localization on the ear and lip. [4][5][6][7] Metastatic cSCC is currently treated by surgical intervention and/or chemotherapy or radiotherapy and is associated with a poor outcome. 8Despite the well-established role of ultraviolet radiation (UVR) in the etiology of cSCC, the molecular events underlying its development remain largely undefined. Inactivation of the tumor suppressor genes TP53 and p16INK4A is a common and early event in cSCC pathogenesis and is characteristic of all histological grades of tumor. 9,10 Recently, genotyping of 60 cSCC identified high rates of loss of heterozygosity (LOH)

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Section: Discussionmentioning

confidence: 99%

“…[4][5][6][7] Metastatic cSCC is currently treated by surgical intervention and/or chemotherapy or radiotherapy and is associated with a poor outcome.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

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Metastatic cutaneous squamous cell carcinoma shows frequent deletion in the protein tyrosine phosphatase receptor Type D gene

Lambert

Harwood

Purdie

et al. 2011

Intl Journal of Cancer

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“…Cheilitis actinica talaján kialakul laphámkarcinóma az esetek 11%-ában ad áttétet, míg keratosis solaris esetén ugyanez az érték mindösszesen 1% (35,54,59).…”

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The differential diagnosis of cheilitis

Németh¹

2012

BVSZ

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“…While the overall rate of metastasis is quite low (on the order of 1-2%) and difficult to assess precisely (for the same reasons as proffered for actinic keratosis incidence above), this rate is greatly increased in certain circumstances. [8][9][10] Traditionally, pathologists have provided clinicians with a template of prognostic indicators when reporting melanomas. This has not been true for squamous cell carcinomas, perhaps in part due to the relatively good prognosis for most of these tumors.…”

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Squamous cell carcinoma: from precursor lesions to high-risk variants

Smoller

2006

Modern Pathology

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Cutaneous squamous cell carcinoma is second only to basal cell carcinoma in its incidence within our population. It is among the most common types of neoplasm afflicting the human race. Most cases are related to exposure to sunlight. This initial portion of the chapter will focus upon the biologic progression that results in the ultimate development of fully formed squamous cell carcinoma. The latter portion will focus upon the histologic features of squamous cell carcinoma, which may be potential prognostic indicators. While pathologists currently provide clinicians with information about many histologic features that may affect the outcome for patients with melanoma, there is little impetus for similar behavior on the part of pathologists when diagnosing squamous cell carcinomas. This is largely due to the relatively low metastasis rate for these tumors compared with melanomas; however, it may be possible for pathologists to separate out those squamous cell carcinomas with a higher chance for recurrence and metastasis. This chapter will examine many of these histologic features and propose a rationale for including this information in pathology reports.

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How Often Does Squamous Cell Carcinoma of the Skin Metastasize?

Cited by 199 publications

References 5 publications

Metastatic cutaneous squamous cell carcinoma shows frequent deletion in the protein tyrosine phosphatase receptor Type D gene

Metastatic cutaneous squamous cell carcinoma shows frequent deletion in the protein tyrosine phosphatase receptor Type D gene

The differential diagnosis of cheilitis

Squamous cell carcinoma: from precursor lesions to high-risk variants

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