Cutaneous neoplasms are more common in renal transplant recipients than in the general population, and are the most common malignancies in these patients.6
The incidence of skin cancer is estimated in 10–40% of patients 10–20 years after transplantation.7
In the transplant recipients, the most common cutaneous non‐melanocytic malignancy is SCC, with an incidence of 40–250 times that in the general population, followed by basal cell carcinoma with an incidence of 10 times that in the general population.8,9,10
The duration of immunosuppression treatment using ciclosporin or tacrolimus‐based regimens,11,12
older age at transplantation, presence of actinic keratosis and verrucae vulgaris, smoking and outdoor occupation are major risk factors associated with SCC.13
The development of SCC in transplant recipients is believed to be caused by the interaction of multiple factors: exposure to ultraviolet radiation, the direct effect of immunosuppressive agents, infection by oncogenic viruses such as human papillomavirus and genetic factors.14
SCCs in the setting of solid organ transplantation tend to evolve more rapidly than in the general population, can be multiple and behave more aggressively, with an increased tendency of recurrence and metastasis.10
Histologically, these SCCs are often poorly differentiated or undifferentiated, and may exhibit a spindle‐cell morphology,15
mimicking other cutaneous spindle‐cell lesions, such as spindle‐cell melanoma, leiomyosarcoma, dermatofibrosarcoma protuberans, fibrosarcoma and atypical fibroxanthoma. The neoplastic spindle cells can sometimes be admixed with pleomorphic osteoclast‐like giant cells (OGCs).16
The origin of the OGCs is not fully understood, as they may present in a wide spectrum of benign and malignant, epithelial and mesenchymal tumours. It is not clear whether they represent a non‐neoplastic mesenchymal component reactively induced in the tumour stroma, or a neoplastic epithelial component. In the pancreas, Sakai et al17
showed the OGCs to be immunoreactive for CD68 and lacking k‐ras
mutations, supporting the fact that OGCs are of reactive and non‐neoplastic origin.
The rhabdoid phenotype is characterised by large polygonal cells with eccentric nuclei, large nucleoli and abundant hyaline filamentous cytoplasmic inclusions. Extrarenal malignant neoplasms with a rhabdoid phenotype and coexpression of epithelial and mesenchymal markers were initially designated as “extrarenal malignant rhabdoid tumours”, and thought to represent a rhabdomyosarcomatous variant of Wilms's tumour. Later, the rhabdoid phenotype was recognised in many tumours at various sites, such as melanoma,17,18
plasmacytoma and diffuse large B cell lymphoma, and malignant peripheral nerve sheath tumour.21
It is currently believed that the rhabdoid phenotype represents a common clonal dedifferentiated end point in malignant tumours of varying histogenesis.22
More recently, it has been suggested that rhabdoid changes may be a type of degeneration, or a preliminary stage before apoptosis or cell necrosis.3
Cutaneous malignant rhabdoid non‐melanocytic tumours are rare, especially cutaneous carcinomas with a rhabdoid phenotype, and tend to grow rapidly and have an early involvement of the regional lymph nodes.5
This report is the first case of cutaneous SCC with a rhabdoid and spindled phenotype with accompanying osteoclastic giant cells arising in a solid organ transplantation. Despite the rhabdoid morphology, the presence of perineural invasion and the immunocompromised status in the current case, no evidence of recurrent or metastatic SCC was seen after 10 months of follow‐up. Whether the rhabdoid or sarcomatoid phenotype confers the aggressive behaviour or occurs because the patient is at a high risk is conjectural. However, it seems that the two rationales are not mutually exclusive.
- Squamous cell carcinoma (SCC) can exhibit a rhabdoid phenotype, uncommonly, in post‐solid‐organ transplantation.
- Osteoclastic giant cells can be seen in SCC.
- SCC with the rhabdoid phenotype may be considered to be a more aggressive form of SCC.
- Unusual morphological variants of SCC may be encountered in transplant patients.