Somatic MT develops in 3-6% of chemotherapy-naïve patients with metastatic GCT containing teratomous components [4, 9]. After platinum-based chemotherapy the incidence of MT increases up to 14% . Histologically, various types of sarcoma and carcinoma have been identified in GCT with MT. The most commonly MTs reported are rhabdomyosarcoma, PNET and adenocarcinoma. Leiomyosarcoma, liposarcoma, chondrosarcoma, Non-Hodgkin’s lymphoma and leukaemia are found less frequently [2, 3, 6]. Renal tumour differentiation is rare. Nephroblastoma (Wilms tumour) have been described  and there is a single report of MT into papillary renal cell carcinoma in a primary retroperitoneal and chemotherapy-naïve GCT . To the best of our knowledge, MT into papillary renal cell cancer within a testicular GCT metastasis following platinum-based chemotherapy has not been previously documented.
It is highly unlikely that the papillary renal cell cancer found was a metastasis originating from the kidneys. We believe the papillary renal cell carcinoma resulted from MT of the teratoma for several reasons. Firstly, the lesion was located within the teratoma. Secondly, both kidneys had normal appearance on multiple abdominal CTs and FDG-PET. Finally, there was no histological evidence of renal cell cancer in the left kidney that was removed en bloc. There was also no family history of papillary renal cell cancer. In cases with more clinical ambiguity, fluorescence in situ hybridisation (FISH) analysis for 12p amplification can be used to confirm the germ-cell origin of somatic-type tumours of uncertain histogenesis .
The characteristic morphology and the immunohistochemical profile confirmed the diagnosis of papillary renal cell cancer. Papillary renal cell cancer is differentiated from other subtypes of renal cell cancer by using CK7 and AMACR immunohistochemical markers . Most papillary renal cell carcinomas are positive for CK7, whereas clear cell renal cell cancer shows either negative or only a focal or expression pattern . A panel of immunohistochemical markers, including CD10, RCC, and vimentin, has been proposed for the identification of renal origin of a metastatic tumour [12, 14]. Identification of the most common chromosomal aberrations in papillary renal cell cancer (trisomy of chromosome 7 and 17 as well as loss of Y chromosome ) were not necessary in our case due to convincing histological and immunohistochemical features.
The role of FDG-PET in evaluating residual masses after chemotherapy differs between seminomatous and non-seminomatous GCTs . FDG-PET can discriminate between viable tumour and fibrosis or necrosis in post-chemotherapy residuals of seminomatous GCT [17, 18]. Therefore, FDG-PET is recommended to decide whether surveillance or surgical therapy is the treatment of choice in patients with residuals > 3 cm . However, in the setting of a non-seminoma post-chemotherapy mass FDG-PET is not recommended . Although it can detect viable tumour in residual masses, it cannot discriminate mature teratoma from fibrosis or necrosis . Therefore FDG-PET is not helpful to decide if surgical therapy is necessary or not in these patients.
In our case of non-seminomatous GCT, FDG-PET was performed contradictory to standard guidelines prior referral to our centre. Histo-pathological examination revealed that the FDG-avid lesion within the retroperitoneal teratoma represented the papillary renal cell cancer. It has been reported that FDG-PET may have a role in detecting metastasis of renal cancer. However this is usually in the setting of clear cell rather than papillary carcinoma .
Due to the wide spectrum and unpredictability of tumour types that occur in MT, the utility of FDG-PET in the setting of MT remains unknown and requires further investigation. Tissue diagnosis is still the gold standard in determining presence of viable malignancy and discriminating between GCT and other types of tumours.
The occurrence of MT is known to worsen the prognosis of GCT, particularly in metastatic disease [6, 22–24]. One reason for this is that many of the tumours found after MT are highly aggressive (i.e. sarcoma, PNET) [25, 26]. If MT remains undetected, a conventional platinum-based chemotherapy approach may fail in treating the new tumour type developed. This may additionally delay diagnosis of MT and lead to worse outcome [27, 28].
Complete surgical resection, if technically possible, should remain the gold standard of therapy as it will achieve the most reliable histopathologic diagnosis, and has been shown to improve the prognosis of patients with MT in metastatic GCT [2, 3, 6, 27]. If MT is found, histological evaluation is mandatory for all synchronously or metachronously detected metastases. In advanced cases with documented spread of the transformed histologic subtype, systemic therapies targeted to the identified tumour type should be considered [6, 9, 27, 29].