Testicular germ cell tumoursBMJ 2013; 347 doi: https://doi.org/10.1136/bmj.f5526 (Published 24 September 2013) Cite this as: BMJ 2013;347:f5526
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We commend the authors of this article which provides a detailed clinical review of testicular germ cell tumour management. However the article manages to exclude almost entirely the role of the histopathologist in the diagnosis and subsequent management of testicular tumours. The role of the pathologist following orchidectomy is summarised here.
1)The histopathologist confirms that the tumour is actually a germ cell tumour. Other tumours such as lymphoma and sex cord stromal tumours (which have a very different natural history) may be in the radiological differential diagnosis. This distinction is usually straightforward, but there are many described examples of pitfalls in the diagnosis of germ cell tumours. For example, Sertoli cell tumour can mimic classical seminoma. These distinctions may require ancillary tests such as immunohistochemistry or tests such as i(12p) FISH, which is a helpful (but not entirely specific marker of germ cell tumours). Germ cell tumours are managed by supra-regional teams, which means the supra-regional pathologist gains considerable experience in these relatively rare tumours.
2)Once the pathologist has decided that the tumour is a germ cell tumour, the tumour must be assigned into the correct tumour group; either seminoma or non-seminomatous germ cell tumour (including combined seminoma/ non-seminoma). As the article describes, these groups are managed quite differently and this distinction is of paramount importance. This is entirely dependent on the pathological examination in marker negative cases.
3)Within each subgroup of tumour, there are important distinctions to be made. In seminoma, classical seminoma must be accurately distinguished from the much less common spermatocytic seminoma which has an excellent prognosis and therefore requires no adjuvant therapy. Within the non-seminomatous germ cell tumours, the proportions of the elements (embryonal carcinoma, yolk sac tumour, teratoma, choriocarcinoma) need to be correctly estimated as a predominance of embryonal carcinoma is strongly associated with disease relapse in stage 1 disease.
4)The pathologist needs to accurately report prognostic factors indicative of disease relapse. This is particularly important in stage 1 disease where the adverse prognostic factors of lymphovascular invasion in non-seminomatous germ cell tumours or rete testis invasion and tumour size in classical seminoma help distinguish which patients can be managed by surveillance and which may need adjuvant therapy. This is less important in classical seminoma where many patients in the UK with stage 1 disease are managed by surveillance.
5)The article makes no mention of TNM staging. The TNM staging system for testis is in need of revision and many of the items used for staging have little evidence base for their inclusion, however, a stage of pT2 due to lymphovascular invasion in non-seminomatous germ cell tumours, as the article states, indicates a relapse rate of up to 50%. Interestingly, the evidence for lymphovascular invasion as an independent prognostic factor of disease relapse in stage 1 seminoma on multivariate analysis is lacking. In stage 1 classical seminoma, the 2 factors which have been shown to be independently predictive of disease relapse are rete testis stroma invasion and size of the tumour (>4cm is an adverse factor)  and these are determined by the pathologist.
6)The unexpected diagnosis of a primary testicular germ cell tumour in a metastasis in the retroperitoneum or lymph node is not uncommon. Many primary germ cell tumours regress with unexpected clinical findings and potentially incorrect management unless a germ cell tumour is suspected. Relapses of germ cell tumours after chemotherapy are challenging and the correct diagnosis, especially in retro peritoneal lymph node dissection will inform management and the choice of chemotherapy.
The role of the pathologist is described in the forthcoming Royal College of Pathologists 3rd edition ‘dataset for the histological reporting of testicular neoplasms’, which is currently under consultation for fellows' comments on the Royal College of Pathologists' website and should be available for wider readership from March 2014 onwards .
 Groll RJ, Warde P, Jewett MAS. A comprehensive systematic review of testicular germ cell tumor surveillance. Crit Rev Oncol Hematol 2007; 64: 182–197.
. Berney DM, Theaker JM, Verrill C. Standards and datasets for reporting cancers. Dataset for the histological reporting of testicular neoplasms. 3rd edition. Royal College of Pathologists 2014; under consultation / in press.
Competing interests: No competing interests
I congratulate Horwich and colleagues for their superb clinical review on testicular germ cell tumors (TGCTs) . I wish to highlight that race appears to play a significant role in the pathophysiology of TGCTs . Walsh and co-workers found that Asian/Pacific Islander boys were more likely than their Caucasian counterparts to have TGCTs . Also, testicular cancer is rare among those of African racial origin .
Racial disparity in the epidemiology of TGCTs has important clinical implications in understanding the biology and identifying potential therapeutic targets for this cancer .
No competing interests
1. Horwich A, Nicol D, Huddart R. Testicular germ cell tumours. BMJ. 2013; 347:f5526.
2. Walsh TJ, Davies BJ, Croughan MS, Carroll PR, Turek PJ. Racial differences among boys with testicular germ cell tumors in the United States. J Urol. 2008; 179(5):1961-5.
3. Hanna NH, Loehrer PJ, Dash A, Buyyounouski MK, Skarecky D. Testicular Cancer. CANCER MANAGEMENT: ONLINE EDITION. 2013. Available. http://www.cancernetwork.com/cancer-management/testicular/article/10165/.... Accessed September 27, 2013.
4. Hayes-Lattin B, Nichols CR. Testicular cancer: a prototypic tumor of young adults. Semin Oncol. 2009; 36(5):432-8.
Competing interests: No competing interests