Surgery versus surveillance in stage I non-seminoma testicular cancer

Abstract

Today, the standard treatment for patients with clinical Stage I non‐seminomatous testicular germ cell tumors (NSTGCT) following orchidectomy is either primary retroperitoneal lymph node dissection (RPLND) or close surveillance with cisplatin‐based polychemotherapy in case of a relapse. Both treatment modalities provide excellent overall survival rates up to 100%. Consequently, selection of the most appropriate management option is not primarily guided by survival considerations. The choice between the available options, each having its merits and its drawbacks, should be made based on a number of factors including treatment‐related morbidity, views and expertise of the physician, patient preferences, the expected degree of patient compliance, and prognostic factor analysis. To date, the role of adjuvant chemotherapy as an alternative management option for patients with clinical Stage I NSTGCT at high risk of occult metastases is limited. This systemic treatment modality would be a realistic alternative if the reliability of prognostic factors to identify high‐risk Stage I patients could be improved. This review addresses relevant issues in the management of patients with clinical Stage I NSTGCT to provide information that will allow a rational selection of the most appropriate management option. Semin. Surg. Oncol. 17:230–239, 1999. © 1999 Wiley‐Liss, Inc.

Prediction of relapse in stage I testicular germ cell tumor patients on surveillance: investigation of biomarkers

“…Presence of embryonal carcinoma is also associated with poorer relapse-free survival. This is in line with previous knowledge which unequivocally support the predictive value of vascular invasion assessment in nonseminoma patients [5,12,[36][37][38][39][40][41][42][43][44][45][46] and further suggest amount of embryonal carcinoma as adjunctive in this context [5]. For seminoma, however, other variables are advanced to help in clinical decision-making: tumor size and rete testis invasion.…”

Interobserver Agreement in Vascular Invasion Scoring and the Added Value of Immunohistochemistry for Vascular Markers to Predict Disease Relapse in Stage I Testicular Nonseminomas

“…Specifically, the aim is to better discriminate those patients who truly benefit from further treatment after orchiectomy from those who can safely follow a surveillance protocol. 6,37,38 The most consistent histological parameter to predict disease recurrence in clinical stage I nonseminoma has been vascular invasion, [11][12][13][14][15][16][17][18][19][20][21][22][23] and our study was no exception, with vascular invasion being the only variable with significant impact on relapsefree survival after multivariable analysis. 39,40 However, more factors apart from vascular invasion have been collected that demonstrate an impact in determining disease relapse, namely the amount of embryonal carcinoma.…”

“…7,8 Vascular invasion has been pointed out as such a marker in various studies, an idea first suggested by Raghavan et al 9 and Peckam et al 10 The presence of vascular invasion is associated with poor prognosis, relapse, and metastases, particularly in nonseminomas. 5,[11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] The relevance of vascular invasion in testicular germ cell tumors is illustrated by its inclusion in the TNM staging system, resulting in a pT2. 26 Given this clinical importance, strict criteria for establishing the diagnosis of vascular invasion are recommended by expert panels, as some representations may result in overdiagnosis and, hence, possible overtreatment of patients.…”

Testicular Cancer

“…In a large study, 15% of patients with a negative lymph node dissection experienced recurrence, usually pulmonary and usually within 18 months [22]. The overall survival rate of patients with pathological stage I is about 99% [23].…”

“…Prognostic factors for patients with stage I disease that may predict the likelihood of occult metastases are the presence of lymphatic or venous invasion in the primary tumour, the presence of embryonal cell carcinoma and the absence of yolk sac elements in the primary tumour [23]. A more sophisticated way to stain proliferating tumour cells in testicular tumours with a monoclonal antibody MIB-1 against Ki-67 in combination with the volume of embryonal cell carcinoma and the transaxial diameter of retroperitoneal lymph nodes in the predicted landing zone allows a low-risk clinical stage I classification [25].…”