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Sequential bilateral testicular tumours presenting with intervals of 20 years and more
© Dieckmann et al.; licensee BioMed Central Ltd. 2013
Received: 7 July 2013
Accepted: 4 December 2013
Published: 9 December 2013
About 3 – 5% of all patients with testicular germ cell tumour (GCT) develop a contralateral cancer, the majority of which arise within 10–15 years. Little is known about the risk of second GCTs after more than two decades. Here we present 3 cases with very late presenting contralateral GCT and provide a summary of similar cases reported previously.
(1) This white Caucasian man underwent right-sided orchiectomy for a nonseminomatous GCT at the age of 22 years. Additional treatment consisted of retroperitoneal lymph node dissection (RPLND) and chemotherapy with 4 cycles of vinblastin / bleomycin. 36 years later, contralateral seminoma clinical stage 1 developed. Cure was achieved by orchiectomy. Histologically, testicular intraepithelial neoplasia (TIN; intratubular germ cell neoplasia) was detected in the tumour-surrounding tissue.
(2) This white Caucasian male had right-sided orchiectomy for nonseminomatous GCT at the age of 29 years. Pathological stage 1 was confirmed by RPLND. 25 years later, he received left sided orchiectomy for seminoma stage 1. Histologically, TIN was found in the tissue adjacent to seminoma. Two brothers had testicular GCT, too, one with bilateral GCT. (3) This 21 year old white Caucasian man underwent left-sided orchiectomy for nonseminomatous GCT. Pathological stage 1 was confirmed by RPLND. 21 years later, he received organ-preserving excision of a right-sided seminoma, followed by BEP chemotherapy for stage 3 disease. Histologically, TIN was found in the surrounding testicular tissue.
22 cases of bilateral GCT with intervals of 20 or more years have previously been reported, thereof three with intervals of more than 30 years, the longest interval being 40 years.
Apart from increased risks of cardiovascular diseases and non-testicular malignancies, patients with GCT face the specific probability of a second GCT in the long run. This risk persists life-long and is not eliminated by chemotherapy. Contralateral testicular biopsy can identify patients at risk by revealing precursor cells of GCT though false-negative biopsies may occur sporadically. However, in view of the multi-facetted late hazards of GCT patients, this minor surgical procedure might somewhat simplify the long-time care of these patients.
The phenomenon of malignant growths occurring in both of the testicles has been known for more than a century. Hamilton and Gilbert conducted the first systematic review in 1942. Based on 144 cases collected from the literature they opened their milestone article with the sentence: “Testicular tumors possess a pronounced tendency to bilateralism” . According to recent reviews, 3 – 5% of patients with testicular germ cell tumour (GCT) develop contralateral cancer which corresponds to a 20–30 fold increased relative risk of tumour [2–4]. About 50% of these events occur within 5 years after diagnosis of the primary while 90% do so within a 10 years time-span . Only few more cancers arise thereafter. So far, little is known about the risk of contralateral GCT after very long intervals of more than two decades. All GCTs are preceded by a common precursor named testicular intraepithelial neoplasia (TIN; also called intratubular germ cell neoplasia unspecified, ITGCNU) which is thought to be present in the testicle many years before the clinical manifestation of GCT [6, 7]. To identify candidates for second GCTs, contralateral testicular biopsy at the time of orchiectomy of the primary is available [8, 9]. However, physicians caring for patients with GCT have widely remained disinclined to this pro-active method of early detection of GCT . Thus clinically, the risk of bilateral testicular tumour needs to be considered during follow-up of patients with GCT. Importantly, as this event may occur beyond the usual 5-years time-span of oncological follow-up, extended observation time is required.
Here we present three cases with exceptionally late onset of second GCT and we provide a survey of the literature regarding the problem of very long intervals between metachronous bilateral testicular tumours.
This Caucasian white male underwent right-sided orchiectomy for a nonseminomatous testicular GCT at the age of 22 years. History was uneventful; in particular there was neither history of undescended testis nor any prior familial events of testis cancer. Bulky retroperitoneal lymph-node metastases were resected by extended retroperitoneal lymph node dissection (RPLND) followed by four cycles of chemotherapy. As cisplatin was not yet available at that time (1976), the patient received treatment with the contemporary Samuels regimen consisting of vinblastin and bleomycin . Possibly as a sequel of transfusion therapy during multi-modal treatment for GCT, a viral hepatitis B infection was diagnosed one year thereafter. This infection entered a chronic non-aggressive course and the patient stayed disease-free with respect to testicular cancer for 36 years.
This white Caucasian man underwent right sided orchiectomy for a testicular teratocarcinoma at the age of 29 years. Pathological stage I was ascertained by RPLND. No further therapy was instituted. After 25 years when aged 54 years, the patient discovered a nodule in his remaining testicle by self-palpation. Imaging procedures including ultrasonography, elastography and MRI disclosed a 1.5 cm mass in the testicle. Serum tumour markers beta HCG, AFP and LDH were not increased. As preoperative hormone analysis had revealed a hypogonadal situation with subnormal testosterone level and increased luteinizing hormone (LH), no surgical attempts were made towards a testis-sparing procedure. Instead, a typical inguinal orchiectomy with insertion of a testicular prosthesis was carried out. Histologically, a classical seminoma was identified, with wide areas of TIN in the surrounding tissue. Chest and abdominal CT scans did not reveal metastases. No further treatment was instituted except for hormone replacement therapy. Follow-up of 12 months so far is uneventful. Family history is of particular note: The off-spring consists of one sister and six brothers, two of whom were also struck by testicular cancer. A younger brother succumbed to testicular choriocarcinoma at the age of 23 years. One older brother survived bilateral testicular cancer at ages 23 and 36 years.
This white Caucasian patient underwent left-sided orchiectomy along with a contralateral biopsy for a testicular teratocarcinoma at the age of 21 years. Histologically, the contralateral biopsy was without evidence of TIN. History was uneventful; in particular there was neither history of undescended testis nor any prior familial events of testis cancer. RPLND revealed pathological stage I. Thus, no systemic treatment was applied. At the age of 42 years, he presented with right-sided flank pain. Magnetic resonance imaging revealed dilatation of the right ureter caused by a huge retroperitoneal mass extending from the renal hilum into the pelvis. Beta HCG was slightly increased to 11.9 U/l (reference <1.0 U/l), as was LDH with 400 U/l (reference < 250 U/l), while AFP was within normal limits. Scrotal ultrasonography revealed a mass of 1.9 cm in diameter in the testicle. Organ preserving surgery was performed along with additional biopsies of the adjacent testicular parenchyma. Histological work-up revealed pure seminoma with abundant TIN in the surrounding tissue. Mediastinal lymphadenopathy in addition to retroperitoneal metastases indicated stage III disease with good prognosis according to IGCCCG. The patient was rendered disease-free by systemic therapy with three cycles of cisplatin, etoposide and bleomycin (BEP). Two years thereafter, the patient is relapse-free and well.
The risk of second (contralateral) cancer in GCT patients is pending life-long.
Chemotherapy does not prevent a second testicular tumour.
Familial clustering of testicular cancer appears to be associated with bilateral disease.
Second tumours may arise despite a contralateral biopsy negative for TIN.
Sequential bilateral testicular germ-cell tumours with interval of 20 years or more
Age at first presentation (years)
Histology first tumour
Reference, first author,
Present case I
Present case II
Present case III
The median age at primary presentation of the patients with very late presenting contralateral testicular tumour is 28.5 years that is not at variance with the over-all median age of patients with germ cell cancer . Yet, there appears to be a slight deviation from the contention that patients with bilateral tumours usually experience a rather early presentation of their primary [12, 34, 35]. All of our cases had a nonseminomatous histology at first presentation which is somehow at variance with the preponderance of seminoma usually encountered in cases with bilateral testicular GCT . Table 1 does not suggest any association of histology with the particular risk of late second GCT. Little is known about clinical stage at primary diagnosis and during relapse for these particular patients. In most of the reports (Table 1) information on clinical staging is not provided. In our series, only one had metastasized disease at primary presentation while two had stage I disease. So, the basic message of this compilation of cases is the information that the risk of contralateral testicular cancer will persist life-long.
(2) Our first case experienced his second tumour despite interval chemotherapy. Pathogenetically, all GCTs are preceded by the premalignant lesion TIN (ITGCNU) that is believed to be present in the contralateral testicle already at the time of the first tumour. Concerns regarding the low sensitivity of chemotherapy to eradicate the precursor in the contralateral gonad had been raised already in the 1980ies . Accordingly, large series of patients with bilateral testicular tumours clearly revealed that chemotherapy does not protect against second tumours [4, 15]. In the largest investigation of bilateral tumours performed on the SEER data base, 39 second tumours (> 1%) were found among 3157 nonseminoma patients receiving chemotherapy . Recently, it was shown that low doses of two cycles of cisplatin-based chemotherapy are probably without any considerable effect on TIN, three or more cycles may eradicate it in about 75% of cases . Our patient had received 4 cycles of chemotherapy, however, that treatment did not involve cisplatin, which clearly is the most efficacious drug. So, one might speculate that the vinblastin/bleomycin regimen could have suppressed TIN only temporarily . Accordingly, it took 36 years for the remaining TIN cells to recover and to finally progress to invasive seminoma. In fact, there is some indication of extended intervals in bilateral GCTs following chemotherapy [13, 15]. Our patient apparently represents the case with the longest lag time between sequential bilateral testicular tumours and interval chemotherapy. So, this case represents an exceptional example showing the low efficacy of chemotherapy to prevent sequential testicular neoplasms.
(3) Two brothers of case #2 had suffered from testicular cancer, too, one of whom had even bilateral disease. Approximately 1-3% of all patients with testicular GCT have close relatives with the same diagnosis . Notably, 6-15% of all familial cases of GCT develop bilateral disease while second GCTs occur in only 3-5% among sporadic cases . Accordingly, a strong hereditary predisposition of testicular GCT is assumed . While the clinical evidence for the involvement of genetic factors in the etiology of GCT is undisputed, the assumed Testicular GCT 1 gene has so far not been identified . From a practical point of view, it is concluded that history of familial testicular cancer should increase the clinician´s vigilance regarding the possible development of contralateral cancer. As elucidated by the case, this event may even occur after a very long lag time.
(4) In one of our patients (#3), contralateral GCT developed despite a previous testicular biopsy negative for TIN. False-negative biopsies do occur in less than 10% of cases . Multiple probing has been recommended to reduce the rate of biopsy-failures. In fact, systematic two-site biopsies revealed an 18% extra yield of contralateral TIN . Whether or not double biopsy would have disclosed the true diagnosis at that time remains elusive, but clearly, multiple biopsies are more sensitive than a single one.
Our three cases highlight one of the manifold problems in the long-time follow-up of patients with testicular GCT. The specific risk of a second testicular tumour is one threat in addition to the well-recognized hazards of metabolic disorders, cardiovascular diseases and non-testicular malignancies . The risk of contralateral GCT is not eliminated by chemotherapy. As all of our patients had TIN in the tumour-surrounding tissue, histologically, a contralateral biopsy at the time of the primary might have identified the impending second tumour. Although not explicitly recommended by current guide-lines [43–45], contralateral testicular biopsy is clearly valuable for exploring the particular risk of second testicular cancer [8, 46].
Written informed consent was obtained from all of the three patients for publication of these Case reports and the two accompanying images. A copy of the written consent is available for review by the Editor of this journal.
This study was supported by the German Ministry of Defence.
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