Bilateral testicular germ cell tumors.

2015 ◽  
Vol 33 (7_suppl) ◽  
pp. 392-392
Author(s):  
Stephanie A. Curreri ◽  
Sarah C. Markt ◽  
Rowan Miller ◽  
Elizabeth O'Donnell ◽  
Brandon David Bernard ◽  
...  
Keyword(s):  
Testicular Cancer ◽  
Germ Cell ◽  
Cause Of Death ◽  
Germ Cell Tumors ◽  
Malignant Neoplasm ◽  
Patient Characteristics ◽  
Second Malignant Neoplasm ◽  
Testicular Germ Cell ◽  
Risk Of Death ◽  
Increased Risk

392 Background: Germ cell tumors (GCTs), both seminomatous and non-seminomatous, account for greater than 90% of testicular cancers. While bilateral testicular GCTs are rare, the incidence of bilateral tumors has increased over time. Methods: 668 cases of bilateral and 38,593 cases of unilateral testicular GCTs were reported between 1973 and 2011 by the SEER database. Patient characteristics and tumor features were analyzed. Results: The incidence of bilateral GCTs among men with testicular GCTs was 1.7% (668 of 39,261 total cases). Among the 668 men with bilateral GCTs, 53% (n=353) of second GCTs occurred within three years after the first cancer. 29% (n=196) of bilateral tumors occurred synchronously. Among patients with bilateral GCTs, 378 first GCTs and 466 second GCTs were seminomatous. 43% of bilateral cases were concordant seminomatous GCTs, 16% were concordant non-seminomas, and 41% were discordant histologies. 68% of unilateral GCTs, 70% of first GCTs, and 82% of second GCTs were staged as Localized disease. Testicular cancer was the cause of death for 4% (n=1,630) of men with a unilateral GCT and 1% (n=8) of men with bilateral GCTs. A second malignant neoplasm (SMN) was the cause of death for 2% (n=736) of men with a unilateral GCT and 2% (n=16) of men with bilateral GCTs. Conclusions: Among men with bilateral testicular GCTs, 59% had concordant histological diagnoses between their first and second tumor. Most (53%) second cancers among men with bilateral tumors occurred within three years after diagnosis of first cancers. Men who experience bilateral testicular GCTs do not appear to have an increased risk of death due to testicular cancer or a subsequent non-germ cell malignant neoplasm compared to men with a unilateral testicular GCT. [Table: see text]

Excellent outcomes in bilateral testicular germ cell tumors over four decades.

2019 ◽  
Vol 37 (7_suppl) ◽  
pp. 523-523
Author(s):  
Ning-Ning Lu ◽  
Aaron Richard Hansen ◽  
Philippe L. Bedard ◽  
Padraig Richard Warde ◽  
Joan Sweet ◽  
...  
Keyword(s):  
Testicular Cancer ◽  
Germ Cell ◽  
Germ Cell Tumors ◽  
Patient Characteristics ◽  
Stage I ◽  
Second Primary ◽  
Time Interval ◽  
Testicular Germ Cell ◽  
Prior Therapy

523 Background: Bilateral testicular germ cell tumours (BTC) form a small minority of testicular cancer and detailed management data are sparse. Methods: Bilateral testicular cancer (BTC) patients managed at a single cancer centre were retrospectively analyzed. Synchronous BTC was defined as uni+contralateral presentation within 3 months. Patient characteristics, treatment and outcomes were collected. Kaplan-Meier method was used to calculate the overall survival (OS) and relapse-free survival (RFS). Results: Between Jan 1971 to Jun 2018, 118 pts were included. Nine patients (7.6%) had cryptorchidism. Twenty-two patients (18.6%) had synchronous BTC at median age of 30(21-54) years, 11 presented with concordant histology (10-seminoma). Median follow-up time was 96(1-220) months. Two of 14 patients (14%) with stage I disease on surveillance had retroperitoneal nodal recurrence, other 3 (21%) had testicular recurrence after partial orchiectomy alone. No recurrence occurred for 8 stage II/III patients (36%) who received stage-appropriate treatment. All patients were alive without disease at last follow-up. For metachronous BTC, the median age was 27(16-68) and 37(19-78) years for first and second diagnosis, respectively. The median time interval was 88 (8-352) months, with shorter interval when second primary was non-seminoma, median 69 vs. 92 months. Concordant histology was present in 58 (38-seminoma) patients and discordant in 38 patients. There were 66, 23, 7 and 84, 9, 3 patients with stage I, II, III disease for first and second testicular cancer (TC), respectively. For all stage I disease, 69% of non-seminoma (n = 33) and 79% of seminoma (n = 81) were on surveillance, of whom the crude relapse rate was 15%. The median follow-up time after second diagnosis was 87 months. In all, 35 patients (30%) with recurrence except 1 were successfully salvaged. The 10-year OS and RFS for whole cohort was 99% and 69.8%, respectively. Conclusions: In our series, seminoma was the more common pathology, and management based on pathology and stage yielded excellent outcomes regardless of prior therapy. Metachronous BTC may occur at extremely long time intervals such that longer follow-up is needed to capture the majority of contralateral primary TC.

Evidence for Altered Hypothalamic-Hypophyseal-Gonadal Axis in Untreated Patients with Testicular Germ-Cell Tumor

1989 ◽  
Vol 75 (5) ◽  
pp. 505-509
Author(s):  
Sergio Crispino ◽  
Gabriele Tancini ◽  
Sandro Barni ◽  
Paolo Lissoni
Keyword(s):  
Testicular Cancer ◽  
Germ Cell ◽  
Germ Cell Tumor ◽  
Venous Blood ◽  
Germ Cell Tumors ◽  
Testicular Germ Cell Tumor ◽  
Cell Tumor ◽  
Testicular Germ Cell Tumors ◽  
Testicular Germ Cell ◽  
Significant Difference

To investigate the function of the hypothalamic-hypophyseal-gonadal axis in testicular germ cell tumors, we evaluated gonadotropin responses to gonadotropin-releasing hormone (GnRH) in 12 untreated patients with testicular cancer (5 seminomas and 7 non-seminomas). GnRH was given i.v. at a dose of 100 μg as a bolus, and venous blood samples were collected at 0, 20, 60, and 120 min. As controls, 14 healthy males were studied. Basal levels of testosterone, estradiol and prolactin were also detected in each patient. Hormonal serum concentrations were measured by the radioimmunoassay. Mean basal testosterone, estradiol and prolactin levels were not significantly different from those of controls. Patients had a lower FSH and LH peak after GnRH than controls, without, however, any significant difference. As regards histology, nonseminoma patients lacked an FSH response to GnRH and had statistically lower mean peak levels than controls. Moreover, non-seminoma patients had statistically lower mean peak values of LH after GnRH than controls. These data show that patients with testicular germ cell tumor, and more particularly those with non-seminomas, have an altered function of the hypothalamic-hypophyseal-gonadal axis, which is already present prior to therapy. Further studies, particularly in stage I patients treated only with orchiectomy, should be performed to confirm and better define the Physiopathologic significance of the altered hypothalamic-hypophyseal-gonadal axis in testicular cancer and to clarify the alteration of fertility, which is frequently present before treatment.

Current Insights into Interethnic Variability in Testicular Cancers: Population Pharmacogenetics, Clinical Trials, Genetic Basis of Chemotherapy- Induced Toxicities and Molecular Signal Transduction

2020 ◽  
Vol 20 (20) ◽  
pp. 1824-1838 ◽  
Author(s):  
Aman Vasistha ◽  
Rishi Kothari ◽  
Adarsh Mishra ◽  
Fernando De Andrés ◽  
Adrián LLerena ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Clinical Trials ◽  
Testicular Cancer ◽  
Germ Cell ◽  
Germ Cell Tumors ◽  
Surgical Removal ◽  
Genetic Determinants ◽  
Testicular Germ Cell ◽  
Aggressive Cancer ◽  
Molecular Signal

Testicular cancer is an aggressive malignancy with a rising incidence rate across the globe. Testicular germ cell tumors are the most commonly diagnosed cancers, and surgical removal of the testes is often a radical necessity along with chemotherapy and radiotherapy. While seminomas are receptive to radiotherapy as well as chemotherapy, non-seminomatous germ cell tumors respond to chemotherapy only. Due to the singular nature of testicular cancers with associated orchiectomy and mortality, it is important to study the molecular basis and genetic underpinnings of this group of cancers across male populations globally. In this review, we shed light on the population pharmacogenetics of testicular cancer, pediatric and adult tumors, current clinical trials, genetic determinants of chemotherapy-induced toxicity in testicular cancer, as well as the molecular signal transduction pathways operating in this malignancy. Taken together, our discussions will help in enhancing our understanding of genetic factors in testicular carcinogenesis and chemotherapy-induced toxicity, augment our knowledge of this aggressive cancer at the cellular and molecular level, as well as improve precision medicine approaches to combat this disease.

Elevated risk of second malignant neoplasms in pediatric germ cell tumor patients.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 10010-10010
Author(s):  
Maria Clarissa de Faria Soares Rodrigues ◽  
Carlos Rodriguez-Galindo ◽  
Karina Braga Ribeiro ◽  
A. Lindsay Frazier
Keyword(s):  
Germ Cell ◽  
Germ Cell Tumors ◽  
Malignant Neoplasm ◽  
Primary Diagnosis ◽  
Second Primary ◽  
Malignant Neoplasms ◽  
Primary Malignancy ◽  
Second Malignant Neoplasm ◽  
Primary Tumors ◽  
Treatment Type

10010 Background: The probability of cure is very high for children with germ cell tumors (GCT), but late effects from cisplatinum can be quite significant. In addition to the immediate effects of oto-, neuro and nephrotoxicity, data from men treated for testicular cancer shows that the rate of second malignant neoplasm (SMN) is doubled and that a man treated before age 20 has a 50% chance of SMN by age 75. This study was designed to assess the risk of SMN among individuals treated for malignant GCT during childhood. Methods: We included all patients 0-19 years old with a primary diagnosis of malignant GCT registered in the Surveillance, Epidemiology and End Results (SEER) in the period 1973-2008. We analyzed tumors occurring at least 12 months after the first primary. Standardized incidence ratios (SIR) and 95% confidence intervals (CI) were calculated using SEER Stat, version 8.0.1. Results: The cohort comprised 1997 patients (798 women and 1,199 men); 86.3% had primary gonadal tumors (91% in men and 79.5% in women). The median age at diagnosis of the primary malignancy was 17 years (17 for males ; 15 for females), and for second malignancies was 27 (27 for males; 30 for females). Fifty eight SMNs were observed (21 in females; 37 in males). Among women, higher risk was observed to developing breast cancer (n=5; SIR=1.29; 95% CI= 0.42-3.02), thyroid cancer (n=5; SIR= 3.40; 95% CI= 1.1-7.93) and brain cancer (n=3; SIR= 9.19; 95% CI=1.89-26.85). Twenty-seven out of 37 second primary tumors observed in men were contralateral testicular tumors, conferring a 16.2 fold higher risk of developing this neoplasm (95% CI= 10.67-23.58). When the analysis excluded testis as a second site, a higher risk was noted for the development of pancreatic cancer (SIR=19.06; 95% CI=2.31-68.83) and leukemia (SIR=3.55; 95% CI=0.43-12.81). Conclusions: Rates of SMN are elevated in both men and women treated as children for pediatric germ cell tumors. Men need to be made aware of risk in contralateral testicle. The rates of SMN may continue to rise with longer follow up. The attribution of treatment type to risk of SMNs is not possible due to the lack of this information in SEER database.

BMI at diagnosis and adverse outcomes among men with malignant testicular germ cell tumors.

2015 ◽  
Vol 33 (7_suppl) ◽  
pp. 400-400
Author(s):  
Sarah C Markt ◽  
Rowan Miller ◽  
Elizabeth O'Donnell ◽  
Laurence Albiges ◽  
Brandon David Bernard ◽  
...  
Keyword(s):  
Testicular Cancer ◽  
Germ Cell ◽  
Clinical Stage ◽  
Germ Cell Tumors ◽  
Cox Proportional Hazards ◽  
Adverse Outcomes ◽  
Tumor Characteristics ◽  
Cancer Death ◽  
Testicular Germ Cell ◽  
Risk Of Relapse

400 Background: Previous studies evaluating the relationship between measures of anthropometry, such as body mass index (BMI), and risk of testicular cancer have been conflicting, with most finding null or inverse associations. Methods: We conducted a retrospective review of 960 germ cell tumors among patients treated at the Dana-Farber Cancer Institute (DFCI) between 1997 and 2012 with information on BMI. BMI at diagnosis, tumor characteristics, IGCCC classification, treatment, relapse and cause of death was ascertained from electronic medical record review. We divided the men and conducted the analyses separately for two groups: 1) men who presented as clinical stage 1 (CS1), and 2) men who presented with metastases or were CS1 at diagnosis and developed metastases (lifemets). We conducted logistic regression to evaluate the association between BMI and characteristics at diagnosis, and Cox proportional hazards regression to investigate the risk of relapse and testicular cancer death. Results: 65% of men (n=628) were overweight or obese at diagnosis. We did not find an association between BMI and tumor characteristics at baseline, such as histology, lymphovascular invasion, or tumor size for either group. Among CS1 patients, men who were overweight or obese had a non-statistically significant reduced risk of relapse compared to men who were normal weight (HR: 0.83, 95% CI: 0.53-1.30). Among the lifemets group, 16% of men relapsed (n=83) and 8% died of testicular cancer (n=43). Although not statistically significant, men who were overweight or obese were less likely to present with intermediate (OR = 0.77, 95 CI: 0.39-1.52) and poor (OR = 0.66, 95% CI: 0.36-1.20) rather than good risk disease when compared to men with normal BMI. After adjusted for confounding variables, BMI was not associated with risk of relapse (HR: 0.94, 95% CI: 0.59-1.51) or risk of testicular cancer death (HR: 1.00, 95% CI: 0.54-1.84) among the lifemets group. Conclusions: We did not find an association between BMI at diagnosis and tumor characteristics at baseline, or risk of relapse or testicular cancer death among men with testicular cancer.

Validation of testicular germ cell tumor (GCT) staging in nationwide cancer registries.

2021 ◽  
Vol 39 (6_suppl) ◽  
pp. 383-383
Author(s):  
Rohit R Badia ◽  
Daniel Wong ◽  
Rashed Ghandour ◽  
Nathan Chertack ◽  
Xiaosong Meng ◽  
...  
Keyword(s):  
Testicular Cancer ◽  
Germ Cell ◽  
Germ Cell Tumors ◽  
Cancer Registries ◽  
Clinical Staging ◽  
Line Treatment ◽  
First Line ◽  
Testicular Germ Cell ◽  
Tumor Registry ◽  
First Line Treatment

383 Background: Nationwide cancer registries such as the National Cancer Database (NCDB) and Surveillance, Epidemiology, and End Results (SEER) rely on accurate data from institutional tumor registries to formulate hypotheses and report outcomes and treatment patterns for patients with cancer. We evaluated the accuracy of our institutional registry for testicular germ cell tumors (GCT) by comparing data abstracted by urologists with data abstracted by our tumor registry. Methods: We performed a retrospective review of patients receiving initial diagnosis and treatment for testicular cancer at our hospital system from 2005-2016. We reviewed registrar coding for American Joint Committee on Cancer clinical staging, overall composite stage grouping, and first-line treatment and compared it with urologist-reviewed staging at the time of diagnosis. Results: Paired staging from registry and urologist was available for 80 patients. T, N, M, and S-staging were accurate for 90%, 81%, 94%, and 54% of records, respectively. Composite staging and first-line treatment were concordant for 39% and 90% of patients, respectively. A separate review of 33 Stage IS patients per registry for composite staging revealed only 15% concordance. Conclusions: We identified significant inconsistencies with data abstracted by our institutional tumor registry for patients with testicular cancer, most notably with regards to S and composite stage. An educational intervention to improve abstraction by registry led to increased concordance. Assuming similar discrepancies may exist at other institutions and for other cancer types, caution should be used when interpreting NCDB and SEER cancer staging data. This sheds light on the need for improved clarification of staging guidelines, dynamic institutional internal auditing, and training reform within cancer registries.

scholarly journals Rare inactivating PDE11A variants associated with testicular germ cell tumors

2015 ◽  
Vol 22 (6) ◽  
pp. 909-917 ◽  
Author(s):  
Anand Pathak ◽  
Douglas R Stewart ◽  
Fabio R Faucz ◽  
Paraskevi Xekouki ◽  
Sara Bass ◽  
...  
Keyword(s):  
Testicular Cancer ◽  
Germ Cell ◽  
Germ Cell Tumors ◽  
Testicular Germ Cell Tumor ◽  
Testicular Tissue ◽  
Transcript Variant ◽  
Coding Region ◽  
Testicular Germ Cell ◽  
Rare Mutations ◽  
Gene Study

Germline inactivating mutations of isoform 4 of phosphodiesterase (PDE) 11A (coded by the PDE11A gene) have been associated with familial adrenocortical tumors and familial testicular cancer. Testicular tissue is unique in expressing all four isoforms of PDE11A. In a prior candidate gene study of 94 familial testicular germ cell tumor (TGCT) subjects, we identified a significant association between the presence of functionally abnormal variants in PDE11A and familial TGCT risk. To validate this novel observation, we sequenced the PDE11A coding region in 259 additional TGCT patients (both familial and sporadic) and 363 controls. We identified 55 PDE11A variants: 20 missense, four splice-site, two nonsense, seven synonymous, and 22 intronic. Ten missense variants were novel; nine occurred in transcript variant 4 and one in transcript variant 3. Five rare mutations (p.F258Y, p.G291R, p.V820M, p.R545X, and p.K568R) were present only in cases and were significantly more common in cases vs controls (P=0.0037). The latter two novel variants were functionally characterized and shown to be functionally inactivating, resulting in reduced PDE activity and increased cAMP levels. In further analysis of this cohort, we focused on white participants only to minimize confounding due to population stratification. This study builds upon our prior reports implicating PDE11A variants in familial TGCT, provides the first independent validation of those findings, extends that work to sporadic testicular cancer, demonstrates that these variants are uncommonly but reproducibly associated with TGCT, and refines our understanding regarding which specific inactivating PDE11A variants are most likely to be associated with TGCT risk.

Treatment of testicular cancer and the development of secondary malignancies.

1995 ◽  
Vol 13 (1) ◽  
pp. 283-292 ◽  
Author(s):  
C Bokemeyer ◽  
H J Schmoll
Keyword(s):  
Testicular Cancer ◽  
Germ Cell ◽  
Solid Tumors ◽  
Alkylating Agents ◽  
Cell Cancer ◽  
Germ Cell Tumors ◽  
Elevated Risk ◽  
High Dose ◽  
Secondary Neoplasia ◽  
Increased Risk

PURPOSE Secondary neoplasia represents one of the worst possible long-term complications of therapy for testicular cancer, frequently leading to death in patients cured of the primary malignancy. The frequency and importance of secondary malignant disease will be reviewed. METHODS The international literature was screened for reports concerning secondary solid cancers or leukemias in patients treated with chemotherapy or radiotherapy for malignant germ cell tumors. RESULTS Patients with testicular germ cell tumors appear to have a twofold significantly increased risk (range, 0.7 to 3.4) for the development of secondary neoplasia. Apart from contralateral testicular cancers, which are not treatment-related, a largely elevated inherited risk for secondary cancers in patients with germ cell tumors seems unlikely. Radiotherapy is associated with a two- to threefold increased risk for secondary solid tumors (range, 1.3 to 7.5). A three- to sevenfold increased risk seems to exist for the development of solid tumors arising in the previous irradiation ports, such as stomach, pancreatic, bladder, and renal cell cancer, and sarcomas. To date, no significantly elevated risk for secondary solid tumors was observed after chemotherapy, even including regimens with alkylating agents, eg, cisplatin and ifosfamide. However, the risk associated with chemotherapy needs to be reexamined when the median follow-up of studies will exceed more than 10 years. An increased relative risk for secondary leukemias after chemotherapy (range, 1.3 to 3.4) has been reported in three of eight studies with more than 300 patients. Four large studies indicate a significantly elevated risk (range, 15 to 25) for the use of conventional-dose etoposide (< 2 g/m2 cumulative dose); however, with a 5-year cumulative incidence of less than 0.5% of all patients, this risk seems small. Concerning high-dose etoposide regimens (> 2 g/m2), further studies are necessary. CONCLUSION Treatment for testicular cancer is associated with a small, but clearly identifiable, risk for secondary solid tumors that can be attributed to radiotherapy, and for secondary leukemia mainly associated with the use of chemotherapy. The frequency of secondary neoplasia observed is rather low, and in the light of the high cure rate, the risk for the individual patient appears negligible and should not alter current treatment strategies for metastatic testicular cancer.

scholarly journals On the Origin of Testicular Germ Cell Tumors: From Gonocytes to Testicular Cancer

2019 ◽  
Vol 10 ◽  
Author(s):  
Tiziano Baroni ◽  
Iva Arato ◽  
Francesca Mancuso ◽  
Riccardo Calafiore ◽  
Giovanni Luca
Keyword(s):  
Testicular Cancer ◽  
Germ Cell ◽  
Germ Cell Tumors ◽  
Testicular Germ Cell Tumors ◽  
Testicular Germ Cell

scholarly journals Burned-Out Testicular Cancer: Really a Different History

2017 ◽  
Vol 10 (3) ◽  
pp. 846-850 ◽  
Author(s):  
Claudia Mosillo ◽  
Simone Scagnoli ◽  
Giulia Pomati ◽  
Salvatore Caponnetto ◽  
Maria Laura Mancini ◽  
...  
Keyword(s):  
Testicular Cancer ◽  
Germ Cell ◽  
Histopathological Examination ◽  
Mature Teratoma ◽  
Germ Cell Tumors ◽  
Testicular Tumor ◽  
Testicular Germ Cell ◽  
Abdominal Lymph Node ◽  
Cell Components ◽  
Histological Regression

Two or more histological types characterize more than 60% of testicular germ cell tumors (GCTs). Burned-out testicular tumor refers to partial or complete histological regression of the primary testicular lesions. The most frequent GCT type involved in this kind of histological regression is choriocarcinoma, followed by embryonal carcinoma. To our knowledge, there are no cases of the burned-out phenomenon in teratoma. We report a case of a 19-year-old man presenting to our institute with a right testicular lesion, evidence of mediastinal and abdominal lymph node metastasis, and high levels of GCT serum biomarkers. After orchiectomy, the histopathological examination showed a mixed GCT: mature teratoma, immature teratoma, and histological features of testicular cancer regression (burned-out phenomenon). The patient underwent first-line chemotherapy (BEP regimen) which resulted in a complete instrumental and biochemical response after 4 cycles. Teratoma is considered a less aggressive type of GCT. In this particular case, metastatic disease seems to result from non-germ cell components which underwent early spontaneous regression.

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