Active clinical trials for "Testicular Neoplasms"

The Engagement of Patients with Advanced Cancer is an intervention that utilizes well-trained lay health coaches to engage patients and their families in goals of care and shared decision-making after a diagnosis of advanced cancer. Although lay health workers have never been tested in this role, we hypothesize that lay health workers can feasibly improve goals of care documentation and help to reduce unwanted healthcare utilization at the end of life for Veterans diagnosed with new advanced stages of cancer and those diagnosed with recurrent disease.

This randomized phase III trial is studying how well Caphosol rinse works in preventing mucositis in young patients undergoing autologous or donor stem cell transplant. Supersaturated calcium phosphate (Caphosol) rinse may be able to prevent mucositis, or mouth sores, in patients undergoing stem cell transplant.

In this study, investigators aim to reveal how the COVID-19 pandemic process affects testicular cancer presentations, tumor stages, the time elapsed between diagnosis and intervention, tumor recurrence and progression, which are oncological outcomes.

This pilot study will explore the relationship of Ochratoxin A (OTA) levels in patients with upper tract transitional cell (TCC), renal cell, and testicular cancers by measuring levels of OTA in serum and tumor samples. Dietary exposure will also be analyzed.

We hope to determine the importance of different genes (including B receptors) in anthracycline-induced cardiomyopathy. This has important benefits to patients exposed to anthracyclines, as this could help determine whether certain individuals have increased susceptibility to cardiac injury.

The incidence of testicular germ cell tumors (TGCT) has increased during the twentieth century and is of particular concern as it primarily affects young men. It is the most common cancer among U.S. males ages 25-34. The only well-described risk factors are cryptorchism (undescended testis), family history of TGCT, and personal history of TGCT. To better understand the environmental and genetic determinants of TGCT risk, a case-control study will be conducted among members of the U.S. armed forces. The study will include men who have donated a blood sample to the Department of Defense Serum Repository (DoDSR) between 1989 and 2000. All DoDSR donors who have developed GCT will be matched to DoDSR donors who have not developed TGCT. Approximately 1,080 men with TGCT, 1,080 controls, and 2,160 mothers will be included in the study. The DoDSR serum sample will be tested for organochlorines levels, gonadotropin levels, and viral antibody titres. Each participant will donate a saliva specimen that will be used in an examination of genetic susceptibility. Each participant will also complete a questionnaire concerning a variety of possible risk factors such as physical activity, medical history, medication history, and other risk factors. The mothers of all participants will be invited to participate by completing a questionnaire concerning perinatal exposures and events and by donating a saliva sample. The three main objectives of this study are to: determine whether environmental endocrine modulators (i.e., chlorinated pesticides and polychlorinated biphenyls) are related to risk of GCT and, if so, whether their effects are augmented by other risk factors. determine whether genetic susceptibility to GCT exists and to characterize the environmental risk factors related to that susceptibility. determine whether there are distinct causes of GCT by relating the tissue structures of the tumors to the risk factors.

BACKGROUND: Evidence has emerged that patients cured with cisplatin-bleomycin chemotherapy from disseminated testicular cancer (TC) develop a large number of cardiovascular risk factors (CRF) several years later. Recently, we observed an increased incidence of cardiac events 10-20 years after chemotherapy, possibly as a result of increased occurrence of CRF. Additional cardiovascular damage was observed after treatment: disturbed diastolic function of the left ventricle, microalbuminuria and increased endothelial damage parameters. Furthermore, a metabolic syndrome (syndrome X) with insulin-resistance, dyslipidemia, hypertension and endothelial damage was found in about one third of our cured patients. The investigators hypothesize that endothelial damage and metabolic changes caused by the bleomycin and cisplatin chemotherapy are the main causes for the observed increase in cardiovascular disease in these young cancer survivors. Genetic susceptibility may be an important determinant of individual risk of toxicity in individual patients. PURPOSE: To identify risk factors for cardiovascular disease (CVD) following testicular cancer. To obtain insight into the pathway(s) of CVD development, by examining whether clinical CVD following testicular cancer is associated with a preceding unfavorable cardiovascular risk factor profile and/or with treatment-related factors. To investigate genetic polymorphisms in pathogenetically important pathways that are potentially involved in the development of treatment related cardiovascular morbidity following testicular cancer. PATIENTS AND METHODS: Patients with non-seminomatous testicular cancer who have been uniformly treated with orchidectomy and cisplatin-bleomycin combination chemotherapy at the University Hospital Groningen, The Netherlands, since 1977 but before 2000 are eligible. 380 patients with non-seminomatous testicular cancer fulfill these criteria. A close routine follow-up of these patients after treatment has been done at the University Hospital Groningen. Clinical characteristics of these patients, treatment details including outcome and long-term follow-up are being registered systematically. From all patients who agree to participate assessment of their cardiovascular risk factors and the presence of subclinical cardiovascular damage will be performed by means of several measurement techniques. Also genomic DNA will be collected for studies on polymorphisms in pathogenetically important pathways. For the total cohort of patients several different late effects phenotypes of cardiovascular damage and cardiovascular risk factor patterns will be derived from the available data. These toxicity phenotypes will be used to select cases and controls from the total cohort to test candidate genetic polymorphisms on their association with occurrence of toxicity. The association of the different genetic polymorphisms with the toxicity phenotype will be estimated by comparing cases with different toxicity phenotypes with controls without that phenotype. POSSIBLE RESULTS This research will provide insight into the pathogenesis of cardiovascular disease after treatment for testicular cancer. The main outcome will be the possibility to select individually those patients who are likely to have an increased risk to encounter specific cardiovascular toxicity during or after chemotherapy treatment for TC. This will provide opportunities for the tailoring of potential toxic treatment and/or guide primary and secondary prevention strategies for serious side effects of chemotherapy treatment.

Chemotherapy drugs improve cancer survival but increase the risk of cardiovascular disease (CVD). VEGF inhibitors (VEGFI) cause severe hypertension, while cisplatin appears pro-thrombotic. Hence while cancer survival may improve, this is at the risk of potentially severe CVD and associated morbidity. Mechanisms underlying the cardiovascular toxicities of VEGFI and cisplatin are unknown, but effects on vascular function may be important. The INTELLECT study will phenotype the endothelial effects of VEGFI and cisplatin using a variety of methods.

incidence is increasing1,2. Whilst the prognosis is very good with the vast majority of patients cured with orchidectomy alone, those with high risk stage one non seminomatous germ cell cancer (NSCGT) or metastatic disease (NSCGT or seminoma) are treated by surgery followed by chemotherapy. Platinum based chemotherapy is associated with long-term cardiovascular sequelae. Endothelial dysfunction is a key component of early atherogenesis and the later stages of obstructive atherosclerosis, plaque rupture and thrombus formation. Whilst endothelial toxic effects of BEP chemotherapy appear to be central in the pathophysiology of associated complications, abnormalities in endothelial function as assessed by measures of brachial artery flow-mediated dilatation (FMD) have not demonstrated a consistent effect over time. When assessed within ten weeks of platinum-based chemotherapy9, no change in FMD was observed whilst marked decreases are seen immediately following treatment11 and also one year following treatment12. Therefore, the time-course of endothelial vasomotor impairment remains incompletely defined in a single prospective cohort.

Rationale: In pharmacokinetic studies, aprepitant was shown to be a moderate inhibitor of CYP3A4 activity. Etoposide is metabolised by CYP3A4. Objective: to investigate the absence of a clinical relevant interaction between aprepitant and etoposide in TC patients treated with (B)EP. Study design: A single centre, prospective, paired observational pharmacokinetic study in 12 patients with TC who are treated with etoposide during 5 days in combination with cisplatin with or without bleomycin conform the standard BEP or EP-protocol and who will be treated with aprepitant from day 3 until day 7 according to the routine antiemetic protocol. The effect of aprepitant on etoposide will be investigated within the same patient. In this study the patient will serve as its own control.