Diagnosis Of Testicular Cancer Research Articles

Second cancer risk following testicular cancer: a follow-up study of 1,909 patients.

Improved survival in testicular cancer has been accompanied by concern about long-term side effects of therapy. We assessed the evolution of second cancer (SC) risk over a prolonged follow-up period, which has been rarely studied in large patient series. We estimated the risk of SCs in 1,909 patients with testicular cancer diagnosed in the Netherlands from 1971 to 1985. Complete medical information was obtained up to at least January 1988 for 92% of patients. Median follow-up was 7.7 years. For 89% of second tumors the diagnosis was confirmed through review of histologic slides; for an additional 8%, the diagnosis was verified by pathology reports only. Seventy-eight patients developed a SC 1 year or more after start of treatment, as compared with 47.6 expected on the basis of incidence rates in the general population (relative risk [RR], 1.6; 95% confidence interval [CI], 1.3 to 2.1). The mean 15-year actuarial risk of all SCs was 9.8% (95% CI, 7.5% to 12.8%). Significantly increased RRs were observed for all gastrointestinal cancers combined (RR, 2.6; 95% CI, 1.7 to 3.9), stomach cancer (RR, 3.7; 95% CI, 1.8 to 6.8), contralateral testicular cancer (CLTC) (RR, 35.7; 95% CI, 21.8 to 55.2), and leukemia (RR, 5.1; 95% CI, 1.4 to 13.0). Patients who had received irradiation to the paraaortic lymph nodes and who survived testicular cancer for more than 5 years were at particularly high risk of developing stomach cancer (RR, 6.9; 95% CI, 3.3 to 12.7). The median interval between the diagnosis of testicular cancer and stomach cancer was 12.4 years. Patients treated with chemotherapy (CT) did not experience an increase in SCs in general. Indeed, CT-treated patients, as compared with those who received radiotherapy (RT), or surgery alone, had significantly reduced risk of CLTC. This finding might be attributed to an eradicating effect of CT on carcinoma in situ or subclinical CLTC. The excess risk of leukemia was not found to be clearly related to CT. Testicular cancer patients who receive RT experience elevated risk of gastrointestinal tumors. CT does not seem to increase SC risk and may even decrease the risk of a CLTC. Following testicular cancer, the 15-year actuarial risk of all SCs is only about half the risk experienced by patients with Hodgkin's disease.

Incidence of second primary cancer following testicular cancer.

The incidence of second primary cancers was investigated in 6187 Danish men diagnosed with testicular cancer in the period 1943-1987. During the course of 59,000 person years, 459 subsequent primary cancers occurred. The relative risks were significantly increased for leukaemia, gastric cancer, pancreatic cancer, bladder cancer, non-melanoma skin cancer and kidney cancer. Increased incidence was furthermore suggested for cancer of the rectum, prostate and lung. The increased incidence of leukaemia appeared in the first 10 years after testicular cancer diagnosis. The excess incidence for gastric cancer, pancreatic cancer, rectal cancer and lung cancer was strongest 10-19 years after testicular cancer, while the relative risk of non-melanoma skin cancer and prostate cancer increased throughout the period of follow-up. The increased incidence of cancer in this cohort is most likely an effect of radiotherapy used for testicular cancer. It is proposed that the different incidence patterns over time after testicular cancer diagnosis reflect differences in the growth rate of tumours originating in different tissues.

Increased incidence of sarcoma in patients treated for testicular seminoma.

In a nationwide cancer registry analysis of second primary malignancies in 6187 men with testicular cancer in the period 1943-1987, 13 sarcomas were found, yielding a 4-fold increase of the relative risk (RR). The majority of sarcomas occurred in men with seminoma, and the increased incidence was seen irrespectively of time since the diagnosis of testicular cancer. The interval between the testicular cancer and the sarcoma varied from 5-34 years. After investigation of the hospital records and re-examination of the histological specimens, 3 patients were excluded. In spite of this, the RR was still considerably increased (at least 3-fold). Seven of the 10 sarcomas were found to be located within the field of the radiation treatment administered and three at the periphery. The absolute number of these secondary sarcomas is low, but the risk of developing such neoplasms and other malignancies should, even so, be kept in mind in the follow-up of testicular cancer patients.

Advances in the diagnosis and treatment of testicular cancer.

Advances in the diagnosis and treatment of testicular cancer.

Birth order and risk of testicular cancer

To explore the etiology of testicular cancer, cases of testicular cancer were identified among members of a cohort of Danish boys born between 1941 and 1957 (inclusive), who had attended schools in Copenhagen and Gentofte and whose school health records were contained in an archive under the supervision of the Danish Cancer Registry. One hundred and eighty-three cases of testicular cancer diagnosed before 31 December 1984 were identified; 366 controls, matched to cases by sex and age, were selected from the same cohort. Information on potential risk factors and confounders was obtained from two sources: school health records and midwife protocols, both of which were recorded prior to the diagnosis of testicular cancer in cases. Relative risks (RR) approximated by the odds ratios were calculated and, in logistic regression analyses, adjustments were done for known or suspected confounders. A decreasing risk of testicular cancer with increasing birth order was observed (P = 0.020). Compared with being firstborn, being number four or more in birth order was associated with a significantly decreased RR for all testicular cancers (RR = 0.3, 95 percent confidence interval [CI] = 0.3-0.8) and testicular seminoma (RR = 0.1, CI = 0.02-0.9). No association was observed between high social class and the risk of testicular cancer (RR = 1.4, CI = 0.8-2.3); neither was age at which the study subjects had mumps or measles related to risk of testicular cancer. No cases of mumps orchitis were observed before or during school years. A slightly increased RR for testicular cancer among boys from small families could be explained by the association between family size and birth order.(ABSTRACT TRUNCATED AT 250 WORDS)

Surveillance after orchidectomy for patients with clinical stage I nonseminomatous testis tumors.

This study was designed to determine the proportion of patients with clinical stage I nonseminomatous germ cell tumors of the testis (NSGCTT) managed with surveillance after orchidectomy who have more advanced disease and, therefore, require further treatment, the time to progression, the sites of progression, and the efficacy of treatment delayed until progression was recognized. One hundred five patients were observed prospectively without further treatment after orchidectomy and full clinical staging. Treatment was given immediately upon detection of marker-positive, clinical, or radiologic evidence of disease. Thirty-seven patients (35.2%) have required further therapy for disease progression, occurring from 2 to 21 months after diagnosis. Thirty-six patients have been successfully treated. Overall, 104 patients (99%) remain alive and free of disease at 12 to 121 months after orchidectomy. Progression occurred in the retroperitoneum in 25 of 37 patients who developed further disease on surveillance. The presence of vascular invasion in the primary tumor was predictive of an increased risk of progression. Surveillance is a valid alternative to immediate retroperitoneal lymph node dissection in patients with clinical stage I NSGCTT but should be recommended only under the close supervision of physicians experienced in the diagnosis and treatment of testicular cancer.

Missed diagnosis of testicular cancer

Missed diagnosis of testicular cancer

Familial testicular cancer: a report of the UK family register, estimation of risk and an HLA class 1 sib-pair analysis

Forty-two families with two or more cases of testicular cancer have been reported to the UK Register for Familial Testicular Cancer, comprising two pairs of identical twins, 27 sets of other brothers (25 pairs, two triples), nine father-son pairs, two pairs of first cousins and two uncle-nephew pairs. In total 91 testicular tumours are described in 86 individuals (42 (46%) pure seminoma, 49 (54%) other germ cell tumours). The median age at diagnosis in these patients was significantly younger than that in a comparable series of non-familial patients (29 c.f. 32.5 years, P less than 0.01). In a case-control comparison of 794 testicular cancer patients, eight patients (1.0%) had a brother and four patients (0.5%) had a father with a previous diagnosis of testicular cancer at the time of their own diagnosis (and these families are all included in this report). Two out of 794 controls (0.3%) had a first degree relative with testicular cancer. The cumulative risk to a brother of a patient for developing testicular cancer by the age of 50 years was estimated to be 2.2% (95% C.I. 0.6-3.8%) which results in a relative risk of 9.8 (95% C.I. 2.8-16.7) in comparison with the general population. HLA Class I typing of 21 affected sib-pairs demonstrated four (19%) sharing two haplotypes, 13 pairs (62%) sharing one and four pairs (19%) sharing none. This did not differ significantly from the expected proportions of 25%/50%/25%. It is unlikely, therefore, that there is a major gene associated with testicular cancer predisposition within or closely linked to the major histocompatibility gene complex on chromosome 6.

DNA Flow Cytometry in Sperm Cells from Testicular Cancer Patients

In 77 patients with testicular cancer, sperm cell density was evaluated before and after treatment together with the following parameters as recorded by DNA flow cytometry: the percentage of condensed and non-condensed haploid sperm cells, and the number of non-haploid cells. The patients received either abdominal radiotherapy, cisplatin-based combination chemotherapy (+/- surgery) or did not undergo antiproliferative treatment at all. Ejaculates with a low sperm cell density had high numbers of non-condensed haploid and non-haploid cells, whereas the percentage of condensed haploid cells was decreased. However, even 'azoospermic' semen samples (by light microscopy) contained haploid cells indicating ongoing sperm cell production. One year after radiotherapy there was a significant decrease in the sperm cell density and the number of condensed haploid cells. Chemotherapy led to a significant reduction of sperm cell density evaluated 1 year after treatment. Three years after the diagnosis of testicular cancer, sperm cell production had recovered in most patients. In patients who did not have radiotherapy or chemotherapy the median density of sperm cells 3 years after treatment significantly exceeded the corresponding figure from the pretreatment situation. A low pretreatment percentage of condensed haploid cells (less than or equal to 90%) was correlated with the lack of 1-year recovery of sperm cell production. It is too early to state whether longitudinal flow cytometric data from ejaculates in testicular cancer patients yield clinically valuable information, in addition to that obtained by light microscopy. From this preliminary observation it seems that DNA flow cytometry in ejaculates from testicular cancer patients may give valuable clinical information about sperm cell production following treatment.

Psychosocial Sequelae in Long-Term Survivors of Testicular Cancer

Eighty-eight men with a diagnosis of either seminomatous or nonseminomatous testicular cancer were recruited for intensive psychosocial assessment by personal interview and psychological testing. The interviews were conducted, on the average, 45 months after treatment had ended. The men experienced significant depletion of energy, increased fear of cancer, interference with sleep and cognitive function, and sexual difficulties during and after treatment. No significant differences in these measures were found between tumor types. A small subset of patients continued to experience substantial difficulties in these areas. The men's scores on psychological tests did not reflect significant levels of syrnptomatology in the sample as a whole.

Testicular cancer.

Testicular cancer, which predominantly occurs in young men, has become increasingly common; it is presently the most common malignancy in men aged 20-34. Despite a lack of knowledge of aetiology, empirical advances, particularly in the management of patients with advanced disease, have been dramatic. Prior to the development of effective chemotherapy in the 1970s, less than 10% of men with metastatic non-seminomatous germ cell tumours were cured; nowadays approximately 90% of patients are potentially curable. The introduction of effective chemotherapy has led to a reappraisal of surgery and radiotherapy in the management of early stage disease and the introduction of a policy of surveillance in patients without evidence of metastases at the time of removal of the primary tumour. Following chemotherapy, surgery is required in approximately 25% of patients with advanced disease to excise residual masses, which in one-fifth of cases will show evidence of residual malignancy. In a proportion of patients, testicular cancer develops on a background of long-standing infertility, whereas in many men there is temporary oligospermia, despite a previous history of fertility. The majority of patients with prior evidence of spermatogenesis recover this function following chemotherapy and there is no evidence that children fathered by such patients have an increased risk of malformation. Despite physician optimism and excellent prospects for cure, significant psycho-social morbidity is associated with the diagnosis and treatment of testicular cancer. Factors contributing to this are being identified and will lead, hopefully, to the minimisation of such problems by appropriate intervention.

Immunological tissue markers in the diagnosis of testicular cancer

Immunohistochemistry greatly contributes to the accuracy of the diagnosis in testicular germ cell tumors (TGCT). Human chorionic gonadotropin (HCG) and alphafetoprotein (AFP) are the most used markers in testicular cancer, where the immunostaining is positive in non-seminomatous TGCT. Pure seminoma does not produce these proteins but some are combined with syncytiotrophoblastic cells which elaborate HCG, producing elevated HCG serum levels and positive immunostaining. Other markers deserve mention. Among these there are placental alkaline phosphatase (PLAP), ferritin (Fe), pregnancy specific beta1-glycoprotein (SP1), human placental lactogen (HPL), carcinoembrionic antigen (CEA) and alpha1-antitrypsin (A1AT). In addition, the recognition of intermediate filament proteins, such as keratin and vimentin, allow differentiation between seminoma and embryonal carcinoma.

Testicular Neoplasm Diagnosed by Ultrasound

The diagnosis of testicular cancer is usually made by the findings of a testicular mass on physical examination. in rare cases a young man will present with retroperitoneal nodes and a normal testicular examination. in such cases a testicular ultrasound may localize the testis which harbors a subclinical neoplasm. in addition serum markers of B-HCG and AFP are essential. As a screening procedure a urine pregnancy test is helpful, since it can be obtained quickly while quantitative B-HCG and APF results are delayed.

Testicular self-examination: validation of a training strategy for early cancer detection.

Testicular self-examination (TSE) can lead to early diagnosis and treatment of testicular cancer, the third leading cause of death in young men. We evaluated the effectiveness of a brief and specific checklist for teaching TSE skills. Ten men were videotaped while performing testicular self-examinations before and after training. The TSE training resulted in large and significant increases in the number of TSE steps completed and duration of the TSE. Two urological validation measures supported the improvements observed in the mens' self-examinations. Subjects reported continued performance of TSE during a follow-up telephone interview. This pilot study indicates that a brief and specific checklist is an effective strategy for teaching early cancer detection skills.

Is SP-1 a marker for testicular cancer?

We measured the serum levels of the pregnancy-associated protein SP-1 by radioimmunoassay in 91 patients with a diagnosis of germ cell testicular cancer. Sixty-seven of the men had active disease, and of these, 52 per cent had elevated levels of SP-1. In contrast, all 24 patients with inactive disease had normal levels. Elevations of SP-1 were associated more often with elevated levels of human chorionic gonadotropin than with elevated levels of alpha fetoprotein, but elevated SP-1 levels also occurred in patients with normal levels of both of these established tumor markers. We studied serial samples from 21 patients, and in 5 the SP-1 level provided clinically valuable information not provided by the other two markers. SP-1 is a clinically useful marker in germ cell testicular cancer. Further studies are needed to determine the role of the two forms of protein, alpha and beta, and to define the conditions under which the SP-1 level is elevated.