Meiosis as a means of cell division in human testicular and ovarian neoplasms.
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Cell Division↗
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Results for “TESTICULAR NEOPLASMS”
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Classification and pathology of testicular germ cell and sex cord-stromal tumors.
Germ cell tumors of the testis are the most frequent testicular neoplasms, with seminoma predominating. The pathologist must be able to discriminate between seminoma and nonseminomatous germ cell tumors as well as sex cord-stromal tumors and metastatic lesions. Appropriate therapy and accurate prognostic information are dependent on the proper classification of testicular neoplasia. Characteristic histologic features, serum markers, and immunohistochemistry are helpful in this regard. Sex cord-stromal tumors comprise a small minority of testicular neoplasms. It remains critically important not to confuse these neoplasms with testicular germ cell or metastatic tumors, and, again, recognition of the characteristic histologic features, immunohistochemical findings, and clinical information is diagnostic. The urologist can provide the pathologist with key clinical information in the attempt to make a correct diagnosis.
Carcinoma, Embryonal↗
Pediatric testicular tumors: evaluation with gray-scale and color Doppler US.
PURPOSE: To evaluate the appearance of testicular neoplasms in pediatric patients at examination with gray-scale and color Doppler ultrasonography (US). MATERIALS AND METHODS: Gray-scale and color Doppler US were performed in seven patients aged 8 1/2 months to 17 years 6 months (mean age, 7.8 years) with testicular neoplasms proved at histologic examination. Gray-scale images were evaluated for echogenicity and presence of testicular masses; color Doppler US was used to assess the presence and distribution of color flow. RESULTS: Gray-scale US showed enlargement of the affected testis in all patients. Testicular echogenicity was normal in four prepubertal patients; discrete masses were seen in all three postpubertal patients. The gray-scale findings correlated with patient age. Color Doppler US demonstrated increased blood flow in six of seven testicular neoplasms. Three of the four patients with normal gray-scale echogenicity had diffuse hypervascularity and one had a focal hypervascular mass on color Doppler scans. CONCLUSION: Color Doppler US is more helpful than gray-scale US in identification of testicular tumor.
Blood Vessels↗
Oncogenes in human testicular cancer: DNA and RNA studies.
Oncogene dosage and expression were studied in 16 testicular neoplasms, 14 of germ cell and two of non-germ cell origin. In comparison with normal DNA, tumour DNA of a total of eight patients (seven with germ cell neoplasm and one with testicular lymphoma) showed increased dosages of KRAS2, PDGFA, EGFR, MET and PDGFB. The most frequent (occurring in six tumours) and prominent (up to 3-4-fold) increases were detected in the dosages of KRAS2 (on chromosome 12p) and PDGFA (chromosome 7p), relative to a reference locus from chromosome 2. Importantly, there was a similar increase in 12p dosage in general in these tumours, suggesting the presence of the characteristic isochromosome 12p marker. On the contrary, possible 7p polysomy (assessed by molecular methods) did not explain the PDGFA (or EGFR) changes in all cases. NRAS, MYCN, CSFIR, MYB, MYC, ABL, HRASI, TP53, and ERBB2 did not reveal any consistent alterations in tumour DNA. In RNA dot blot assays the expression of KRAS2, PDGFA, EGFR, or MYC was generally not increased in the tumour samples when compared to that in normal testicular tissue of the same patients although there was interindividual variation in mRNA levels. It thus appears that while oncogene dosage changes occur in a proportion of testis cancers, they are often part of changes in large chromosomal regions or whole arms and are seldom accompanied by altered expression.
Actins↗
Identity of M2A (D2-40) antigen and gp36 (Aggrus, T1A-2, podoplanin) in human developing testis, testicular carcinoma in situ and germ-cell tumours.
Testicular germ-cell tumours of young adults are derived from a pre-invasive intratubular lesion, carcinoma in situ (CIS). In a recent genome-wide gene expression screening using cDNA microarrays, we found PDPN over-expressed in CIS compared to normal adult testis. PDPN encodes podoplanin (Aggrus, human gp36, T1A-2), a transmembrane glycoprotein expressed in lymphatic endothelium and various solid tumours. To examine a potential role for PDPN in testicular neoplasms and during testicular development, we investigated its expression pattern during the development of human testis and in a series of testicular CIS, gonadoblastoma and overt germ-cell tumours. We established by RT-PCR and by immunohistochemistry with a gp36 antibody that PDPN mRNA and the protein product were expressed in testes with germ-cell neoplasms but not in the normal adult testis. We also found gp36 expression in early foetal gonocytes and immature Sertoli cells, similar to the expression pattern of M2A antigen, a previously identified marker for CIS and seminoma. This reinforced our previous proposal that M2A (D2-40) antigen was identical to gp36 (podoplanin, Aggrus, T1A-2). Our findings also suggest that podoplanin has a function in developing testis, most likely at the level of cell-cell interactions among pre-meiotic germ cells and immature Sertoli cells.
Adolescent↗
Invasion of the inferior vena cava by testicular seminoma: demonstration by computed tomography and venography.
Involvement of the inferior vena cava (IVC) by testicular neoplasms is unusual and often clinically unsuspected. We present a patient with testicular seminoma that involved the IVC secondarily and caused multiple pulmonary emboli requiring the placement of a caval filter. The radiographic features of this phenomenon are presented with special emphasis on the computed tomographic (CT) appearance of caval thrombosis and pulmonary embolus. The characteristically low density lymphadenopathy of seminoma may obscure the diagnosis of caval thrombosis on CT. Although the findings are nonspecific, tumor invasion of the IVC should be suspected in all patients with testicular neoplasms who demonstrate caval thrombosis radiographically.
Adult↗
Familial testicular cancer in a single-centre population.
Familial occurrence of testicular cancer suggests a genetic predisposition to the disease. A genetic susceptibility may also be reflected by the occurrence of bilateral testicular neoplasms and the high rates of urogenital developmental anomalies in families prone to testicular cancer. In this study, the proportion of familial testicular cancer cases was analyzed retrospectively in a single-centre population of 693 testicular cancer patients treated between 1977 and 1997 and the relative risk (RR) for first-degree relatives of patients was estimated. In addition, the existence of bilateral testicular neoplasms and urogenital developmental anomalies in familial testicular cancer patients was evaluated. 24 of the 693 patients (3.5%) had a first-degree relative with testicular cancer. These 24 cases belonged to 17 families; in 7 of these 17 families both affected first-degree family members were part of the study population of 693 patients. Consequently, the 693 studied patients belonged to a total of 686 families. Thus, the actual proportion of familial testicular cancer was 2.5% (17 of 686 families). The familial cases consisted of 11 brother pairs, including 2 pairs of identical twins and 1 pair which also had two affected cousins, and 6 father-son pairs (in total 36 cases, 12 treated elsewhere). Estimates of the RR to first-degree relatives showed a 9- to 13-fold increased RR to brothers (P < 0.001) and a 2-fold increased RR to fathers (P = non-significant (n.s)) of testicular cancer patients. Among the 36 patients with familial testicular cancer, 2 (5.6%) had bilateral testicular cancer, 4 (11.1%) had undescended testis, 3 (8.3%) had inguinal hernia, and 1 (2.8%) showed renal hypoplasia. The present data on familial occurrence of testicular cancer may lend support to a role of genetic factors in the aetiology of testicular cancer.
Adult↗
Isolated testicular polyarteritis nodosa mimicking testicular neoplasm-long-term follow-up.
Polyarteritis nodosa is a systemic vasculitis characterized by segmental necrotizing lesions of medium and small-size arteries. Rarely, the inflammatory process is isolated and involves a single organ without systemic manifestations. We describe a patient with isolated polyarteritis nodosa of the testis who presented with a testicular mass mimicking primary testicular tumor. The postoperative laboratory evaluation was negative. Long-term follow-up, without systemic treatment, showed no evidence of recurrence in the remainder of the testis or development of systemic vasculitis.
Adult↗
[Testicular microlithiasis].
Testicular microlithiasis is an uncommon condition in which calcified concretions fill the lamina of seminiferous tubules. It has a specific appearance on sonography with diffuse intra testicular echogenic foci without acoustic shadows. Testicular microlithiasis can be associated with various entities and frequently with primary testicular neoplasm. The authors report a new case of testicular microlithiasis diagnosed by sonography in a 14-year-old boy with epididymo-orchitis. Based on a review and discussion of the literature, the authors emphasize the importance of regular and protracted ultrasound follow-up and monitoring of serum tumour markers to allow early detection of primary testicular neoplasm.
Adolescent↗
Childhood embryonal carcinoma of testis, report of two unusual cases, and the implication on clinical management.
Primary testicular neoplasms are not common childhood tumors, comprising about 1% of all childhood malignancies [1]. Embryonal carcinoma is the most common childhood testicular neoplasm. It has been described in a variety of histologic variants as embryonal carcinoma of infancy, orchioblastoma, yolk sac tumor, endodermal sinus tumor, Teilum tumor, and adenocarcinoma with clear cells. Because of the rarity of the tumor, there is no general concensus concerning the management. Recently we encountered two children with embryonal carcinoma of testis who had rather unusual clinical courses. We believe that a report of these cases may contribute to further design of the most suitable therapeutic regimen.
Castration↗
Retroperitoneal malignancies several years after initial treatment of germ cell cancer of the testis.
Three patients (aged 56, 40, and 38 years, respectively) presenting with large retroperitoneal masses 10 to 18 years after prior orchiectomy for testicular neoplasms (seminoma and embryonal carcinoma) are presented. Despite aggressive chemotherapy in all three patients and surgical excision of the tumor in two, two of the men subsequently died 11 to 16 months after initial diagnosis of the retroperitoneal tumors, and one is living with the disease. Theoretic etiologic mechanisms for the development of late retroperitoneal tumors in these men are discussed, including (1) metastatic disease from a second primary tumor in the remaining testicle, (2) a primary extragonadal retroperitoneal tumor, and (3) delayed transformation of metastatic teratomatous retroperitoneal tumor from the original primary into malignant neoplasm.
Adult↗
Lifespan carcinogenicity tests with native carrageenan in rats and hamsters.
Native carrageenan (Gelcarin), a widely used food additive, was tested for carcinogenicity in MRC rats and Syrian golden hamsters through lifespan studies. Three groups of 30 males and 30 females from these species received carrageenan at dose levels of either 5%, 2.5% or 0.5% in the diet daily for the animal's lifespan. A trend toward an increased incidence of benign mammary tumors in females and testicular neoplasms in males occurred at the median dose level (2.5%); however, the incidence of these tumors was not statistically significant. Hamsters did not develop neoplasms in response to treatment at any dose levels. From the results of this experiment, carrageenan demonstrated no carcinogenic effects in either species.
Adenofibroma↗
Induction of testicular sarcomas in Fischer rats by intratesticular injection of nickel subsulfide.
Nickel subsulfide (Ni3S2) was injected in various amounts into the testis of adult Fischer rats for the study of the acute and chronic effects of Ni3S2 on testicular cells. Rats given injections of 0.6 to 10 mg of Ni3S2 developed an immediate inflammatory response at the site of injection, followed by a delayed, slowly evolving coagulation necrosis of seminiferous tubules and interstitial cells. The extent of testicular necrosis was dose dependent, but at doses of 5 or 10 mg of Ni3S2 the rats invariably developed subtotal destruction of the testis. The testis became atrophic, without regeneration of seminiferous tubules. No damage was seen in the other testis, and no systemic effects were noted. Malignant testicular neoplasms developed in 16 of 19 rats within 20 months after an injection of 10 mg of Ni3S2. These neoplasms were classified by light and electron microscopy as fibrosarcomas, malignant fibrous histiocytomas, and rhabdomyosarcomas. None of the testicular neoplasms was derived from germ cells or genital cord cells. The occurrence of rhabdomyosarcomas in the testis, an organ normally devoid of striated muscle, suggests that Ni3S2 induces malignant transformation of undifferentiated, pluripotential mesenchymal cells.
Animals↗
[Gynaecomastia and male infertility as symptoms of a nonpalpable Leydig cell tumour].
A 35-year-old man and his partner were referred for intracytoplasmic sperm injection treatment (ICSI) because of secondary infertility due to severe oligoasthenoteratospermia. Three years earlier he had presented elsewhere with left unilateral gynaecomastia. A hypertrophic mammary gland had been excised one year later. Histopathological investigation showed benign hypertrophy. One year later he developed gynaecomastia on the other side. Physical examination and incomplete hormonal screening showed no abnormalities. The couple were referred to our tertiary clinic for ICSI treatment. The patient still had unilateral gynaecomastia. Hormonal screening showed not only severe oligoasthenoteratospermia, but also an elevated serum oestrogen level. Scrotal ultrasound revealed a 17 mm mass in his right testicle. Subsequently unilateral orchidectomy was performed. Histology showed a benign Leydig cell tumour for which no further therapy was required. Four months after surgery the gynaecomastia diminished, oestrogen levels became normal and improvement in semen parameters followed. Patients with severe male infertility or gynaecomastia are at a higher risk of developing a testicular neoplasm. Besides history taking, physical examination of breasts and testicles, hormonal screening and scrotal sonography should be performed as some testicular neoplasms are not apparent on palpation.
Adult↗
Electronic data base systems support the evaluation of male infertility factors, example cryptorchidism.
BACKGROUND: A new data base system was applied to analyse our patient group with two aims: (a) to analyze the effects of former cryptorchidism on the fertility of OUR infertility patients in comparison with the data of the literature and (b) to evaluate this system in a clinical study. MATERIALS AND METHODS: Using the electronic data base Winsperm 2000, 1,648 infertility patients, 79 patients with testicular cancer and 201 healthy semen donors were examined. RESULTS: A history of cryptorchidism, treated at 6.8 +/- 3.3 years of life, was found in 10.1% of our infertility patient group. The routine spermiogram parameters, as well as basal hormone concentration of FSH, LH and testosterone, differed significantly from those of the healthy semen donor group. Comparison between patients with former unilateral and bilateral cryptorchidism differed significantly only in total sperm count. 27.7% of patients with a history of unilateral and 5.4% of patients with a history of bilateral cryptorchidism showed a sperm concentration within the normal range (p < 0.01). Azoospermia was detected in 13.1% of patients with unilateral cryptorchidism and in 29.7% of patients with former bilateral cryptorchidism (p < 0.05). The patients responding to our conception questionnaire realised a total conception rate of 46.1% in the 'non-cryptorchidism group' and of 20.6% in the 'cryptorchidism-group' (p < 0.05), whereas the conception rates did not differ between former unilateral and bilateral cryptorchidism (p > 0.05). Sixteen (20.3%) of the 79 patients with testicular neoplasm were previously treated for cryptorchidism. CONCLUSION: The results of our patient group underline the significance of former cryptorchidism for infertility and testicular neoplasm. The new data base system facilitates rapid data retrieval and examination.
Adult↗
Involvement of dysadherin and E-cadherin in the development of testicular tumours.
Testicular neoplasms are comprised of a variety of histologically different forms, and their pathogenesis has not been elucidated. Dysadherin is a recently described cell membrane glycoprotein, which has an anticell-cell adhesion function and downregulates E-cadherin. In this study, we examined immunohistochemically the expression of E-cadherin and dysadherin in 120 testicular neoplasms (37 seminomas-26 classic, five spermatocytic and six anaplastic-, 45 embryonal carcinomas, 10 mixed germ cell tumours, two yolk sac tumours, 10 mature and eight immature teratomas and eight non-Hodgkin B-cell lymphomas), clinical stage I. The intensity, the expression pattern and the percentage of neoplastic cell staining was recorded and correlated with the histologic type and vascular/lymphatic invasion. Dysadherin was not expressed in non-neoplastic germ cells, neither in CIS/ITGCNU, but it was highly expressed in all types of germ cell tumours, that demonstrated either embryonic phenotype or somatic differentiation, in most terminally differentiated neoplasms, and in all lymphomas. Dysadherin expression did not correlate with vascular invasion. Increased dysadherin expression was correlated with aberrant E-cadherin expression in most tumours. In 17% of embryonal carcinomas colocalisation of dysadherin and membranous E-cadherin staining was noted. This is the first report on dysadherin expression and its association with E-cadherin in testicular tumours. Since dysadherin is not normally expressed in non-neoplastic testis, it is conceivable that it plays a role in the neoplastic transformation of germ cells. In testicular tumours, as in other neoplasms, dysadherin downregulates E-cadherin expression, at least in part.
Adolescent↗
Morphological pattern of testicular tumors.
OBJECTIVE: To find out the mode of presentation, age distribution and the prevalence of various histological subtypes of testicular tumors. METHOD: All consecutive cases of testicular tumors diagnosed in the department of pathology, the Aga Khan University Hospital, Karachi, during the period of eight years (1991-98) were included in this study. Relevant clinical details such as age, clinical presentation and side of involvement of the testis were also recorded, where available. RESULTS: During the span of eight years (1991-98), 170 cases of testicular tumors were diagnosed at the Aga Khan University Hospital, Karachi. Most of the tumors were diagnosed in the third and fourth decade of life. Scrotal mass or swelling was the predominant mode of presentation. There was a slight predominance of right-sided testicular tumors. Germ cell tumors constituted 83.5% of all malignant testicular neoplasms. Amongst these seminoma was the most common (36.5%) tumor followed by mixed germ cell tumors (28.82%). Yolk-sac tumor was the commonest testicular neoplasm in children while lymphoma was the predominant neoplasm in the elderly population. CONCLUSION: The overall relative frequency of testicular malignancy in this series correlated with that reported in the international literature.
Adolescent↗
Current concepts in clinical therapeutics: testicular cancer.
The incidence and epidemiology, pathophysiology, diagnosis and staging, and therapy of testicular cancer are reviewed. Although relatively rare, testicular cancer is an important disease because it is the first disseminated solid tumor occurring in adults for which truly effective therapy has been developed. More than 90% of testicular neoplasms are of germ-cell origin; about 40% of cases involve pure seminoma, 15%-20% are pure embryonal carcinoma, and the rest are of mixed types. Clinically, the major distinction is between pure seminoma and other types because of therapeutic differences. Most men with testicular neoplasms initially complain of a painless testicular mass. Surgical exploration follows, with orchiectomy and complete excision of the spermatic cord if a neoplasm is documented. Seminoma is a highly radiosensitive tumor, and overall cure rates now approach 95%-98%. Combination therapy with cisplatin has been effective in treating patients with extensive disease. Nonseminomatous testicular cancer patients who do not have metastases are treated with a traditional orchiectomy and retroperitoneal lymph-node dissection; about 10% of patients will relapse and must be treated with antineoplastic agents. Patients with disseminated disease require systemic treatment with cisplatin-based combination drug therapy. Reduction of toxicity and identification of patients who can be spared extensive treatment are the current thrusts of research; efficacy is excellent for several regimens. Major advances have been made over the last two decades in curing patients with testicular cancer.
Antineoplastic Combined Chemotherapy Protocols↗