Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 56-year-old patient is described who presented with retroperitoneal lymph node metastases 2 years after resection of a Leydig cell tumor of the left testis. The patient did not suffer from endocrinological imbalance. Surgical removal of the metastases alleviated abdominal symptoms for 1 year. o,p'-Dichlorodiphenyl-dichloroethane (o,p'-DDD) treatment was started at the time of recurrence of the retroperitoneal mass and the appearance of a hepatic metastasis. Tumors were remarkably responsive to o,p'-DDD, since 2 complete remissions could be obtained for extended periods. The o,p'-DDD was tolerated reasonably well and serum levels of 15 to 20 mg./l. were sustained for many months. Unfortunately, the patient could not be cured with this effective treatment.
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PMID:Malignant Leydig cell tumor of the testis in complete remission on o,p'-dichlorodiphenyl-dichloroethane. 140 49

During a routine long-term drug safety study, lasting approximately 2 1/2 yr, male Wistar rats, treated with a prolactin-inhibiting compound, developed an excess of Leydig cell tumors (LCTs). Most tumors were typical for the rat but a small number showed an unusual variation and some appeared malignant. The variation consisted of glandular and/or tubular structures within the tumor mass which occasionally anastomosed and contained an eosinophilic periodic-acid Schiff (PAS) positive material. In a few of these variants, malignant features such as cellular atypia, capsular, and lymphatic invasion and necrosis were seen. No metastases were detected. Detailed morphological and immunohistochemical investigations were conducted in order to establish the cell of origin of these variants. Glandular/tubular structures were found to stain with varying intensity for vimentin and cytokeratin, but were always negative for beta-tubulin. The results indicated that the cell of origin of these LCT variants was indeed the Leydig cell and that glandular and/or tubular structures within LCTs represented a form of Leydig cell metaplasia.
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PMID:Morphologic and immunohistochemical characterization of Leydig cell tumor variants in Wistar rats. 172 33

The transplantable Leydig cell tumor of Wistar rats, LTW(m), caused decreased food consumption and weight loss in the host within 2 weeks of implantation. The tumor was small, did not metastasize, and did not affect several parameters of biochemical function. When the tumors were removed, increases in food intake and body weight occurred within 72 hours and were sustained. Reimplantation of tumors caused anorexia to recur. Parabiotic pairs of rats with tumor in one partner also experienced weight loss. Those rats in parabiosis with tumor-bearing rats gained less weight than those in parabiosis with control rats. These observations suggest that the LTW(m) tumor causes anorexia and that this anorexia is mediated by a circulating substance.
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PMID:Tumor-induced anorexia in the Wistar rat. 694 77

The light microscopic and ultrastructural characteristics of a hormonally active Leydig cell tumor are described. Evidence is adduced that strongly suggests that the Leydig cell tumor was malignant and that functioning metastases were present.
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PMID:Malignant interstitial cell tumor of the testis. 720 56

The incidence of testicular tumours in dogs is higher than in other species. The main three types are: Sertoli cell tumour, seminoma, and Leydig cell tumour. Metastases are rare. Sertoli cell tumours, and to a lesser extent Leydig cell tumours, are often associated with feminization, which occurs in 19% and 5% of cases, respectively. Seminomas are rarely associated with feminization. Feminization seems to be the result of an excessive oestrogen production by the tumour. In severe cases this may lead to bone marrow depression. Atrophy of the contralateral testis is a common finding. It is not clear whether this is a result of feminization or of age because most tumours occur in older dogs. By investigating the morphology of the testis, and the endocrinological and fertility status of the dog this phenomena is hopefully going to be explained. Extra attention is given to the pathogenesis of feminization.
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PMID:[Testicular tumors in dogs: a literature review]. 861 21

Inactivation of the DCC (Deleted in Colon Carcinoma) tumor suppressor gene by allelic loss and/or reduced expression is associated with the development of colon cancer, gliomas, gastric and prostatic malignancies. In a total cohort of 51 testicular germ cell tumors (GCT) of different histologies we analyzed restriction fragment length polymorphism (RFLP) for DCC at two specific DNA sites in 37 GCT and DCC mRNA expression compared to that of the adjacent normal testicular tissue in 41 GCT, one Leydig cell tumor and one testicular metastasis of a non-small cell lung cancer (NSCLC). Two of 17 tumors (11.7%) informative for the Msp I polymorphic site of the DCC gene and 6/25 tumors (24.0%) informative for variable number of tandem repeat (VNTR) showed loss of heterozygosity (LOH). DCC expression was analyzed by semi-quantitative polymerase chain reaction after initial reverse transcription (RT-PCR). Thirty of 41 GCT (73.1%) and both, the Leydig cell tumor and the testicular metastasis of NSCLC, had a nearly complete or total loss of DCC mRNA expression. Six of 11 (54.5%) seminomas and 24/30 (80.0%) nonseminomas had this loss of expression. Twelve of 17 (70.5%) localized tumors, 9/13 (69.2%) tumors with lymph node involvement and 9/11 (82.2%) tumors with distant metastases showed decreased or absent DCC expression. This data suggests that inactivation of the DCC gene, especially the loss of DCC expression, is associated with the development and progression of human GCT.
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PMID:Analysis of the DCC tumor suppressor gene in testicular germ cell tumors: mutations and loss of expression. 911 74

We reported the case of a 35-year-old man with Klinefelter's syndrome and a malignant Leydig cell tumor of the testis. Bilateral gynecomastia and right testicular enlargement led the patient to seek medical assistance. Despite initial orchidectomy two years later the patient developed lung and iliac lymph node metastases. The tumor appeared to be refractory to chemotherapy and to hormonal treatments including op'DDD. Finally, the patient died within 20 months of developing metastases. Leydig cell tumor is an exceedingly rare tumor, especially when associated with Klinefelter's syndrome. This association as well as presentation, pathologic features, hormonal abnormalities, clinical course and response to therapy of malignant Leydig cell tumors are discussed.
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PMID:Malignant Leydig cell tumor of the testis associated with Klinefelter's syndrome. 1065 Jul 98

690 patients were treated for testicular tumour in the course of 18 years. The histology of 7 cases showed Leydig cell tumour. In 4 of the 7 cases, a metastatic process leading to death was observed. At the time of diagnosis, 5 patients were found to have low stage, whereas 2 of the patients had advanced lymphatic involvement. The hematogenous and lymphatic metastases proved to be resistant to chemotherapy. Contrary to the major part of the literature, retroperitoneal lymphadenectomy should be performed with this histological type for the exact pathological staging immediately following orchiectomy.
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PMID:High frequency of metastatic Leydig cell testicular tumours. 1097 Nov 69

A case of malignant Leydig cell tumour is presented. It is a rare primary malignant tumour of the testis and occurs exclusively in adults. The present case is of interest because it occurred at the young age of 25 years which is rare. Histologically it showed almost all features which suggest malignancy and also had metastases to the lungs and liver. The clinical details and pathology of this tumour are discussed.
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PMID:Malignant Leydig cell tumour of the testis. 1180 71

Leydig cell tumors of the testis are rare, mostly presenting as a testicular mass or as endocrinological symptoms. Here, three patients who were admitted for investigation of primary infertility and one patient presenting with a testicular mass are reported. The histological features were reviewed and an immunohistochemical study was done using a panel of antibodies against cytokeratin, vimentin, inhibin A, S-100, Ki-67, follicle-stimulating hormone, luteinizing hormone, prolactin, p53, bcl-2, and c-erbB2. The latter case (lost during follow up of metastatic disease) demonstrated massive tumor necrosis, extension through the tunica albuginea, and a high mitotic activity and MIB-1 score. Only this malignant case was bcl-2 positive. Of the two oncogenic markers studied, none of the cases were positive for c-erb2, while p53 was positive in more than 50% of cells in the malignant case and in one case of infertility with a large tumor, hemorrhage, focal necrosis and atypical cytological features. We recommend the evaluation of infertile men for Leydig cell tumors, and we believe that a panel of antibodies, including Ki-67, p53 and bcl-2, used for immunohistochemical analysis could be of diagnostic value in the identification of malignant and borderline cases of Leydig cell tumor.
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PMID:Leydig cell tumor of the testis: comparison of histopathological and immunohistochemical features of three azoospermic cases and one malignant case. 1188 32


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