ABSTRACT
Objective@#To explore the color Doppler ultrasonic characteristics of testicular Leydig cell tumors (LCT) and improve the clinical diagnosis of the disease.@*METHODS@#We retrospectively analyzed 4 cases of testicular LCT diagnosed and treated in our hospital and summarized the experience in the ultrasonic diagnosis of LCT with a review of the relevant literature.@*RESULTS@#All the 4 testicular LCTs were solitary and quasi-round, 1 in the left and 3 in the right. The smallest mass was 1.8 × 1.5 cm and the largest 3.1 × 2.5 cm, and 2 were complicated by hydrocele of tunica vaginalis. The margins of tumors were distinct in 2 cases and indistinct in 1, and changed from distinct to indistinct in another during the follow-up. Hypoechoes were revealed in all the 4 cases in ultrasonography, 2 with abundant internal blood flow, 1 with abundant peripheral blood flow, and the other with abundant internal blood flow changed from circular blood flow surrounding the mass.@*CONCLUSIONS@#A typical sporadic LCT was ultrasonically manifested as an isolated hypoechoic infracentimetric mass with a clear demarcation from the adjacent pulp. It exhibited intrinsic hypervascularization associated with a typical peripheral rim pattern. Larger lesions more often presented a lobulated shape and intense hypervascularization. Although these ultrasonic characteristics do not reveal the nature of LCT with certainty, they can help the surgeon with the decision on testis-sparing surgery or perhaps even on the active monitoring for the smallest lesions in a population with impaired fertility.
ABSTRACT
<p><b>OBJECTIVE</b>To study the clinicopathologic features and biological behavior of spermatocytic seminoma.</p><p><b>METHODS</b>A retrospective analysis of patients diagnosed as seminoma, spermatocytic seminoma between January 2003 and May 2011, was performed. Clinical data, HE stained section and immunohistochemical staining (SP method) were reviewed with follow-up.</p><p><b>RESULTS</b>Sixty-six cases of seminoma and 5 cases of spermatocytic seminoma were identified. The average age at the diagnosis of 5 cases of spermatocytic seminoma was 53 years, and no patient had a history of crytorchidism or germ cell tumor. All five patients had stage pT1 tumor. Immunohistochemical studies showed that spermatocytic seminoma was negative for CK, vimentin, OCT3/4, PLAP, and LCA, and PAS staining was also negative. All five patients were well after operation. In contrast, the average age at diagnosis of the 66 cases of seminoma was 37 years, in which 12% had a history of crytorchidism and 11% were in stage pT2 or the above. Immunohistochemical studies showed that seminoma was positive for OCT3/4, PLAP, and CD117. During the follow-up, 2 patients developed metastasis and 3 patients died of the disease.</p><p><b>CONCLUSIONS</b>Spermatocytic seminoma is rare and appears to follow a benign clinical course Due to its favourable prognosis, further treatment is not necessary after orchidectomy. Accurate pathologic diagnosis is critical for patient management and for avoiding over-treatment.</p>
Subject(s)
Adult , Aged , Humans , Male , Middle Aged , Alkaline Phosphatase , Metabolism , Diagnosis, Differential , Follow-Up Studies , GPI-Linked Proteins , Metabolism , Isoenzymes , Metabolism , Neoplasm Staging , Octamer Transcription Factor-3 , Metabolism , Orchiectomy , Proto-Oncogene Proteins c-kit , Metabolism , Retrospective Studies , Seminoma , Metabolism , Pathology , General Surgery , Spermatocytes , Pathology , Testicular Neoplasms , Metabolism , Pathology , General SurgeryABSTRACT
<p><b>OBJECTIVE</b>To investigate further the possible mechanism of carcinogenesis and portal invasion of hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>Samples of the primary tumors, cancer cells emboli in the portal veins and normal liver tissues adjacent to the tumor were collected from 20 cases of primary HCC. Expression of TIMP-3 (tissue inhibitor of metalloproteinases-3) protein was detected using Western blot. Expression of TIMP-3 mRNA was detected by RT-PCR. Methylation of TIMP-3 gene promoter was detected using methylation-specific PCR (MSP).</p><p><b>RESULTS</b>Expression of TIMP-3 protein and mRNA were obtained in all of the normal liver tissues adjacent to tumor. However, loss of TIMP-3 protein expression was found in 5 and 36 cases respectively in the primary tumors and tumor cell emboli in portal veins. Expression of TIMP-3 protein and mRNA in primary tumors and tumor emboli were significantly lower than that in the normal liver tissues. Promoter methylation of TIMP-3 gene could be detected in primary tumors (7 cases) and cancerous emboli (9 cases) in HCC, while no methylation found in normal liver tissues. In all the HCC cases with promoter gene methylation including primary tumors and cancerous emboli in portal veins, 13 cases showed complete loss and 6 cases showed low expression of TIMP-3 protein and mRNA. Promoter methylation of TIMP-3 was noticed not related with the histological grading of HCC.</p><p><b>CONCLUSIONS</b>There is a close relationship between loss or low expressions of TIMP-3 and carcinogenesis and portal invasion of HCC. The loss and low expression of TIMP-3 gene and protein were caused by methylation of the gene promoter.</p>