Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-nine patients with assumed extragonadal germ-cell tumors (retroperitoneum: 39, mediastinum: 8, CNS: 2) were included in the present study. The patients were treated with 'high' (40 mg cisplatin/m2 and 200 mg etoposide/m2 daily x 5) or 'conventional' (20 mg cisplatin/m2 and 100 mg etoposide/m2 daily x 5) doses of cisplatin and etoposide together with bleomycin, depending on the presence or absence of poor prognosis factors. Forty-six patients were evaluable for response and 3 patients were classified as non-responders (1 early death, 2 toxic deaths). Eighty percent obtained complete remission and 76% are alive without evidence of disease after a median observation time of 41 months (88% of patients with primary tumor in the mediastinum, 72% with tumor in the retroperitoneal area, 87% of patients with seminoma and 71% with non-seminoma, respectively). In 48 patients testicular biopsies were performed. In 42% of patients with primary retroperitoneal tumors, carcinoma in situ testis (CIS) was diagnosed. None of the patients with tumors in mediastinum or CNS had CIS in the testicles. The therapeutic outcome for patients with extragonadal germ-cell tumors is now similar to that of patients with very advanced testicular cancer when considered in relation to the presence of prognostic factors. The coexistence of CIS and retroperitoneal tumor could indicate that these tumors are not truly extragonadal or that these lesions have a common malignant progenitor.
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PMID:Management of extragonadal germ-cell tumors and the significance of bilateral testicular biopsies. 132 76

Distribution of intermediate filament proteins (IFs) and several special markers was studied in 39 testicular germ cell tumors and 8 embryos and foetuses. The similarity and difference between development of germ cell tumor and embryogenesis were immunohistochemically investigated. Seminoma and embryonal carcinoma, as tumoral counterparts of undifferentiated germ cells, were characterized by little IF expression. This study revealed that the maturing and differentiating process in germ cell tumor is different from normal embryonal development and the tumor cells showed leaping maturing steps in tumorigenesis. Immunostaining for IFs helped to discover the further differentiation occurring in embryonal carcinoma and to demonstrate heterogeneous elements in non-seminoma germ cell tumors, which sometimes might not be apparent by light microscopical observation of H&E staining section. According to the findings, two patterns in mixed germ cell tumors are suggested; i.e., combined and diffuse types. The mechanism of tumorigenesis of the two types is supposed to be different. Clinically, the prognosis of most patients with testicular germ cell tumor is fairly good because of the improved chemotherapies that are dependent on histological diagnosis.
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PMID:Expression of intermediate filaments and other special markers by testicular germ cell tumors. With reference to embryogenesis. 133 51

The strong association of intratubular germ cell neoplasia (ITGCN) with adult germ cell testicular tumors is well known, but studies noting the absence of ITGCN in certain germ cell neoplasms such as spermatocytic seminoma, childhood teratoma, and infantile yolk sac tumor (YST) have raised the issue of whether these latter neoplasms follow a different path of tumorigenesis, accounting for their more benign behavior. A case study illustrating the association of ITGCN with infantile YST is presented to challenge this hypothesis. In addition to the usual characteristic features that included strong cytoplasmic glycogen deposits, and focal placental alkaline phosphatase immunoreactivity, the atypical intratubular germ cells manifested triploidy by in situ hybridization using as probe a telomeric tandem repeat sequence, p1-79, specific to chromosome 1. The invasive YST cells, in contrast, showed evidence of tetraploidy by both in situ hybridization and flow and image cytometric studies, excluding the possibility that the atypical intratubular germ cells represented intratubular invasion by adjacent YST. These findings challenge the belief that the infantile YST follows a different path of tumorigenesis than its adult germ cell counterpart and suggest other hypotheses that might better explain its more benign behavior.
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PMID:Intratubular germ cell neoplasia in infantile yolk sac tumor. Verification by tandem repeat sequence in situ hybridization. 134 58

We reviewed the clinical characteristics, treatment methods, and outcome of 26 patients presenting with seminoma arising in an undescended testis. The tumor-bearing testis was located in the iliac fossa in 17 patients and in the inguinal canal in nine. The most common presenting symptoms were pain or an enlarging mass. At diagnosis, the tumors tended to be relatively advanced, and 16 of 26 patients (62%) had nodal metastases. In addition to the paraaortic nodes, metastases were frequent to the ipsilateral iliac and inguinal nodes even in the absence of prior inguinal-scrotal surgery. Four patients had documented pelvic peritoneal tumor seeding. All patients received treatment in addition to resection of the primary tumor. Fifteen patients received radiotherapy only, 10 received chemotherapy only, and one received both modalities. At a median follow-up of 9.6 years, only one patient had relapsed. He was initially treated with radiation and after relapse was successfully salvaged with chemotherapy. The 5 and 10-year disease-free rate was 96%, and the 5 and 10-year survival rates were 92% and 79%, respectively. Appropriate treatment of seminoma arising in an undescended testis results in an excellent outcome equivalent to that observed for the more usual scrotal seminomas.
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PMID:Treatment of seminoma arising in cryptorchid testes. 135 81

Glutathione S-transferase (GST) isoenzyme expression is altered in a variety of neoplasms and the enzymes are implicated in metabolism of carcinogens and resistance to drugs, including cisplatin. We have studied GST Alpha, Pi, Mu and microsomal isoenzyme expression by immunohistochemistry in normal and cryptorchid testes, intratubal germ cell neoplasia (ITGCN), seminoma and non-seminomatous germ cell tumours. In 16 stage II-IV malignant teratoma intermediate (MTI) both orchidectomy and post-treatment residual surgical masses were studied. All four isoenzymes were strongly expressed in Leydig and Sertoli cells. GST Pi was absent from normal spermatogonia but strongly expressed by the neoplastic germ cells of ITGCN and seminoma. GST Pi was strongly expressed in all elements of teratoma, irrespective of differentiation. There were no qualitative differences in expression between primary and post-chemotherapy metastases. GST Alpha expression in teratoma correlated with epithelial differentiation. GSTs may be important in normal spermatogenesis and protection of germ cells from teratogens and carcinogens. They may have a role in testicular tumour drug resistance but this role is not well defined. GST Pi is a new marker for ITGCN.
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PMID:Glutathione S-transferase expression in the human testis and testicular germ cell neoplasia. 135 63

Seminomas are germ cell tumors that are rarely associated with hypercalcemia. In this report, four cases of seminoma with concomitant hypercalcemia are presented and another three from the literature are reviewed. All seven patients exhibited hypercalcemia with a normal serum concentration of inorganic phosphorus and no evidence of skeletal metastases. The peripheral venous level of parathyroid hormone (PTH) was normal in four of the five patients in whom it was measured. The serum concentration of calcitriol was elevated in the two patients in whom it was measured. After systemic chemotherapy, the serum "corrected" total calcium concentration returned to normal and remained normal; the decrease in the levels temporally paralleled the decrease in tumor volume. Both patients with elevated calcitriol levels remained eucalcemic after treatment of the malignancy, suggesting that the increased serum calcitriol level was linked to the development of hypercalcemia as this humoral agent was inappropriately elevated by patients with this syndrome. In contrast to many forms of malignancy, the development of hypercalcemia did not adversely affect the prognosis of the patients with seminoma, since all seven patients entered complete remission. Hypercalcemia appears to be heretofore unrecognized paraneoplastic syndrome associated with seminoma.
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PMID:Humoral hypercalcemia in seminomas. 137 70

Current opinions differ as to the biological significance and treatment of pure seminoma associated with the serological establishment of beta-human chorionic gonadotropin. Between December 1987 and April 1990, 147 patients with malignant testicular tumors were treated. Of these patients 47 (32%) had a pure seminoma. In 35 of the 47 patients we measured the tumor markers beta-human chorionic gonadotropins and alpha-fetoprotein in the cubital vein blood and testicular vein blood. There were elevated beta-human chorionic gonadotropin levels in the cubital veins of 26% of the patients, in agreement with the literature. However, elevated levels were found in the testicular veins of 80% of the patients, which reflects the high sensitivity of marker identification in testicular vein blood. Apparently, most seminomas produce beta-human chorionic gonadotropin even if it is not detectable in the cubital vein. We believe that the presence of this marker in patients with pure seminoma is not an indication of greater tumor aggressiveness but of tumor mass.
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PMID:Spermatic cord beta-human chorionic gonadotropin levels in seminoma and their clinical implications. 137 58

Recent ultrastructural, cytogenetic, and ploidy analyses indicate that seminoma acts as a precursor from which other forms of testicular germ cell tumor may originate. Ten cases of primary or metastatic testicular germ cell tumors were investigated that showed possible transformation of seminoma to yolk sac tumor. Such transformation was identified in six cases in which foci of abrupt change from seminoma to various patterns of yolk sac tumor occurred, often at the periphery of otherwise pure lobules of seminoma. Immunostains for cytokeratins, placental-like alkaline phosphatase, and alpha-fetoprotein demonstrated the expected changes in reactivity at the foci of such transformation. Four additional cases were regarded as either seminomas with artifactual microcystic change or the close association of seminoma and yolk sac tumor but lacking evidence for transformation. These data support the theory that seminoma is not an "endpoint" neoplasm but may serve a precursor role in the progression to nonseminomatous germ cell tumors.
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PMID:Evidence for the transformation of seminoma to yolk sac tumor, with histogenetic considerations. 155 10

Serum levels of AFP, hCG and CEA were initially and serially measured in 59 patients with testicular germ cell tumors, and serially in 37 with ovarian and 3 with extragonadal germ cell tumors. Patients with seminoma/dysgerminoma or mature teratoma had normal serum AFP and sporadically slightly elevated hCG. Some patients with embryonal carcinoma, pure or with admixture of seminoma, had serum AFP elevated to maximum 100 U/ml, yet its use for monitoring therapy was limited. Patients with yolk sac tumors had elevated AFP and sometimes CEA levels, those with choriocarcinoma had elevated hCG, and those with compound tumors had one or more of the markers highly elevated. High AFP and/or hCG levels indicated the presence of the relevant tumor cells both in the primary and in residual tumor and/or metastases, also those missed in histological material, and thus were useful in restaging. Unfortunately, their absence in serum did not exclude the presence of marker-negative subpopulations of tumor cells. Changes in marker values paralleled the effects of treatment: the level increasing from any nadir heralded recurrence in patients in remission; elevated or increasing levels during therapy implied resistance to the therapy; decreasing levels indicated regression even though a return to the normal range did not mean eradication of all tumor cells.
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PMID:Serum AFP, hCG and CEA in the management of patients with testicular, ovarian and extragonadal germ cell tumors. 137 75

Preliminary studies of RAS mutational activation in human testicular germ cell neoplasms have yielded conflicting results. Whereas two studies of clinical material revealed a significant incidence of N- and KRAS mutations, two studies of a variety of germ cell lines failed to document RAS mutations. To clarify the incidence of RAS mutations in these tumors, we studied archival paraffin-embedded, formalin-fixed orchiectomy specimens from 25 nonseminomas (NSGCT), 18 seminomas (SEM), and one Leydig cell tumor. For 14 of the 44 neoplasms, DNA was also available from nonmalignant testis adjacent to the tumor. Six age-matched patients had testes removed because of nonmalignant disease and were studied as controls. Polymerase chain reaction (PCR) amplified the K-, N-, and HRAS 12, 13, and 61 codons of these specimens, and mutations were detected with mutation-specific oligonucleotide probe hybridization of Southern and slot blots. Four mutations were found in KRAS 12 (4/44;[9.1%]). One seminoma [1/18(5.6%)] contained the mutation GGT(GLY)----CGT(ARG), and three NSGCT [3/25(12%)] were found to have GGT(GLY)----GAT(ASP) mutations. One of the NSGCT mutations was detected in adjacent nonmalignant tissue, but the corresponding tumor did not contain any detectable mutation. No mutations were detected at KRAS 13 or 61, in NRAS or HRAS 12, 13, or 61, or in the control normal testes. PCR, slot blots, and hybridizations were performed twice by two separate investigators for confirmation of results. PCR-generated mutation-specific positive controls were created for all possible RAS mutations, and these along with wild-type DNA controls were integral to interpretation of the oligonucleotide mismatch hybridization assay. By using positive and negative controls, we have detected a relatively low incidence of RAS mutations in archival human testicular germ cell tumors.
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PMID:Detection of RAS mutations in archival testicular germ cell tumors by polymerase chain reaction and oligonucleotide hybridization. 138 46


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