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testicular neoplasms/glutathione
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Cisplatin-induced long-term hearing impairment is associated with specific glutathione s-transferase genotypes in testicular cancer survivors.
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OBJECTIVE
Cisplatin, a cornerstone of combination chemotherapy in the treatment of testicular cancer, induces hearing impairment with considerable interindividual variations. These differences might be a result of functional polymorphisms in cisplatin-detoxifying enzymes like glutathione
Selective induction of glutathione S-transferases in round spermatids from the Brown-Norway rat by the chemotherapeutic regimen for testicular cancer.
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Chemotherapeutic drugs can affect DNA in male germ cells, thereby impacting on the integrity of the genome transmitted to offspring. Drug metabolizing enzymes can protect cells from xenobiotic insult. We analyzed the expression pattern of such enzymes in isolated round spermatids from rats exposed
[Histochemical study on glutathione S-transferase in patients with testicular tumor].
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Tumor tissue and nontumorous tissue of 31 patients with testicular tumor were examined by the peroxidase antiperoxidase (PAP) procedure using the primary antibody against glutathione S-transferase (GST). Histology of primary tumor was classified as seminoma in 10 cases, non-seminoma in 18 (including
Genotype and phenotype of glutathione S-transferase mu in testicular cancer patients.
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The incidence rate of testicular cancer has been steadily increasing during the last 50 years, and only cryptorchidism, i.e. undescended testes, has been identified as an important risk factor. An interplay between changing environmental factors and genetic susceptibility e.g. in foreign compound
Association between long-term neuro-toxicities in testicular cancer survivors and polymorphisms in glutathione-s-transferase-P1 and -M1, a retrospective cross sectional study.
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BACKGROUND
To assess the impact of polymorphisms in Glutathione S-transferase (GST) -P1, -M1, and -T1 on self-reported chemotherapy-induced long-term toxicities in testicular cancer survivors (TCSs).
METHODS
A total of 238 TCSs, who had received cisplatin-based chemotherapy at median twelve years
Glutathione S-transferase expression in the human testis and testicular germ cell neoplasia.
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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
The role of phase I and II genetic polymorphisms, smoking, alcohol and cancer family history, in the risk of developing testicular cancer.
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[Malignant testicular tumors: cytogenetic and molecular biology principles].
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The common cytogenetic finding characteristic of human malignant testicular germ-cell tumors is the presence of an isochromosome of the short arm of chromosome 12, i(12p), suggesting alterations in the proto-oncogenes (e.g., c-Ki-ras2) or putative tumor suppressor genes (TSG) that are localized
Pi-class glutathione S-transferase: regulation and function.
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Our laboratory has been involved in the study of Glutathione S-transferase pi (GST pi) for many years, both in terms of regulation of gene expression and in trying to understand the endogenous function(s) of this enzyme and also what role it may play in the carcinogenic process [1]. Over-expression
Identification of genetic polymorphisms at the glutathione S-transferase Pi locus and association with susceptibility to bladder, testicular and prostate cancer.
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Two variant glutathione S-transferase cDNAs have been described at the GSTP1 locus, which differ by a single base pair (A-G) substitution at nucleotide 313 of the GSTP1 cDNA. This results in an amino acid substitution which alters the function of the enzyme. In this study, a novel PCR assay has been
Role of oxidative stress in single-dose, cadmium-induced testicular cancer.
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Treatment of rats with a single carcinogenic dose of CdCl2 (i.e., 30 mumol/kg) caused severe hemorrhagic damage in the testis within the first 12 h after the metal. Subsequently, atrophy with calcification developed in the next 2-3 mo. Atrophied tissues regenerated during the 1 yr after exposure.
Effects of curcumin on bleomycin‑induced oxidative stress in malignant testicular germ cell tumors.
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Bleomycin is commonly used in the treatment of testicular cancer. Bleomycin generates oxygen radicals, induces the oxidative cleavage of DNA strands and induces cancer cell apoptosis. Curcumin (diferuloylmethane) is a potent antioxidant and chief component of the spice turmeric. No study
Effects of N-acetyl-L-cysteine on bleomycin induced oxidative stress in malignant testicular germ cell tumors.
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Testicular cancer is a very common cancer in males aged 15-44 years. Bleomycin is used in chemotherapy regimens in the treatment of patients having testicular germ-cell tumor. Bleomycin generates oxygen radicals, induces oxidative cleavage of DNA strand and induces apoptosis in cancer cells. There
Clinically atypical seminomas with yolk sac tumor features.
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BACKGROUND
A small subset of young men die from seminoma. Studying these high risk, clinically atypical seminomas (CASs)-aggressive tumors with visceral metastases and chemotherapy resistance-may provide clues to the nature of drug resistance and the origin of testicular cancers. We explored the
Protective effect of hemin against cadmium-induced testicular damage in rats.
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The protective effect of hemin, the heme oxygenase-1 inducer, was investigated in rats with cadmium induced-testicular injury, in which oxidative stress and inflammation play a major role. Testicular damage was induced by a single i.p. injection of cadmium chloride (2mg/kg). Hemin was given for
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