Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma spermidine concentrations were measured by radioimmunoassay in normal subjects and in patients with various tumours of the breast, prostate or the testis. The sensitivity of the method was 0.45 pmol spermidine/20 microliter plasma and the cross reactivity was 13% with putrescine and 2% with spermine. Plasma spermidine concentrations were raised in 25% of the patients with prostatic cancer (mean concentration 316.7 +/- 240.69 nmol/l) and in 8% of the patients with benign prostatic hyperplasia (mean concentration 198.9 +/- 169.92 nmol/l). No correlation was found between elevated plasma levels of spermidine in the prostatic cancer patients and tumour stage or metastatic status of the patients. No correlation of plama spermidine concentrations and age was found in 61 normal male subjects (mean concentration 200.3 +/- 137.71 nmol/l plasma). Only 29% of the patients with breast carcinoma had elevated levels of spermidine compared to normal female subjects. Plasma spermidine concentrations did not correlate with clinical stage or oestrogen receptor status in these patients. Patients with testicular tumours had elevated mean concentrations of plasma spermidine. One out of five patients with seminoma of the testis and six out of 16 patients with teratoma of the testis had significantly elevated concentrations.
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PMID:Plasma spermidine concentrations in patients with tumours of the breast or prostate or testis. 615 39

Most urologists perform adjuvant radiation therapy for stage 1 (TxN0M0) testicular seminoma after orchiectomy, although the majority of patients with clinical stage 1 seminoma do not have occult metastases and therefore do not require elective nodal irradiation. However, there are currently no clinical or histological parameters that can be used to distinguish patients who need radiation therapy from those who do not. We reported previously that estimates of volume-weighted mean nuclear volume (MNV) were a better predictor of the prognosis of prostate cancer and renal cell carcinoma than subjective histological grading. Here, we examined the usefulness of estimation of MNV for predicting the prognosis of primary testicular seminoma. A retrospective study of 57 patients with testicular seminoma diagnosed between April 1981 and March 1997 at Kobe City General Hospital was performed. Unbiased estimates of MNV data were compared for prognostic value with the level of beta-human chorionic gonadotropin (beta-HCG), alpha-fetoprotein (AFP), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH). Fifty patients were stage 1 (TxNoMo), and 7 patients were stage 2 (TxN1-2M0). All patients received orchiectomy, followed by radiation therapy. Estimates of MNV of stage 2 patients were significantly larger than that of stage 1 patients (P = 0.0142). Although the LDH level was also significantly higher in stage 2 (P = 0.001), there were no significant differences between stages 1 and 2 with respect to beta-HCG (P = 0.997), ALP (P = 0.226), and AFP (P = 0.467). Multivariate logistic regression analysis revealed that the estimate of MNV was the only variable predicting lymph node metastasis (P = 0.0315). In stage 1 patients, only the estimate of MNV was significantly correlated with progression-free survival (P = 0.0118). These findings indicate that the estimate of MNV may be an important prognostic indicator for testicular seminoma. Estimates of MNV may also be useful for excluding patients from surveillance protocols.
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PMID:Prognosis of primary testicular seminoma: a report on 57 new cases. 1078 78

The contribution of specific genes on the Y chromosome in the etiology of prostate cancer has been undefined. Genetic mapping studies have identified a gonadoblastoma locus on the human Y chromosome (GBY) that predisposes the dysgenetic gonads of XY sex-reversed patients to tumorigenesis. Recently a candidate gene, the testis-specific protein Y-encoded (TSPY) that resides on the GBY critical region, has been demonstrated to express preferentially in tumor cells in gonadoblastoma and testicular germ cell tumors. TSPY shares high homology to a family of cyclin B binding proteins and has been considered to possibly play a role in cell cycle regulation or cell division. To address the possible involvement of the TSPY gene in prostate cancer, both in situ mRNA hybridization and immunohistochemistry techniques were used to study the expression of this putative GBY gene in prostate specimens. Our results demonstrated that TSPY was expressed at low levels in normal epithelial cells and benign prostatic hyperplasia (BPH), but at elevated levels in tumor cells of prostate cancers at various degrees of malignancy. Sequence analysis of RT-PCR products obtained from both prostatic and testicular tissues using specific primers flanking the open reading frame of the TSPY mRNA revealed a complex pattern of RNA processing of the TSPY transcripts involving cryptic intron splicing and/or intron skipping. The variant transcripts encode a variety of polymorphic isoforms or shortened versions of the TSPY protein, some of which might possess different biochemical and/or functional properties. The abbreviated transcripts were more abundant in prostatic cancer tissues than the testicular ones. Although the exact nature of such variant TSPY transcripts and proteins is still unclear, their differential expression suggests that the TSPY gene may also be involved in the multi-step prostatic oncogenesis besides its putative role in gonadoblastoma and testicular seminoma.
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PMID:Expression pattern of a gonadoblastoma candidate gene suggests a role of the Y chromosome in prostate cancer. 1468 91

In the Congress of European Cancer Organisation (ECCO)/European Society for Medical Oncology (ESMO), which took place in Stockholm between 23 and 27 September 2011, urological cancers were the subject of various oral presentations and posters. A selection of the more innovative researches, likely to change the patients' management was performed. In prostate cancer, abiraterone acetate should be indicated in patients previously treated with docetaxel and sipuleucel-T in patients with asymptomatic or minimally symptomatic castrate-resistant prostate cancer. Alpharadine should be indicated in patients with symptomatic bone metastases and denosumab in non-metastatic prostate cancer patients with a high risk of developing bone metastases. In metastatic renal clear cell carcinoma, the genetic polymorphisms are predictive for efficacy of anti-angiogenic agents. Targeting both vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) pathways is a very promising strategy. In urothelial cancer, two molecules are promising, the belinostat and the bortezomib. Other news on penile cancer and testicular seminoma are discussed.
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PMID:[Urological cancers: ECCO/ESMO congress 2011]. 2263 46

TFDP3 has been previously identified as an inhibitor of E2F molecules. It has been shown to suppress E2F1-induced apoptosis dependent P53 and to play a potential role in carcinogenesis. However, whether it indeed helps cancer cells tolerate apoptosis stress in cancer tissues remains unknown. TFDP3 expression was assessed by RT-PCR, in situ hybridization and immunohistochemistry in normal human tissues, cancer tissues and prostate cancer tissues. The association between TFDP3 and E2F1 in prostate cancer development was analyzed in various stages. Apoptosis was evaluated with annexin-V and propidium iodide staining and flow-cytometry. The results show that, in 96 samples of normal human tissues, TFDP3 could be detected in the cerebrum, esophagus, stomach, small intestine, bronchus, breast, ovary, uterus, and skin, but seldom in the lung, muscles, prostate, and liver. In addition, TFDP3 was highly expressed in numerous cancer tissues, such as brain-keratinous, lung squamous cell carcinoma, testicular seminoma, cervical carcinoma, skin squamous cell carcinoma, gastric adenocarcinoma, liver cancer, and prostate cancer. Moreover, TFDP3 was positive in 23 (62.2%) of 37 prostate cancer samples regardless of stage. Furthermore, immunohistochemistry results show that TFDP3 was always expressed in coordination with E2F1 at equivalent expression levels in prostate cancer tissues, and was highly expressed particularly in samples of high stage. When E2F1 was extrogenously expressed in LNCap cells, TFDP3 could be induced, and the apoptosis induced by E2F1 was significantly decreased. It was demonstrated that TFDP3 was a broadly expressed protein corresponding to E2F1 in human tissues, and suggested that TFDP3 is involved in prostate cancer cell survival by suppressing apoptosis induced by E2F1.
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PMID:TFDP3 was expressed in coordination with E2F1 to inhibit E2F1-mediated apoptosis in prostate cancer. 2440 21

Positron emission tomography/computed tomography (PET/CT) technology has been a significant, but expensive addition to the oncologist's armamentarium. The aim of this review was to determine the clinical utility of PET/CT in urological oncology, its impact on disease outcome and cost-effectiveness. We searched MedLine and peer reviewed journals for all relevant literature available online from the year 2000 until January 2014 regarding the use of PET/CT in the management of urological malignancies. (11)C-choline PET/CT has emerged as a powerful tool for assessment of biochemical relapse in prostate cancer. Use of novel radiotracers like (124)I-girentuximab has shown promise in the diagnosis of clear cell renal carcinoma. Fluorodeoxyglucose PET has a proven role in seminoma for the evaluation of postchemotherapy residual masses and has shown encouraging results when used for detection of metastasis in renal, bladder, and penile cancer. Introduction of novel radiotracers and advanced technology has led to a wider application of PET/CT in urological oncology. However, testicular seminoma aside, its impact on disease outcome and cost-effectiveness still needs to be established.
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PMID:Management of urological malignancies: Has positron emission tomography/computed tomography made a difference? 2562 71