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

A sensitive RIA (500 fg/tube) has been developed for assay of testosterone in male saliva and extensively validated. In normal male saliva samples, morning concentrations (368 +/- 167 pmol/l) were significantly higher than evening samples (212 +/- 132 pmol/l). The circadian rhythm was confirmed by COSINOR analysis. Levels of testosterone in saliva, in response to HCG stimulation, accurately reflected the increase observed in matched plasma samples. Synacthen administration, although increasing circulating cortisol levels, caused no significant change in plasma and salivary testosterone concentrations. Prostatic cancer patients on diethylstilboestrol therapy had low salivary (47--122 pmol/l) and plasma (1.0--2.8 nmol/l) testosterone concentrations. Correct assessment of testicular function following stimulation and treatment regimens requires multiple sampling. Since saliva samples are easily collected by non-invasive techniques they represent an attractive alternative to plasma for evaluation of androgenicity.
 ...
PMID:Assessment of testicular function by the radioimmunoassay of testosterone in saliva. 740 98

Present status of tumor markers in urological malignancies for diagnosis and follow-up was reviewed. Although many researches have been performed, specific tumor markers in kidney, urothelium and penis cancers have not identified. In testicular tumors, AFP and beta-subunit of HCG are widely used. Especially, using biological half time, these substances are very useful in the judgement of presence of residual tumor or tumor recurrence. In prostate cancer, the determination of PSA has been confirmed to be the most useful tumor marker in solid tumor. World standardization of PSA assays and evaluation of PSA subtypes are necessary.
 ...
PMID:[Tumor markers in urological malignancies]. 869 21

Most testicular germ cell tumors have serological tumor markers such as alpha-fetoprotein (AFP) and human chorionic gonadotropin beta-subunit (beta-HCG). On the other hand, molecular staging of these tumors has not been well established compared to other urogenital malignancies like prostate cancer. Recently, melanoma antigen (MAGE) which is one of the tumor-associated antigens recognized by cytotoxic T lymphocytes (CTL) has been found to be present in a variety of malignant tumor types and normal testis. In addition, Wilms' tumor-associated gene WT1 has been found to be expressed in some testicular cancers. Thus, we examined the expression of these genes in testicular cancer tissues and peripheral blood of cancer-bearing patients using reverse transcription-polymerase chain reaction (RT-PCR). The expression of the MAGE1-3 genes was examined in 34 testicular germ cell tumors (24 seminomas and 10 nonseminomas). Of the seminomas and nonseminomas, 87.5% and 40% were positive for MAGE1, 91.7% and 60% for MAGE2, and 83.3% and 30% for MAGE3, respectively. The expression of the MAGE genes was not correlated with the tumor stage. The expression of the WT1 gene was quantified in 26 testicular germ cell tumors. WT1 was highly expressed in 5 of the 7 high stage cases, but in only 4 of the 19 low stage cases (p < 0.01). The mRNA of these genes could not be detected from the peripheral blood of patients with high stage tumors. These results suggest that MAGE genes may be useful tumor markers for molecular staging of testicular cancer, especially seminoma, and that the WT1 gene may be a tumor marker for high stage testicular germ cell tumors. However, these genes cannot yet be used for molecular staging of testicular germ cell tumors.
 ...
PMID:[Molecular staging of testicular cancer using polymerase chain reaction of the testicular cancer-specific genes]. 1050 Sep 69

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.
 ...
PMID:Prognosis of primary testicular seminoma: a report on 57 new cases. 1078 78

The genetic mechanisms of prostate cancer recurrence during hormonal therapy are largely unknown. So far, data from conventional karyotype analysis on hormone-refractory prostate carcinomas have not been published, mainly because of the difficulties in obtaining fresh hormone-refractory prostate carcinoma samples and getting metaphases from them. Here, we have studied chromosomal changes in 12 locally recurrent, hormone-refractory prostate carcinomas using karyotyping and CGH that revealed genetic aberrations in all tumors. Loss of the Y chromosome was the most common (89%) finding, and tetraploidy or near-tetraploidy was detected in all tumors. Also non-random translocations were found in 56% of the tumors. The present study indicates that clonal chromosomal aberrations in hormone-refractory prostate carcinomas are more common than in untreated primary tumors, and also, further studies on the frequency and significance of translocations in prostate carcinoma progression during hormonal therapy are warranted.
 ...
PMID:Chromosomal changes in locally recurrent, hormone-refractory prostate carcinomas by karyotyping and comparative genomic hybridization. 1173 23

Clinical oncologists have always shown great interest in circulating tumor markers. There are several markers that in the clinical routine are a signal of particular tumor types; some of them are strictly tissue-specific such as prostatic specific antigen (PSA) for prostatic cancer, AFP and HCG for germ cell tumors of the testis and ovary, others such as CA 15.3, CA125, CEA or cytokeratins are less specific since their elevations can be found in different varieties of cancers even if they are preferentially associated to a certain tumor type, thus are considered markers for breast, ovarian cancer and colon adenocarcinoma. The most useful clinical applications of these parameters is their determination during the follow-up of the treated patients, in order to detect the tumor recurrence early, and also to evaluate the evolution of the disease by monitoring the treatment responses. During follow-up, increasing levels of tumor markers can be observed even several months before the clinical demonstration of cancer recurrence. The association of tumor marker tests with imaging modalities can lead to several advantages: the first is to confirm the diagnosis of relapses, possibly before the appearence of the related clinical symptoms due to tumor growth; the second is to localize the sites of lesions, while tumor markers provide only a general indication of the existence of metastases; the third is to make possible a correct whole body restaging. In the assessment of cancer response tumor markers are often very reliable and their changes are faster than the morphological ones. Among all the imaging modalities, nuclear medicine plays an important role in detecting recurrences and metastatic localizations as it is able to investigate functional rather than morphological aspects of tumors, and provide different information in comparison to morphologic imaging. In addition, the scintigraphic techniques offer the possibility to evaluate treatment responses, confirming or not the information from biochemical changes. This review aims to show some examples (breast, prostate and ovarian cancer) in which the combination of nuclear medicine imaging modalities and tumor marker tests is proposed for clinical practice. The advantages and some critical aspects are discussed on the basis of the clinical findings and the most important clinical indications are described.
 ...
PMID:Circulating tumor markers and nuclear medicine imaging modalities: breast, prostate and ovarian cancer. 1211 72

A detailed analysis of chromosome 6 in DNAs from prostate cancers was performed, to define a region for subsequent search for cancer genes. DNA from 4 prostate cancer cell lines and 11 xenografts was used for CGH and whole-chromosome allelotyping with polymorphic microsatellite markers. Loss of proximal 6q was studied in more detail by high-density allelotyping of xenografts, cell lines and 19 prostate tumour specimens from TURP. Seven of 15 xenografts and cell lines showed deletion of proximal 6q by CGH. Gain of 6q was found in 2 samples. Six samples showed 6p gain, and 1 had 6p loss. Allelotyping results were consistent with CGH data in 11 of 15 DNAs. In LNCaP and DU145 cells, CGH showed 6p loss and 6q loss, respectively, but 2 allelic bands were detected for many polymorphic markers on these chromosome arms. These apparent discrepancies might be explained by aneuploidy. In cell line TSU, allelotyping demonstrated chromosome 6 deletion, which was not clearly detected by CGH, indicating loss of 1 copy of chromosome 6 followed by gain of the retained copy during progressive tumour growth. Loss of heterozygosity was detected in 9 of 19 TURP specimens. Combining all data, we found a common minimal region of loss at 6q14-16 with a length of 8.6 Mbp flanked by markers D6S1609 and D6S417. One hundred and twenty-three STSs, ESTs, genes and candidate genes mapping in this interval were used to screen xenografts and cell lines for HDs, but none was detected. In summary, chromosome region 6q14-16 was deleted in approximately 50% of the prostate cancer specimens analysed. The high percentage of loss underscores the importance of genes within this region in prostate cancer growth.
 ...
PMID:Deletion of chromosomal region 6q14-16 in prostate cancer. 1238 9

Metastasis is responsible for most deaths from cancer. Currently, little is known about the early genetic events in the metastatic evolution. Here we describe the application of a newly developed strategy for an in-depth characterization of genomic changes in micrometastatic cells. Unique tumor cell lines were established from bone marrow of patients with cancer of the prostate and analyzed by multiplex-FISH (M-FISH) and array CGH. M-FISH revealed that the occult disseminated cells were characterized by very complex numerical and structural aberrations. Many of these aberrations resulted in chromosomal gains and losses, such as losses of 8p, 13q, and 18q and gains of 8q, 9q, 20, and the X chromosome, which are typically observed in prostate cancer. Array CGH allowed an unprecedented high-resolution assessment of copy number changes, pinpointing commonly gained or lost regions, which should narrow down the identification of regions critically involved in metastasis. Thus, occult micrometastatic cells are now amenable to detailed analyses of their genome. Markers for prognosis and treatment decisions can now be established.
 ...
PMID:High-resolution genomic profiling of occult micrometastatic tumor cells. 1250 44

In the course of the last decades, dramatic advances in the field of molecular biology have greatly increased our knowledges regarding the chromosomal aberrations associated with both hereditary and sporadic tumours. The development of new techniques (RELF, FISH, CGH, cDNA array analysis and functional oncogenetics, etc.) has provided powerful new tools for identification of onco- and oncosuppressor predisposing-genes. The most logical consequence of genetic research is the gene-therapy by directing treatment to the site of the chromosomal defect. The implementation of gene-directed technologies (gene-replacement or augmentation, antisense, interfering small -RNAs, etc.) into clinical practice stands as a model of translational research from laboratory to bedside. Prevention and therapy may be widely influenced by the experience of these techniques. On the other hand, some chemoprevention trials are carried out in subjects with hereditary risk for prostate cancer. The paper aims to outline the advances of genetics in urogenital hereditary tumours on the basis of a review of the literature in this field.
 ...
PMID:[Inheritance in neoplastic urogenital pathology]. 1461 Apr 36

Prostate cancer is known for its highly heterogeneous histological appearance. Data concerning the cytogenetic content of areas with different histology are sparse. We have genetically evaluated 10 prostatic adenocarcinomas with intermediate histopathological grades (Gleason score 7) that showed two distinctive growth patterns with different pathologies, that is, Gleason grades 3 and 4 (G3 and G4). The G3 and G4 tumor specimens were taken from spatially separated regions within the cancer mass. Array-based comparative genomic hybridization (aCGH) was performed to obtain genotypes from the 10 pairs of G3 and G4 cancer areas. The cancer DNAs were retrieved from formalin-fixed and paraffin-embedded tissues allowing optimal recognition and selection of target cells. A genome-wide 2,400-element BAC array that provided high-resolution detection of both deletions and amplifications was used. In the 20 G3 and G4 areas, 252 genomic aberrations (88 gains, 164 deletions) were noted, of which 86 were concurrent in G3 and G4 areas (34% overlap). Ninety-five of the 252 alterations were defined by a single BAC clone (54 gains, 41 deletions). Overlapping changes were more frequent for deletions (46%) than for gains (13%). Frequent coinciding deletions (> or = 20% of tumors) were seen on 8p (60%), 6q (30%), 1p (20%), 2q (20%), proximal 8q (20%), 10q (20%), 13q (20%), 16q (20%), and 18q (20%). A frequent overlapping gain (> or = 20% of tumors) was detected on distal 13q (20%). The patterns of imbalance could be found to coincide in the G3 and G4 areas of the majority of cancers. Array-based CGH can be used as a tool for the evaluation of genetic patterns in prostate cancer.
 ...
PMID:Evaluation of genetic patterns in different tumor areas of intermediate-grade prostatic adenocarcinomas by high-resolution genomic array analysis. 1473 26


<< Previous 1 2 3 4 Next >>