Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P52742 (pT3)
 1,034 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostate cancer is the second-leading cause of cancer-related death among men and the seventh most common cause of death in the United States overall. As prostatic carcinoma is a slowly growing cancer depending on the tumor burden, use of PSA results in early cancer detection. pT2 tumors can be cured with low morbidity by radical prostatectomy. Five years after operation only few patients will experience further PSA recurrences. Adjuvant radiation therapy is effective in about half of patients with pT3 tumors in case of PSA recurrence. Most prostate cancers are androgen-dependent, meaning that they respond to androgen-ablation therapy. However, these tumors eventually become androgen-independent and grow despite androgen ablation. Since androgens are essential to the survival of prostate cells, a major question is how a prostate cell survives after androgen-ablation therapy. The mechanisms by which a prostate cancer cell survives after androgen-ablation therapy are conflicting. Specific targeting of genes involved in such pathways may further increase the chance of inventing new therapeutic options. So far, chemotherapy with docetaxel has been proved to prolong survival time and minimize cancer induced side effects in patients with hormone refractory prostate cancer.
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PMID:[The hormone refractory prostate cancer - a challenge for the internal specialist]. 1749 9

The standard treatment options based on the risk category (stage, Gleason score, PSA) for localized prostate cancer include surgery, radiotherapy and watchful waiting. The literature does not provide clear-cut evidence for the superiority of surgery over radiotherapy, whereas both approaches differ in their side effects. The definitive external beam irradiation is frequently employed in stage T1b-T1c, T2 and T3 tumors. There is a pretty strong evidence that intermediate- and high-risk patients benefit from dose escalation. The latter requires reduction of the irradiated normal tissue (using 3-dimensional conformal approach, intensity modulated radiotherapy, image-guided radiotherapy, etc.). Recent data suggest that prostate cancer may benefit from hypofractionation due to relatively low alpha/beta ratio; these findings warrant confirmation though. The role of whole pelvis irradiation is still controversial. Numerous randomized trials demonstrated a clinical benefit in terms of biochemical control, local and distant control, and overall survival from the addition of androgen suppression to external beam radiotherapy in intermediate- and high-risk patients. These studies typically included locally advanced (T3-T4) and poor-prognosis (Gleason score >7 and/or PSA >20 ng/mL) tumors and employed neoadjuvant/concomitant/adjuvant androgen suppression rather than only adjuvant setting. The ongoing trials will hopefully further define the role of endocrine treatment in more favorable risk patients and in the setting of the dose escalated radiotherapy. Brachytherapy (BRT) with permanent implants may be offered to low-risk patients (cT1-T2a, Gleason score <7, or 3+4, PSA <or=10 ng/mL), with prostate volume of <or=50 ml, no previous transurethral prostate resection and a good urinary function. Some recent data suggest a benefit from combining external beam irradiation and BRT for intermediate-risk patients. EBRT after radical prostatectomy improves disease-free survival and biochemical and local control rates in patients with positive surgical margins or pT3 tumors. Salvage radiotherapy may be considered at the time of biochemical failure in previously non-irradiated patients.
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PMID:Evidence-based radiation oncology: definitive, adjuvant and salvage radiotherapy for non-metastatic prostate cancer. 1753 94

In the current study, we analysed the prognostic value of vascular endothelial growth factor receptor-1 (VEGFR-1) in clinically-localized prostate cancer (PCa). Forty patients who had undergone radical prostatectomy (RP) for clinically-localized PCa were included. Two groups were compared: 17 patients who experienced cancer progression following RP (group 1) and 23 patients who remained free of recurrence after intervention (group 2). Paraffin-embedded sections obtained from the RP specimens of the 40 patients were used to build tissue microarrays. The expression of VEGFR-1 was examined in the RP specimens using immunohistochemistry and was compared between the groups of patients. The two groups had similar tumor characteristics in terms of PSA, Gleason score and pathological stage of cancer. The median intensity score of VEGFR-1 expression was significantly higher in pT3 tumors than in pT2 tumors. Nevertheless, the intensity scores of VEGFR-1 expression were similar in the two groups of patients. Our results suggest that VEGFR-1 expression is not associated with the risk of cancer progression following RP. Therefore, VEGFR-1 may not be of prognostic value in clinically-localized PCa.
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PMID:The association of vascular endothelial growth factor receptor-1 with the risk of cancer progression following radical prostatectomy. 1809 92

Seeking insight into the possible role of estrogens in prostate cancer (PCa) evolution, we assayed serum E2, estrone (E1), and estrone sulfate (E1S) in 349 PCa and 100 benign prostatic hyperplasia (BPH) patients, and in 208 control subjects in the same age range (50-74 years). E1 (pmol/L+/-S.D.) and E1S (nmol/L+/-S.D.) in the PCa and BPH patients (respectively 126.1+/-66.1 and 2.82+/-1.78, and 127.8+/-56.4 and 2.78+/-2.12) were significantly higher than in the controls (113.8+/-47.6 and 2.11+/-0.96). E2 was not significantly different among the PCa, BPH, and control groups. These assays were also carried out in PCa patients after partition by prognosis (PSA, Gleason score (GS), histological stage, and surgical margins (SM)). Significantly higher E1S levels were found in PCa with: PSA>10 ng/L (3.05+/-1.92) versus PSA<or=10 ng/mL (2.60+/-1.55), stage pT3-T4 (2.99+/-1.80) versus pT2 (2.58+/-1.58), and positive (3.26+/-1.95) versus negative margins (2.52+/-1.48). E1 was higher in poor- than in better-prognosis PCa. E2 was significantly higher in PCa with GS>or=4+3 (109.5+/-43.8) versus GS<or=3+4 (100.6+/-36.5) and increased significantly when GS increased from 3+3 to 4+4. Estrogens, especially E1S appeared to be possible markers of PCa progression. Attempting to identify potential sources of E2 in PCa according to prognosis, as well as in BPH, we found a significant correlation coefficient between E1S and E2 (0.266-0.347) in poor-prognosis PCa and no correlation in BPH (0.026) and better-prognosis PCa (0.013-0.104). It is as though during progression of PCa from good to poor prognosis there were a shift in the E1 to E2 metabolic pathway from predominantly oxidative to predominantly reductive.
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PMID:Estrone sulfate (E1S), a prognosis marker for tumor aggressiveness in prostate cancer (PCa). 1833 90

Resistin is a member of adipokine family involved in the regulation of inflammatory reactions and insulin sensitivity. In presented study its possible role in the development of benign prostate hyperplasia and prostate cancer was evaluated. Blood samples and prostate specimens were collected from 26 patients with benign prostate hyperplasia (BPH) and from 42 patients with prostate cancer (PCa) stage pT2 (n=18) and pT3 (n=24). Selected metabolic and biochemical parameters and serum resistin levels were measured and anthropometric measurements were performed as well as tissue immunohistochemistry for resistin. Serum resistin levels did not differ significantly between benign hyperplasia and prostate cancer but in cancer patients there was a trend towards decrease with higher cancer stage. Moreover, serum resistin levels were significantly lower in patients with seminal vesicle invasion in comparison to those without invasion. While in BPH serum resistin levels correlated with insulin resistance, inflammatory status and cortisol, in PCa positive correlation with F/T PSA ratio and cortisol was observed. Tissue immunohistochemistry did not show any differences in staining pattern between benign and neoplastic prostate tissue. We conclude that serum resistin levels do not significantly differ between patients with benign prostate hyperplasia and prostate cancer, but there is a trend towards decrease in resistin serum levels in advanced cancer cases.
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PMID:Serum resistin levels in benign prostate hyperplasia and non-metastatic prostate cancer: possible role in cancer progression. 1866 56

We have previously shown that endoglin (CD105) is upregulated in prostatic fluid of men with large volume prostate cancer. We chose to assess endoglin levels in urine and serum from men with prostate cancer or at increased risk for the disease: Urine samples were collected after digital rectal examination (DRE) from 99 men whose cancer status was confirmed by biopsy, and serum samples were collected from 20 men without prostate cancer at low risk for the disease and from 69 men diagnosed with prostate cancer that subsequently underwent radical prostatectomy (30 pT2, 39 pT3). Endoglin levels were assessed by ELISA. Urinary endoglin was elevated in men with biopsy-positive prostate cancer compared to biopsy-negative men (p=0.0014). Urinary endoglin levels in men with prostate cancer correlated with radical prostatectomy tumor volume. The area under the receiver operating characteristic (ROC) curve was 0.72 for urinary endoglin and 0.50 for serum prostate-specific antigen (PSA; sensitivity for cancer detection 73%, specificity 63%). There were no differences in serum endoglin between normal and cancer cases, but there were increases in serum endoglin in non-organ confined (NOC, pT3+) versus organ-confined (OC, pT2) cases (p=0.0004). The area under the ROC curve was 0.75 for serum endoglin and 0.63 for PSA for predicting NOC status, with a sensitivity of 67% and a specificity of 80%. In conclusion, elevations in post-DRE urinary endoglin suggest there may be value in further studying endoglin as a urinary biomarker of prostate cancer. Endoglin levels in both urine and serum may aid in prostate cancer detection and prognostication.
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PMID:Endoglin (CD105) as a urinary and serum marker of prostate cancer. 1900 9

OBJECTIVE To evaluate a contemporary series of patients with incidental prostate cancer detected by transurethral resection of the prostate (TURP) and undergoing radical prostatectomy (RP). PATIENTS AND METHODS Between 1998 and 2004, 1931 patients had TURP for obstructive voiding symptoms and suspected BPH. Incidental prostate cancer was found in 104 (5.4%); 26 of these patients had a RP. The pathological staging and treatment of these patients were reviewed retrospectively and the follow-up results obtained. RESULTS Of the 26 patients who had RP, 17 had T1a and nine had T1b carcinoma of the prostate. After RP, six (35%) in the T1a group had no residual tumour (pT0) and 11 (65%) had pT2 cancer; the respective incidence in those with T1b was two and seven, with no pT3 disease in either group. The preoperative Gleason grading did not correspond well with that after RP; 30% of the patients had upgraded Gleason scores and 42% showed either downgrading or no residual tumour, with 81% having Gleason scores of <7. After a median follow-up of 47 months, one patient is receiving hormonal therapy because of biochemical relapse. Conclusion Subsequent to stringent PSA testing and prostate biopsy when indicated, the rate of incidental prostate cancer is low. Furthermore, substantially many patients will harbour either no residual cancer or tumours with favourable characteristics in their RP specimens. However, there is currently no possibility to reliably predict the absence of aggressive prostate cancer after TURP, and thus safely recommend observation instead of further therapy. Therefore, patients with incidental prostate cancer need to be counselled individually. The decision 'treatment or no treatment' should be determined by the patients' age and life-expectancy, tumour aggressiveness in the TURP specimen and the prostate-specific antigen level after TURP.
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PMID:Outcome of radical prostatectomy for incidental carcinoma of the prostate. 2126 82

Minute prostatic adenocarcinomas are considered to be of insufficient virulence. Given recent suggestions of TMPRSS2-ERG gene fusion association with aggressive prostatic adenocarcinoma, we evaluated the incidence of TMPRSS2-ERG fusion in minute prostatic adenocarcinomas. A total of 45 consecutive prostatectomies with minute adenocarcinoma were used for tissue microarray construction. A total of 63 consecutive non-minimal, Gleason Score 6 tumors, from a separate PSA Era prostatectomy tissue microarray, were used for comparison. FISH was carried out using ERG break-apart probes. Tumors were assessed for fusion by deletion (Edel) or split (Esplit), duplicated fusions and low-level copy number gain in normal ERG gene locus. Minute adenocarcinomas: Fusion was evaluable in 32/45 tumors (71%). Fifteen out of 32 (47%) tumors were positive for fusion. Six (19%) were of the Edel class and 7 (22%) were classified as combined Edel+Esplit. Non-minute adenocarcinomas (pT2): Fusion was identified in 20/30 tumors (67%). Four (13%) were of Edel class and 5 (17%) were combined Edel+Esplit. Duplicated fusions were encountered in 5 (16%) tumors. Non-minute adenocarcinomas (pT3): Fusion was identified in 19/33 (58%). Fusion was due to a deletion in 6 (18%) tumors. Seven tumors (21%) were classified as combined Edel+Esplit. One tumor showed Esplit alone. Duplicated fusions were encountered in 3 (9%) cases. The incidence of duplicated fusions was higher in non-minute adenocarcinomas (13 vs 0%; P=0.03). A trend for higher incidence of low-level copy number gain in normal ERG gene locus without fusion was noted in non-minute adenocarcinomas (10 vs 0%; P=0.07). We found a TMPRSS2-ERG fusion rate of 47% in minute adenocarcinomas. The latter is not significantly different from that of grade matched non-minute adenocarcinomas. The incidence of duplicated fusion was higher in non-minute adenocarcinomas. Our finding of comparable rate of TMPRSS2-ERG fusion in minute adenocarcinomas may argue against its value as a marker of aggressive prostate carcinoma phenotype.
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PMID:TMPRSS2-ERG gene fusion status in minute (minimal) prostatic adenocarcinoma. 1973 49

We examined whether the tumor volume (TV) is a good predictor of PSA recurrence after radical prostatectomy. Data were collected for 158 patients with clinically localized prostate cancer undergoing radical prostatectomy without neoadjuvant hormonal therapy in our hospital since April 2005 to September 2007. Along with the routine pathological assessment, TV was assessed in all prostatectomy specimens. PSA recurrence was defined as PSA levels of greater than 0.2 ng/ml. The TVs were 1.81+/-1.66 ml (mean +/-SD) ranging from 0.02 to 8.20 ml. The TV in cT1c was 1.77+/-1.64, and 1.89+/-1.72 ml in cT2 (not significant). Significant differences were observed between TV and pT. The TVs in pT2a, pT2b and pT3/4 were 0.54+/-0.54, 1.63+/-1.47 and 2.67+/-1.80 ml, respectively. The median follow-up period was 32.3 months (range from 15 to 45) after radical prostatectomy, and PSA recurrence was observed in 32 cases. Patients with smaller TV (TV <1.3 ml) had a higher PSA-free survival rate (89.5%) than those with a larger TV (TV > or = 1.3 ml, 66.7%) with a significant difference atp <0.001 (log-rank test). A multivariate analysis was performed for PSA, TV, pT, Gleason Score (GS), and surgical margins. Significant differences were observed for GS, and surgical margins, but not for TV. Clinically organ-confined disease in Japanese patients with prostate cancer included various cancers from clinically insignificant to locally advanced ones. In our series, TV was not regarded as a predictor of PSA recurrence after radical prostatectomy.
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PMID:[Relationship between tumor volume and PSA recurrence after radical prostatectomy]. 2018 93

External beam radiotherapy (EBRT) is a well established curative treatment for prostate cancer. Retrospective studies demonstrate similar biochemical recurrence free survival rates of radical prostatectomy and EBRT for patients in comparable prognostic subgroups, so that patient information should particularly include the respective toxicity spectrum. In principle, EBRT can be offered to every patient without distant metastases and a life expectancy of at least 5-10 years. The decision involves the selection of a suitable technique, dose, target volume and the option of a combination with antiandrogen therapy. Prospective randomized studies showed the advantage of a dose escalation up to total doses of 76-78Gy concerning biochemical tumor control; additionally concerning disease-specific survival for high risk patients. Other randomized trials demonstrated a survival benefit for patients with locally advanced or high risk cancers who received an additional adjuvant antiandrogen therapy to EBRT. Based on the results of randomized studies, an adjuvant post-prostatectomy EBRT of the prostatic fossa with doses in the range of 60-66 Gy can be recommended in case of positive surgical margins or pT3 tumors - reducing the risk of metastases and increasing survival. In case of a biochemical (or macroscopic) recurrence after radical prostatectomy, EBRT is the only curative treatment option for the patient - favorable prognostic factors are low pre-EBRT PSA (prostate-specific antigen) levels, long PSA doubling doubling time, long interval between prostatectomy and recurrence, low Gleason score, positive margins and an absent seminal vesicle involvement. Total doses of at least 70 Gy should be administered in case of macroscopic recurrences, but the curative chances are considerably lower in comparison to a biochemical recurrence alone.
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PMID:External beam radiotherapy for prostate cancer. 2104 76


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