Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous tumours of the rat small intestine are extremely rare. A control Sprague-Dawley male rat from a carcinogenicity bioassay had a mucinous adenocarcinoma in the ileum. Tumour metastasis was observed in the mesenteric lymph node, lung, and seminal vesicles. Gross and histopathological features of this neoplasm are described and discussed.
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PMID:Spontaneous metastasizing mucinous adenocarcinoma in the ileum of a Sprague-Dawley rat. 796 68

Since 1976, 126 patients with clinically localized carcinoma of the prostate have been managed by radical retropubic prostatectomy. All patients with tumour spread beyond the capsule or metastasis in lymph nodes received radiotherapy. Tumour category pT3 was divided into invasion of the capsule or infiltration of the seminal vesicle. The disease-free 10-year survival rate in patients with minimal invasion of the capsule was 72% and in patients with infiltration of the seminal vesicles it was 26%. Unilateral lymph node metastases were classified as microscopic disease or macroscopic infiltration. The disease-free 10-year survival rate in patients with metastasis in 1 lymph node (micro- and macro-metastasis) was 65% in contrast to 0% in patients with bilateral disease.
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PMID:Influence of microinvasion of the capsule and/or micrometastasis of regional lymph nodes on disease free survival after radical prostatectomy. 797 9

To assess the mechanisms and prognostic significance of seminal vesicle involvement (SVI) by prostatic adenocarcinoma, we analyzed 312 radical prostatectomy specimens obtained from patients with T1-T3 prostate cancer. Detailed pathological examination demonstrated three patterns of SVI. Type I involvement was direct spread along the ejaculatory duct complex into the seminal vesicles. Type II involvement was spread outside of the prostate, through the capsule, and then into the seminal vesicle. Type III involvement was characterized by the finding of isolated deposits of cancer in the seminal vesicle with no contiguous primary cancer in the prostate. We found SVI in 64 patients (21%), who have been followed for a mean of 31 months (range 1-101). A defining criterion for progression was clinically apparent local or distant recurrence or a postoperative serum prostate specific antigen (PSA) > or = 0.4 ng/ml (Hybritech). Type I SVI was found in 17 (26%), Type II in 21 (33%), and Type III in 8 (13%) cases. In 18 patients (28%), the pattern of SVI appeared to be a combination of types I and II (categorized as Type I+II). Type III (isolated metastasis) SVI was associated with significantly smaller cancers (median, 3.13 vs. 6.7 cc; p < 0.0005) and fewer positive margins (0 vs. 32%; p = 0.05) than in other types. Type II SVI, with direct extension through the capsule, was associated with a significantly higher risk of lymph node metastasis (8 vs. 33%; p < 0.05). When patients with lymph node metastases were excluded, there was a trend toward a more favorable prognosis (p = 0.09) for patients with type III SVI than with other types. Overall, patients with type III SVI had a progression-free survival rate similar to that of 83 patients with extracapsular extension without SVI. We conclude that the prognostic significance of SVI may not be uniformly ominous; instead, it may depend on the specific mechanism of involvement and the pathologic features of the primary tumor.
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PMID:The mechanisms and prognostic significance of seminal vesicle involvement by prostate cancer. 823 32

The objective of this article is to determine the relationship between microvascular invasion and seminal vesicle invasion in prostatic adenocarcinoma. Radical prostatectomies with seminal vesicle involvement were examined histologically and immunohistochemically with antibodies directed against S-100 protein and factor VIII. Microvascular invasion of the seminal vesicles showed a positive correlation with microvascular and capsular invasion of the prostate (P = 0.006 and 0.048, respectively) and lymph node metastases. Tumor progression was found in 8 of 14 (57%) patients with microvascular invasion of the seminal vesicles, compared with 3 of 22 (14%) without microvascular invasion (P = 0.001). Microvascular invasion of the seminal vesicles is predictive of tumor progression and lymph node metastases in prostatic adenocarcinoma.
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PMID:Microvascular invasion of the seminal vesicles in adenocarcinoma of the prostate. 865 72

We report a rare case of bilateral primary seminal vesicle carcinoma in a 73 yr old Australian man. To our knowledge this case report is the 48th histologically confirmed case of primary seminal vesicle neoplasia and only the fourth reported case of primary bilateral seminal vesicle carcinoma. Macroscopically the tumor was localized to both seminal vesicles and the adjacent right lobe of the prostate. Histologically the tumor and metastases displayed a PSA, PAP and CEA negative, well differentiated papillary adenocarcinoma resembling the pattern of normal seminal vesicle epithelium. No other primary carcinoma in the body was demonstrated. The patient survived for 3 yrs and 4 mths without recurrence of tumor. The pathological criteria for acceptance of primary seminal vesicle carcinoma, difficulties in clinical/radiological detection of seminal vesicle tumors and CA-125 immunoreactivity are discussed.
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PMID:Bilateral primary seminal vesicle carcinoma. 874 30

In a series of 1623 men with a follow-up of 5 +/- 3 years (range 1-13) after anatomic RRP for clinically localized prostate cancer, 17% (276/1623) have shown recurrence. A detectable PSA was the only evidence of recurrence in 7.9%, whereas 2.5% have recurred locally and 5.4% have developed distant metastases. The overall actuarial progression-free rate for these men at 10 years was 68%. Actuarial rates at 10 years were 18% for development of an isolated PSA recurrence, 8% for local recurrence, and 9% for distant recurrence. The actuarial likelihood of a postoperative recurrence increased with increasing clinical stage, Gleason score, preoperative PSA level, and pathologic stage. Although not shown in our previous report, the actuarial rate of recurrence of tumors with a Gleason score of 7 was statistically different from that of tumors of higher Gleason score (8-10). As well, men with preoperative PSA levels of 10.1 to 20 ng/mL experienced recurrence at a significantly lower rate than did men with preoperative PSA levels greater than 20 ng/mL. By using a combination of Gleason score, pathologic stage, and surgical margin status, we demonstrated that the presence of a positive surgical margin did not dramatically affect recurrence in tumors of Gleason scores 2 to 6 with capsular penetration. Surgical margin status was important in high-grade tumors with capsular penetration. In fact, tumors with capsular penetration, Gleason score of at least 7, and a positive surgical margin behaved similarly to tumors with invasion of the seminal vesicles. Preservation of potency did not adversely influence cancer control. The Gleason score, presence or absence of seminal vesicle or lymph node involvement, and the timing of PSA recurrence are all important variables in predicting eventual local versus distant failure associated with an isolated rise in serum PSA. Overall actuarial cause-specific survival at 5 and 10 years was 99% and 93%. Although there was no difference in survival among men grouped by TNM stage or preoperative PSA, advancing histologic grade and pathologic stage did have an effect on actuarial cause-specific survival. Men undergoing RRP for clinically localized prostate cancer showed a 16% actuarial rate of development of metastatic disease at 10 years. This is considerably better than conservative therapy and justifies RRP as the treatment of choice for men with clinically localized disease who are otherwise healthy and have a greater than 10-year life expectancy.
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PMID:Prostate-specific antigen after anatomic radical retropubic prostatectomy. Patterns of recurrence and cancer control. 912 37

Despite recent advances in staging modalities, nearly 30-40% of patients undergoing radical prostatectomy for clinically localized prostate cancer have residual disease. In these cases, one or more of the following conditions may be present: extracapsular disease, positive margins, invasion of the seminal vesicles, lymph node metastases or the postoperative persistence of PSA values above the biological threshold. The optimal management for residual prostate cancer remains controversial and in this setting adjuvant therapy could be appropriate. In the present review we examine the conditions in which hormonal adjuvant therapy can be indicated and the results available from retrospective or non-randomized studies. From the data in the literature and in the absence of randomized prospective studies, prudent conclusions could be drawn on the efficacy of adjuvant hormonal therapy. In cases of small volume, low grade (Gleason score < 7) prostate cancer in stage C or D1, radical surgery coupled with adjuvant hormonal therapy leads to survival rates in stage C similar to those in the intraprostatic stage, and in stage D1 with minimal lymph involvement, seems to delay clinical development of metastases. Finally, the quality of life associated with adjuvant therapy and the drug regimens available for this therapy are reviewed.
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PMID:Adjuvant hormone therapy after radical prostatectomy: indications and results. 922 23

Radical prostatectomy may cure most patients in whom the malignant tumor has not invaded through the prostatic capsule. Advances in surgical technique and accumulation of experience have decreased the complication rate significantly. Long-term results of surgical treatment are now better than those of other forms of treatment; hence radical prostatectomy is now recommended for men with life expectancies longer than 10 years. Between 1988 and 1995, 164 men with clinical stages T1 or T2 adenocarcinoma were admitted for radical prostatectomy. Most were not offered a nerve-sparing procedure, so as to allow wider, more complete resection. Those who wanted preservation of sexual function underwent the nerve- preserving procedure. In 6 patients operation was discontinued when metastases to the mac lymph nodes were detected and in 1 when invasion of the pelvic wall was found, 157 underwent radical prostatectomy. Preoperative biopsy revealed a low-grade lesion (Gleason 2-4) in 19.1%, intermediate grade (Gleason 5-6) in 61.8% and high-grade (Gleason 7-9) in 19.1%; however, pathologic grading revealed that only 7.0% had grade 2-4 tumor, 60.5% grade 5-6 and 32.5% grade 7-9. Pathologic staging revealed T2 tumor in 58%, T3 in 38.8% (including microscopic invasion of the capsule or seminal vesicles); microscopic lymph node metastases were found in 3.2%. Tumor invasion through the capsule was found in only 2 of 13 treated with neoadjuvant androgen blockade, compared with 40% in those who did not receive this treatment. There was no operative mortality and only 14.7% has complications. All had urinary incontinence immediately after operation, but regained continence after an average of 4-5 months, 24 were incontinent for more than 12 months, but most of them had only mild stress incontinence. Most patients were impotent after the procedure. There was tumor recurrence, diagnosed by rise in serum PSA, in 26 during an average followup of 26.4 months (range 3-93). Cure rate of prostatic cancer by radical prostatectomy may be increased by improved preoperative staging methods and better patient selection; long term follow up is required for determining cure rate.
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PMID:[Radical retropubic prostatectomy]. 933 69

Our laboratory has developed two cellular models of human prostate cancer progression. The LNCaP prostate cancer progression model is based upon the well-known cellular interaction between human prostate or bone stromal cells and LNCaP cells in vivo. The marginally tumorigenic LNCaP cells acquired tumorigenic and metastatic potential upon cellular interaction with either prostate or bone fibroblasts. A subline termed C4-2 was observed to grow readily in castrated animals and acquired metastatic potential spreading from the primary tumor site to the lymph node, the seminal vesicles, and the axial skeleton, resulting in an intense osteoblastic reaction. The second model is ARCaP, where prostate cancer cells derived from the ascites fluid of a man with metastatic disease exhibited an Androgen- and estrogen-Repressed Prostate Cancer cell growth and tumor formation in either a hormone-deficient or a castrated environment. However, the growth of either the tumor cells in vitro or the tumors in vivo was suppressed by both estrogen and androgen. While the tumor cells expressed low levels of androgen receptor and prostate-specific antigen (PSA), they were highly metastatic when inoculated orthotopically. Distant metastases to a number of organs were detected, including the liver, lung, kidney, and bone. We have employed a human prostate cancer progression model as a system to study the efficacy of gene therapy. Results of the study show that whereas universal promoters, such as Cytomegalovirus (CMV) and Rous Sarcoma Virus (RSV) promoter-driven tumor suppressors (e.g. p53, p21, and p16), were effective in inhibiting prostate tumor growth, the advantages of driving the expression of therapeutic toxic genes using a tissue-specific promoter prostate-specific antigen (PSA) and a tumor--but not tissue-specific promoter, osteocalcin (OC), are preferred. In the case of the PSA promoter, we can achieve cell-kill in PSA-producing human prostate cancer cells. To circumvent the supporting role of bone stroma for prostate cancer epithelial growth, we have recently developed a novel concept where the expression of therapeutic toxic genes is driven by a tumor--but not a tissue-specific OC promoter. Osteocalcin-thymidine kinase (OC-TK) was found to efficiently eradicate the growth of osteosarcoma, prostate, and brain tumors both in vitro and in vivo. We observed that androgen-independent human prostate cancer cells lines expressed OC-TK at higher levels than androgen-dependent human prostate cancer cell lines. We have obtained data to suggest that Ad-OC-TK plus a pro-drug acyclovir (ACV) may be used as an effective therapy to treat prostate cancer bone metastasis in models where the growth of androgen-independent PC-3 and C4-2 tumors in the bone has occurred.
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PMID:Human prostate cancer progression models and therapeutic intervention. 943 28

Immunohistochemistry with antibodies for high-molecular-weight cytokeratin labels basal cells and is used as an ancillary study in diagnosing prostate carcinoma, which reportedly lacks expression of high-molecular-weight cytokeratin. A recent report questioned the specificity of this marker, describing immunopositivity for high-molecular-weight cytokeratin in a small series of metastatic prostate cancer. We have also noted rare cases of prostate lesions on biopsy with typical histological features of adenocarcinoma showing immunopositivity for high-molecular-weight cytokeratin, either in tumor cells or in patchy cells with the morphology of basal cells. In some of these cases, it was difficult to distinguish cancer from out-pouching of high-grade prostatic intraepithelial neoplasia. To investigate whether prostate cancer cells express high-molecular-weight cytokeratin, we studied 100 cases of metastatic prostate carcinoma and 10 cases of prostate cancer invading the seminal vesicles from surgical specimens. Metastatic sites included regional lymph nodes (n = 67), bone (n = 19), and miscellaneous (n = 14). Cases with any positivity for high-molecular-weight cytokeratin antibody (34betaE12) were verified as being of prostatic origin with immunohistochemistry for prostate-specific antigen and prostate-specific acid phosphatase. Only four cases were detected positive for high-molecular-weight cytokeratin. In two cases (one metastasis, one seminal vesicle invasion) there was weakly diffuse positivity above background level. Two metastases in lymph nodes showed scattered strong staining of clusters of tumor cells, which represented <0.2% of tumor cells in the metastatic deposits. These positive cells did not have the morphology of basal cells. We conclude that prostate cancer, even high grade, only rarely expresses high-molecular-weight cytokeratin. This marker remains a very useful adjunct in the diagnosis of prostate cancer.
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PMID:Rare expression of high-molecular-weight cytokeratin in adenocarcinoma of the prostate gland: a study of 100 cases of metastatic and locally advanced prostate cancer. 998 40


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