Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multivariable analysis was used to investigate the relationship between risk of disease progression or death in patients who were treated with adjuvant therapy after definitive treatment for prostatic adenocarcinoma and the components of the National Prostatic Cancer Treatment Group (NPCTG) and Gleason systems for pathologic grading of prostatic cancer. Data were available for 203 patients who were treated on NPCTG Protocols 900 and 1,000, which involve surgical and radiation therapy as definitive treatment. Since less than 10 per cent of these patients have died, analysis of survival was not attempted. The study focus was progression-free survival, which is the minimum of time to progression or death. The analysis demonstrates that a new measure, the NPCTG score (the sum of the glandular and nuclear grades) is superior to the previously reported NPCTG grade (the maximum of the two grades). In addition, the Gleason score is somewhat superior to the new NPCTG score. All of this, however, applies only to the primary tumor and not the nature of any present or future metastatic lesions.
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PMID:Comparative evaluation of National Prostatic Cancer Treatment Group and Gleason systems for pathologic grading of primary prostatic cancer. 396 53

In this preliminary report, evaluation of nontraditional agents has been used to evaluate control of metastasis. This androgen-sensitive rate prostatic adenocarcinoma has been subject to the treatments of heparin, indocin, and castration, as well as combinations of castration, heparin, indocin, and cyclophosphamide. Tumor volume, metastasis, and determination of regression of primary tumor have been evaluated. Heparin and indocin both reduced metastasis without affecting tumor volume in this study. The combination of castration and cyclophosphamide was most effective in reducing tumor volume when compared to the other groups.
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PMID:Nb rat prostate adenocarcinoma model androgen-sensitive tumor: metastasis control. 688 34

Two hundred fifteen patients have undergone pelvic node dissection in clinical Stages A1, A2, B1, and B2 adenocarcinoma of the prostate as a final staging procedure. Two hundred four patients have had the tumor grade assessed adequately and the influence of the grade on the results of the node dissection evaluated. As the grade of the primary tumor worsens in each clinical stage, the incidence of positive nodes increases.
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PMID:Prostatic carcinoma. Influence of tumor grade on results of pelvic lymphadenectomy. 723 56

In 42 patients with metastatic adenocarcinoma of the prostate, histopathologic specimens of the original prostatic biopsy and lymphatic metastasis were classified using the grading system of tumor differentiation described by Gleason et al. The observed similarity between prostatic biopsy morphologic and the morphology in the corresponding lymphatic metastasis supports the concept that the histologic growth pattern of the primary tumor is reduplicated in the metastatic lesions. The observation that a more anaplastic pattern did not appear in the metastatic deposits implies that factors other than cellular loss of differentiation are responsible for the cells' ability to metastasize.
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PMID:Comparative morphology of primary and secondary deposits of prostatic adenocarcinoma. 723 97

Pelvic lymphadenectomy was performed in 300 patients with apparently localized adenocarcinoma of the prostate. Pelvic lymph node metastases were identified in 119 patients (40%) and in 35 of these cases (29%) the metastases involved a solitary lymph node. The incidences of metastases for clinical stage B1, B2 and C tumors were 7, 43, and 60%, respectively. The extent of the metastases in terms of the number and distribution of the involved nodes correlated directly with the clinical stage of the primary tumor. The incidences of metastases associated with well-differentiated, moderately differentiated and poorly differentiated tumors were 27, 45, and 70%, respectively. The degree of tumor differentiation, however, had no apparent impact on the incidence of metastases among patients with clinical stage B1 and C neoplasms. Since tumor stage, tumor grade, and pelvic lymph node metastases have each been demonstrated to be of prognostic significance in prostatic cancer, the status of the pelvic lymph nodes should not be considered an isolated prognostic parameter in patients with otherwise localized prostatic cancer.
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PMID:The incidence and extent of pelvic lymph node metastases in apparently localized prostatic cancer. 726 Aug 81

There were 122 patients with biopsy-proved adenocarcinoma of the prostate and negative radioisotopic bone scan who were subjected to lymphangiography, determination of serum prostatic acid phosphatase, measurement of the size of the lesion, recent pathologic grading of the needle biopsy of the primary tumor and staging pelvic node dissection. The purpose of this study was to determine which of these variables would be most accurate in predicting the presence or absence of positive nodes. Patients with a Gleason scale of less than 5 had only a 13 per cent chance of having positive nodes, whereas patients with a high Gleason scale of 9 or 10 had a 100 per cent chance of having positive nodes. Lymphangiography, size of the prostatic lesion and serum acid phosphatase were not sufficiently accurate to act as predictors of lymphatic extension and precluded the necessity for staging pelvic node dissection.
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PMID:Predictors of lymphatic spread in prostatic adenocarcinoma: uro-oncology research group study. 742 May 58

The benzothiophene antiestrogen, raloxifene (LY156758), has selective estrogen pharmacological antagonist activity in rats. The PAIII rat prostatic adenocarcinoma model was used to evaluate the effects of this agent on the lymphatic and pulmonary metastasis and survival in tumor-bearing male Lobund-Wistar (LW) rats. Raloxifene was inactive against colony formation of PAIII cells in vitro. Similarly, following subcutaneous (s.c.) implantation of 10(6) PAIII cells in the tail, s.c. administration of raloxifene (2.0, 10.0, or 20.0 mg/kg/day) for 30 days failed to demonstrate cytoreductive activity against primary tumor growth in the tail. However, in these same animals, raloxifene administration produced significant (P < 0.05) inhibition of PAIII metastasis from the primary tumor in the tail to the gluteal and iliac lymph nodes (maximal responses = 89% and 81% from control values, respectively). PAIII metastasis to the lungs was significantly inhibited by raloxifene treatment. Numbers of pulmonary foci in PAIII-bearing rats were significantly (P < 0.05) reduced by raloxifene administration in a dose-related manner (maximal reduction = 97% from control values). In these animals, maximal regression of 20% for ventral prostate and 21% for seminal vesicle were also seen after raloxifene administration (P < 0.05 for both). Coadministration of E2B and raloxifene had no consistent antagonistic effect upon the antitumor responses produced by raloxifene. Raloxifene (40.0 mg/kg/day for 28 days) produced marked decreases in PAIII metastasis in the lymphatic and pulmonary components. Continued administration of the compound produced significant (P < 0.05) extension of survival of PAIII-bearing rats. Further studies are needed to define the maximal antitumor efficacy and the mechanism of action of raloxifene in urogenital solid tumor animal models. These data support the contention that raloxifene represents a class of active antimetastatic agents with potential efficacy in the treatment of hormone-insensitive human prostatic cancer.
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PMID:Raloxifene (LY156758) produces antimetastatic responses and extends survival in the PAIII rat prostatic adenocarcinoma model. 747 89

It has been shown that prostatic adenocarcinoma differentiation correlates with prostatic-specific marker and neuroendocrine expression; that is, the more undifferentiated the tumor, the less it expresses prostatic markers and the more neuroendocrine cells are found in it. Complete absence of prostatic markers together with marked neuroendocrine expression has been associated with small cell morphology. This report describes a case of a metastatic, prostatic marker-negative, non-small cell prostatic adenocarcinoma with a prominent neuroendocrine component. The architecturally well-organized luminal-exocrine cells appeared ultrastructurally undifferentiated, however, displaying an almost empty cytoplasm. This contrasted with the prostatic marker-positive control cases of prostatic carcinoma, which contained relatively numerous cytoplasmic vacuoles. The neuroendocrine cells could be identified by light microscopy as eosinophilic cells. The number of the latter cells was markedly increased in the metastatic foci compared with the primary tumor. Light microscopically and ultrastructurally, the eosinophilic cells in this case differed from the Paneth-like cells described in prostatic carcinoma in previous reports. This case provides support for the general concept of multidirectional differentiation in human epithelial cancers and in particular for the association of poor tumor differentiation with neuroendocrine expression in prostatic carcinoma. In addition, in contrast with previous reports describing absence of basement membrane in metastatic foci of prostatic carcinoma, in the current case well-formed basal laminae were identified.
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PMID:Prostatic marker-negative amphicrine carcinoma of the prostate. 752 Jun 42

The more differentiated components of a primary tumor may produce substances that reduce the growth rate and metastatic potential of more aggressive components. In the Dunning R-3327 prostatic adenocarcinoma model, cancer cell motility is required for metastatic potential. Medium conditioned by the non-motile, non-metastatic G subline contains proteins of molecular weight 50-100 kDa that inhibited the motility of the highly motile, highly metastatic MAT-LyLu subline. G subline-conditioned medium was separated by DEAE-cellulose chromatography using a linear gradient of 0-0.5 M NaCl in 100 mM Tris at pH 8.3. The motility inhibitory activity of G-conditioned medium was localized to column fractions 51-70 that contained 18% of the applied protein and only 6.5% of the proteins secreted by the G cells. Analysis of pooled fractions 51-60 and 61-70 by two-dimensional gel electrophoresis identified five protein families, with a total of 12 charged proteins of molecular weights approximating 66, 54, 50, 41 and 34 kDa, that were not present or present in reduced quantities in column fractions that did not inhibit motility. Isolation and identification of motility inhibitory protein may prove it the first substance discovered that is produced by a more differentiated component of a neoplasm that directly inhibits a metastasis-associated property.
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PMID:Detection of candidates for cancer cell motility inhibitory protein in the Dunning adenocarcinoma model. 758 5

The fact that tumors require polyamines for growth has been repeatedly demonstrated. In vivo polyamines are available both from endogenous (intracellular biosynthesis) and exogenous sources (food and intestinal microflora). We investigated in rats grafted with Mat-Lylu prostatic adenocarcinoma the distribution between tumor and tissues of orally administered (14C) putrescine (Pt). The amount of radioactivity retained by tumors was directly proportional to the tumor volume. In a tumor of 25 cm3 19% of the totally retained radioactivity was found. The accumulation of Pt by intestinal brush-border membrane vesicles prepared from tumor-bearing animals was significantly higher than by vesicles from healthy rats. Our results indicate that the presence of a tumor induces an adaptive response in the small intestine which stimulates the uptake of exogenous polyamines. Our therapeutic strategy was to realise a total blockade of all endogenous and exogenous sources of polyamines by feeding animals with a drug (DFMO, MDL 72527, antibiotics) containing polyamine deficient chow. We observed that polyamine deprivation largely reduced both primary tumor and metastatic development. Natural Killer cell cytotoxic activity and blood formula were restored to normal values after treatment. Furthermore polyamine deprivation enhanced anti-tumoral efficacy of chemotherapy.
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PMID:[The involvement of polyamines in the malignant proliferative process. The anticancer effect of polyamine deprivation]. 765 90


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