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We report a rare case of clinically significant secondary prostatic neoplasm. In a patient with outflow obstruction, a transurethral resection of the prostate revealed a metastasis of a signet ring cell carcinoma of the stomach in the resected prostatic tissue.
Five experiments designed for various purposes [mainly for the study of colon carcinogenesis in inbred F344 male rats given sc injections of 3,2'-dimethyl-4-aminobiphenyl (DMAB)] were reviewed as to the production and presence of neoplastic lesions of the prostate gland. The overall incidence of prostate proliferative lesions among 293 animals exposed to DMAB was 32% (95 animals). Early in situ carcinomas were present in 66 animals, larger intra-acinar carcinomas in situ in 28, and invasive carcinoma in 1. None of the control animals in these studies exhibited prostate neoplasms. The conclusion, therefore, is that DMAB can induce adenocarcinomas in the rat prostate gland.
Earlier studies have demonstrated an unexplained depletion of the epidermal growth factor receptor (EGFR) protein expression in prostatic cancer. We now attribute this phenomenon to the presence of a variant EGFR (EGFRvIII) that is highly expressed in malignant prostatic neoplasms. In a retrospective study, normal, benign hyperplastic and malignant prostatic tissues were examined at the mRNA and protein levels for the presence of this mutant receptor. The results demonstrated that whilst EGFRvIII was not present in normal prostatic glands, the level of expression of this variant protein increased progressively with the gradual transformation of the tissues to the malignant phenotype. The selective association of high EGFRvIII levels with the cancer phenotype underlines the role that this mutant receptor may maintain in the initiation and progression of malignant prostatic growth, and opens the way for new approaches in the management of this disease including gene therapy.
Prostatic neoplasms are the second cause of mortality due to cancer in men. Brain metastases are a rare presentation, whereas epidural localizations are relatively frequent. However both occur late in the evolution of the cancer. Thus a reliable, fast and non-invasive diagnosis would be useful in this setting. Regarding the prognosis of such disease, earlier treatment may probably influence the quality of life and postpone fatal evolution. However improved survival is more hypothetical. We report the case of a 69-year old man with a hormone refractory adenocarcinomatous prostatic cancer presenting with diffuse intracranial metastases. An MRI analysis using T2 perfusion images, diffusion weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps excluded intra-axial brain metastases and concluded to the existence of voluminous nodular dural metastases. We discuss the imaging techniques and review literature of neurological complications of prostate cancer.
BACKGROUND: Any carcinoma of prostatic origin which is not an acinary adenocarcinoma of the prostate is considered to be an atypical carcinoma. One member of this group of atypical prostatic tumors is the oat-cell carcinoma, or small cell carcinoma (SCC) of the prostate. This variety of carcinoma constitutes the histologic basis of <1% of all prostatic neoplasms. METHODS: Between 1992 and 1997, four patients were diagnosed with SCC of the prostate at our hospital. In 3 of the 4 cases, the histopathological diagnosis was pure SCC, and in the 4th case there was a component of prostatic adenocarcinoma associated with the SCC. At the time of diagnosis, extracapsular extension of the tumor was present in all 4 cases, with T3 or higher stages in all of them (T(3A)N(0)M(1), T(3A)N(0)M(0), T(3B)N(0)M(1), and T(4)N(0)M(0)). Because of the presence of extracapsular extension, radiotherapy and radical surgery were ruled out for all 4 patients. They were all offered systemic chemotherapy with cyclophosphamide (1 g/m(2)), doxorubicin (50 mg/m(2)) and vincristine (1.2 mg/m(2)). This therapeutic protocol was carried out in only 2 cases. RESULTS: Survival was <1 year in the 3 patients with pure SCC, and the patient with a mixed tumor is alive with detectable disease 9 months after diagnosis. CONCLUSIONS: This poor vital prognosis in SCC stresses the need for early diagnosis a timely and appropriate therapeutic intervention in this condition.
Acquisition of metastatic ability by prostate cancer cells is the hallmark of their lethal trait and outcome. However, the genetic alterations underlying the clinical progression and pathogenesis of prostate cancer are not well understood. Several studies involving loss of heterozygosity (LOH) and comparative genomic hybridization analysis have identified distinctively altered regions on various human chromosomes, and genomic imbalance of chromosome 20 was implicated in progression and recurrence of prostate tumors. To examine the role of chromosome 20 in prostate neoplasms, we introduced this chromosome into highly metastatic rat prostate cancer cells using the microcell-mediated chromosome transfer technique. Introduction of the chromosome resulted in significant suppression of the metastatic ability of the hybrid cells, by as much as 98%, without any interference with the in vivo growth rate or tumorigenicity of primary tumor in SCID mice. Our STS-PCR analysis on 10 hybrid clones indicates that the suppressor activity of chromosome 20 is located in the p11.23-12 region. Further examination of the hybrid clones by experimental metastasis assay and histologic analysis as well as Matrigel invasion assay suggests the involvement of the suppressor region at an early stage of invasion and extravasation. We also investigated the status of the chromosome 20 suppressor region in pathology specimens from human prostate cancer patients and detected the frequent loss of this region in high-grade tumors. These results suggest the presence of a putative suppressor gene on human chromosome 20 that is functionally involved in development of prostate cancer metastases.
An unusual prostatic neoplasm characterized by a carcinoid-like light microscopic pattern together with argyrophilia of tumor cells is described. Immunoperoxidase stain for prostatic specific antigen, however, was positive, indicating that this neoplasm was an argyrophilic prostatic carcinoma. Although the clinical significance of a carcinoid-like pattern and/or argyrophilia in prostatic carcinoma is currently unknown, pathologic recognition of these features is of paramount importance because prostatic carcinoma with these features has to be distinguished from true primary prostatic carcinoid tumor or, in areas of metastasis, from metastatic carcinoid originating from other sites such as the gastrointestinal or respiratory tracts. The value of the immunoperoxidase technique for prostatic specific antigen as well as prostatic acid phosphatase in this differentiation is stressed.
Compared with normal prostatic tissue, the level of basic fibroblast growth factor (bFGF) is elevated in prostatic tumors. This suggests that bFGF may play a role in the development of prostatic neoplasms. The current study was undertaken to identify the cellular distribution of bFGF in benign prostatic hyperplasia (BPH) and prostatic carcinoma using a polyclonal antiserum against recombinant bFGF. In paraffin sections of prostatic tumors immunoreactive bFGF was found in fibroblasts, smooth muscle cells, and endothelial cells. Distinct staining was seen in most nuclei of these cells and a less intense immunoreaction occurred in the cytoplasm of smooth muscle cells. No immunostaining was seen in prostatic epithelial cells of prostatic tumors whether benign or malignant. With digoxigenin-labeled oligonucleotides in nonradioactive in situ hybridization, the presence of mRNA for bFGF was shown in smooth muscle cells of the stroma, suggesting that these cells are the main source of bFGF in BPH. Because no immunostaining for bFGF was obtained in the carcinoma cells, a specific role for bFGF cannot be seen for the development of malignant prostatic tumors.
PURPOSE: In order to investigate the possible involvement of a tumor suppressor gene(s) on chromosome 13 in prostatic neoplasms, we performed loss of heterozygosity (LOH) analysis on normal and tumor pairs from 36 prostate cancer patients. MATERIALS AND METHODS: Pure DNA was obtained from carcinoma cells and normal epithelium by tissue microdissection. The DNA had previously been analyzed for LOH on chromosomes 8 and 16. After an initial pilot experiment to determine the region(s) of significant LOH from 9 loci on chromosome 13q, 3 loci at and near the Rb1 locus (D13S153, D13S1319, and D13S1303) were chosen for further study. RESULTS: The overall rate of LOH on chromosome 13 was 27.3%. Four tumors exhibited LOH at all 3 loci. Two tumors exhibited LOH at D13S153 but not at the other, more telomeric loci; two additional tumors had loss at D13S1303 or D13S1319 but not D13S153. These data suggest that a tumor suppressor gene involved in prostate cancer may be located just telomeric to Rb1. Analysis of clinical and pathological data from carcinomas with and without loss shows that chromosome 13q LOH is correlated with advanced stage prostate cancer. CONCLUSIONS: Our LOH data suggests that there may be a tumor suppressor gene telomeric to Rb1 that is potentially involved in prostate cancer progression. Identification of this gene may be valuable in providing diagnostic and prognostic information for prostate cancer patients.
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In a retrospective review the response of 67 patient with metastatic adenocarcinoma of the prostate to the administration of exogenous testosterone was analyzed. Among 52 patients in whom objective and/or subjective responses were evaluable 45 experienced unfavorable responses. There was prompt regression of most unfavorable responses with testosterone withdrawal. The duration of treatment required to evoke an unfavorable response was related to the clinical status of the patient. Twenty-five per cent of patients with symptomatic metastases who had received no prior treatment, 36 per cent in symptomatic remission after endocrine therapy and 94 per cent with symptomatic relapse after endocrine therapy experienced unfavorable responses within 30 days of treatment. No patient had objective evidence of tumor regression during testosterone therapy but 7 patients, 6 with remission and 1 untreated, experienced symptomatic benefit. We conclude that the response of patients with metastatic prostate cancer to exogenous testosterone is related to the mass and endocrine treatment status, and that exogenous testosterone can stimulate prostatic neoplasms that proliferate in the absence of normal endogenous testosterone levels.
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