Chromosome rearrangements in a metastatic adenocarcinoma of the prostate

Cytogenetic analysis of a metastatic tumor derived from an adenocarcinoma of the prostate revealed a hypodiploid karyotype with the presence of six marker chromosomes. The findings are discussed in relation to cytogenetic findings in other cancers, including those in prostatic cancer.     

MicroRNA 100: a context dependent miRNA in prostate cancer

OBJECTIVE:

MicroRNAs are noncoding RNA molecules involved in the development and progression of tumors. We have found that miRNA-100 is underexpressed in metastatic prostate cancer compared to localized disease. Conversely higher levels of miR-100 are related to biochemical recurrence after surgery. This suggests that miR-100 may be a context-dependent miRNA, acting as oncogene or tumor suppressor miRNA. Our aim is to demonstrate the role of miR-100 in the control of predicted target genes in prostate cancer cell lines.

METHODS:

Cell lines DU145 and PC3 were transfected with miR-100, antimiR-100 and after 24 h and 48 h of exposure, qRT-PCR and western blot were performed for mTOR, FGFR3, THAP2, SMARCA5 and BAZ2A.

RESULTS:

There was reduction in mTOR (p = 0.025), THAP2 (p = 0.038), SMARCA5 (p = 0.001) and BAZ2A (p = 0.006) mRNA expression in DU145 cells after exposure to miR-100. In PC3 cells, mTOR expression was decreased by miR-100 (p = 0.01). There was a reduction in the expression levels of proteins encoded by studied genes, ranging from 34% to 69%.

CONCLUSIONS:

We demonstrate that miR-100 is a context-dependent miRNA controlling BAZ2, mTOR, FGFR3, SMARCA5 and THAP2 that might be involved in PC progression. The elucidation of the roles of miRNAs in tumors is important because they can be used as therapeutic targets in the future.     

Mucinous adenocarcinoma of the prostate

A case of mucinous adenocarcinoma of the prostate that was diagnosed with the aid of prostate-specific antigen immunoperoxidase staining is reported. Focal areas of the tumor, which were morphologically similar to the remainder of the tumor, stained with neuron-specific enolase by an immunoperoxidase technique and with the Grimelius stain. This tumor is best thought of as a variant of the classic acinotubular adenocarcinoma of the prostate with well-differentiated cells that secrete mucin, rather than as a completely different type of cancer, as proposed previously.     

Nutrition, dietary supplements and adenocarcinoma of the prostate

Three well-known and indisputable risk factors contribute to the development of prostate cancer, namely heredity, ethnic origin and increasing age. Geographic variations in incidence rates are considerable and it has, therefore, been suggested that environmental factors may also play a role. Migration studies clearly show that men with the same genetic background raised in different environments show a similar risk of developing the disease to those in their country of residency. Prostate cancer is a good candidate for studies on primary prevention thanks to specific features such as high prevalence, long latency, hormonal dependency, serum markers for monitoring (prostate-specific antigen) and histological precursor lesions (prostatic intraepithelial neoplasia). Nutritional factors that may influence the disease include total energy intake (as reflected by body mass index), dietary fat, cooked meat, micronutrients and vitamins (carotenoids, retinoids, vitamins C, D and E), fruit and vegetable intake, minerals (calcium, selenium), and phytoestrogens (isoflavonoids, flavonoids, lignans). Most published studies have been case–control analyses. The selenium and vitamin E cancer prevention trial (SELECT), however, was a population-based, prospective, randomized clinical trial that examined the effect of selenium and vitamin E alone or in combination on prostate cancer risk reduction. The trial was recently discontinued due to no evidence of benefit from either agent. Nevertheless, lifestyle changes can still be recommended for men at risk of developing clinical prostate cancer.     

前列腺硬化性腺病——一种类似前列腺癌的良性病变

目的探讨前列腺硬化性腺病与小腺泡结构前列腺癌的病理鉴别诊断。方法报道1例前列腺硬化性腺病,结合有关文献从临床、病理形态和免疫组化等方面分析它与前列腺癌的区别。结果硬化性腺病在HE切片中与小腺泡结构前列腺癌十分相似,但缺乏明显增大的核仁,腺管周围有增厚的基膜以及34βE12、p63、CK5/6、S-100蛋白和SMA标记( )的基底细胞围绕。结论前列腺硬化性腺病是一种罕见的容易误诊为前列腺癌的良性病变,有明显的结构和细胞学不典型性以及AM-ACR标记( )等异常表现。富于细胞性间质,腺管周围有完整的基底细胞层围绕和基底细胞的肌上皮细胞化生,是与癌鉴别的重要特征。     

Mucinous adenocarcinoma of the prostate: description of a case

INTRODUCTION: We report an occasional biopsy of primary mucinous adenocarcinoma of the prostate with review of the literature and discussion about all criteria used to classify this clinical-pathological entity. MATERIALS AND METHODS: Histochemical (Alcian Blue and P.A.S.) and immunohistochemical (P.A.P. and P.S.A.) stainings were performed.     

Microsatellite instability in adenocarcinoma of the prostate.

Instability of dinucleotide tandem repeat sequences has been reported to play a major role in the carcinogenic pathway of familial colon cancer, as well as a potential role in the carcinogenesis of other sporadic neoplasms. To determine the frequency of short tandem repeat instability in adenocarcinoma of the prostate, we studied 40 tumors that were stratified according to tumor grade. The tissue samples were screened with di-, tri- and tetranucleotide markers spanning a wide range of chromosomal loci, including an androgen receptor gene trinucleotide repeat. Microsatellite instability was observed overall in only one of the 40 (2.5%) prostate adenocarcinomas studied. This replication error-positive tumor demonstrated repeat length alterations at two loci. Five other tumors showed an alteration in microsatellite size at a single locus. These tumors were not considered to have the microsatellite instability phenotype. All changes were identified either within tetranucleotide sequences or within the androgen receptor gene repeat (4 or 20 total markers analyzed). Both repeat length expansions and contractions were identified. The replication error-positive case also included separate metastatic nodal tissue. Additional microsatellite analysis of the metastatic tumor tissue revealed allelic patterns identical with the normal tissue control. Our data indicate that microsatellite instability is rare in prostate adenocarcinoma. Therefore, observation of this low replication error frequency suggests that most prostate carcinomas develop in the absence of widespread accumulation of somatic mutations in short tandem repeat sequences. Additionally, these genetic alterations appear to occur more often in tetranucleotide repeat sequences as well as in an androgen receptor gene trinucleotide repeat.     

beta hCG as a prognostic marker in adenocarcinoma of the prostate.

AIMS: To assess the importance of immunohistological detection of beta-human chorionic gonadotrophin (beta hCG) in localised prostatic adenocarcinoma with regard to prognosis and clinical applications. METHODS: Eighty consecutive cases of clinically localised adenocarcinoma of the prostate were studied retrospectively. Immunohistological analysis on formalin fixed, paraffin wax embedded prostate tissue from transurethral resections was related to clinical outcome and survival. Prognosis was also related to tumour grade. RESULTS: beta hCG was detected in 12 cases. Nine of these patients were found to have metastases (75%) at follow up and 11 (92%) were dead within 18 months. There was no correlation with grade and prognosis in this group. Of the 68 beta hCG negative cases, 21 had developed metastases (31%) and 25 (37%) had died within 18 months. In the beta hCG negative group there was an association between histological grade and survival. CONCLUSION: The demonstration of beta hCG in prostatic adenocarcinoma identifies a group of patients with poor prognosis, irrespective of histological grade. This additional information will be extremely valuable in the subsequent clinical management of such patients.     

Diagnosis of limited adenocarcinoma of the prostate

This article provides an overview of the diagnosis of limited prostate cancer on needle biopsy. A few of the more common mimickers of prostate cancer, such as adenosis, partial atrophy, and high-grade prostatic intraepithelial neoplasia, are also covered. A systematic approach to diagnosing prostate cancer by evaluating architectural, nuclear, intraluminal and ancillary features is presented. The use of immunohistochemistry, including its pitfalls and limitations, is described and illustrated. By the use of a systematic diagnostic approach as outlined in this article, the threshold for diagnosing limited carcinoma of the prostate can be decreased. If a pathologist is not comfortable in diagnosing carcinoma in a particular small focus, this review will help them to recognize these foci as atypical and suspicious for carcinoma, so that further workup might lead to a more definitive diagnosis. Some of the more common situations leading to an atypical diagnosis have also been presented to help prevent the overdiagnosis of prostatic malignancy.     

Prostatic carcinosarcoma: a case originating in a previous ductal adenocarcinoma of the prostate

Ductal adenocarcinoma of the prostate is a variant of prostatic carcinoma that appears to originate in the ducts of the prostate. Carcinosarcoma of the prostate is an uncommon and aggressive tumour composed of an intimate admixture of adenocarcinoma and sarcoma. In this report we describe the clinicopathological and immunohistochemical characteristics of a case of prostatic carcinosarcoma that appeared in a 66-year-old man who had had a ductal adenocarcinoma of the prostate diagnosed 3 years previously. The patient died of the disease 3 months after the carcinosarcoma was diagnosed. This case may represent further evidence of the dedifferentiation theory in the origin of carcinosarcoma. The case also illustrates that this dedifferentiation may occur from any type of prostatic carcinoma.     

前列腺基底细胞腺癌

目的：探讨前列腺基底细胞腺癌和腺瘤诊断和鉴别诊断标准。方法：对基底细胞腺瘤３例,基底细胞腺瘤１例,复习其临床和病理资料及进行随访。再次常规切片ＨＥ染色和采用ＬＳＡＢ法,对ＰＳＡ、ＰＡＰ、ＣＫ、ＣＥＡ、ＰＣＮＡ、ｂｃｌ－２、ｐ５３和ｃ－ｅｒｂＢ－２８种抗体标记结果进行观察。结果：前列腺基底细胞腺癌为分化差的帝体癌在底细胞癌样排列,核分裂象多,癌巢中央伴坏死,可见局灶性鳞状细胞,移行细胞或腺管分化,     

Prostate-specific antigen as a serum marker for adenocarcinoma of the prostate

To compare the clinical usefulness of the serum markers prostate-specific antigen (PSA) and prostatic acid phosphatase (PAP), we measured them by radioimmunoassay in 2200 serum samples from 699 patients, 378 of whom had prostatic cancer. PSA was elevated in 122 of 127 patients with newly diagnosed, untreated prostatic cancer, including 7 of 12 patients with unsuspected early disease and all of 115 with more advanced disease. The PSA level increased with advancing clinical stage and was proportional to the estimated volume of the tumor. The PAP concentration was elevated in only 57 of the patients with cancer and correlated less closely with tumor volume. PSA was increased in 86 percent and PAP in 14 percent of the patients with benign prostatic hyperplasia. After radical prostatectomy for cancer, PSA routinely fell to undetectable levels, with a half-life of 2.2 days. If initially elevated, PAP fell to normal levels within 24 hours but always remained detectable. In six patients followed postoperatively by means of repeated measurements, PSA--but not PAP--appeared to be useful in detecting residual and early recurrence of tumor and in monitoring responses to radiation therapy. Prostate massage increased the levels of both PSA and PAP approximately 1.5 to 2 times. Needle biopsy and transurethral resection increased both considerably. We conclude that PSA is more sensitive than PAP in the detection of prostatic cancer and will probably be more useful in monitoring responses and recurrence after therapy. However, since both PSA and PAP may be elevated in benign prostatic hyperplasia, neither marker is specific.     

Schistosomiasis and adenocarcinoma of prostate: a morphologic study

A case of prostatic adenocarcinoma coincident with Schistosoma mansoni infestation of the prostate is documented. To the authors' knowledge, this association has not been reported previously. In view of the presence of numerous eggs within the tumor and the youth of the patient, a possible causal relation is suggested.     

Secretory component in pulmonary adenocarcinoma and mesothelioma

The distribution of secretory component was examined by an immunoperoxidase method in 40 pulmonary adenocarcinomas, 11 malignant pleural mesotheliomas and areas of normal lung adjacent to the tumours. Secretory component was demonstrated in tumour cells in 25 (67%) adenocarcinomas. Its presence correlated with the degree of differentiation but was not related to tumour pattern. In the normal lung secretory component can be demonstrated in bronchial ciliated cells, bronchial gland serous cells, bronchiolar epithelium and hyperplastic alveolar epithelium. Although not usually detectable in normal mucous cells it was frequently present in mucin-producing tumours. None of the mesotheliomas examined contained secretory component and this may be an additional useful feature in the differential diagnosis between mesothelioma and adenocarcinoma.