Secondary rectal linitis plastica caused by prostatic adenocarcinoma-magnetic resonance imaging findings and dissemination pathways:A case report

BACKGROUND Secondary rectal linitis plastica(RLP)from prostatic adenocarcinoma is a rare and poorly understood form of metastatic spread,characterized by a desmoplastic response and concentric rectal wall infiltration with mucosal preservation.This complicates endoscopic diagnosis and can mimic gastrointestinal malignancies.This case series underscores the critical role of magnetic resonance imaging(MRI)in identifying the distinct imaging features of RLP and highlights the importance of considering this condition in the differential diagnosis of patients with a history of prostate cancer.CASE SUMMARY Three patients with secondary RLP due to prostatic adenocarcinoma presented with varied clinical features.The first patient,a 76-year-old man with advanced prostate cancer,had rectal pain and incontinence.MRI showed diffuse prostatic invasion and significant rectal wall thickening with a characteristic"target sign"pattern.The second,a 57-year-old asymptomatic man with elevated prostatespecific antigen levels and a history of prostate cancer exhibited rectoprostatic angle involvement and rectal wall thickening on MRI,with positron emission tomography/computed tomography PSMA confirming the prostatic origin of the metastatic spread.The third patient,an 80-year-old post-radical prostatectomy,presented with refractory constipation.MRI revealed a neoplastic mass infiltrating the rectal wall.In all cases,MRI consistently showed stratified thickening,concentric signal changes,restricted diffusion,and contrast enhancement,which were essential for diagnosing secondary RLP.Biopsies confirmed the prostatic origin of the neoplastic involvement in the rectum.CONCLUSION Recognizing MRI findings of secondary RLP is essential for accurate diagnosis and management in prostate cancer patients.

Intraductal Prostatic Carcinoma: Epidemiological and Anatomopathological Aspects in Dakar

Introduction: Intraductal carcinoma is often associated with high-grade, high-stage adenocarcinoma. Its frequency is variable and it is considered a poor prognostic factor. In our context, when prostatic carcinoma is diagnosed, pathologists do not always report the presence of this anatomopathological entity. We therefore conducted a study to determine the epidemiological and anatomopathological profile of patients with this lesion in Dakar. Materials and Methods: This is a retrospective descriptive study covering a 1-year period from January to December 2022. It focused on cases of intraductal carcinoma diagnosed among prostatic carcinomas collected in the anatomopathology laboratories of Hôpital Général Idrissa Pouye (HOGIP) and Hôpital Militaire de Ouakam (HMO). It was based on archives of anatomopathological reports, blocks and slides. A total of 200 cases of prostatic carcinoma were collated and reviewed to identify those presenting with intraductal carcinoma according to the diagnostic criteria of Guo and Epstein. Results: 87 cases of intraductal carcinoma were found, representing 43.5% of prostatic carcinomas. The mean age was 71 years. Patients in their seventh decade were the most represented, i.e. 42.5%. The majority of samples examined were biopsies (72.4%). The mean PSA level was 965.91 ng/ml, with extremes ranging from 0.03 to 10,000 ng/ml. Histologically, 96.5% of cases (N = 84) were invasive prostatic carcinoma. Gleason score 8 (4 + 4) was the most common, accounting for 42.53% (N = 37). On average, the study found four (04) foci of intraductal carcinoma per specimen, with extremes ranging from 1 to 30. Dense cribriform architecture accounted for 78.16%, loose cribriform for 11.5%, solid for 8.04% and micropapillary for 2.3%. Six cases (6.9%) showed foci of comedonecrosis. The vast majority of radical prostatectomies (87.5%) were classified as pT3. Node invasion and perineural sheathing were observed in 12.5% and 52.32% of cases respectively. Conclusion: Intraductal carcinoma is a poor prognostic factor that must be systematically reported in the anatomopathological report. In Senegal, it is often associated with advanced stage, high-grade carcinoma and high PSA levels.

Concurrent occurrence of adenocarcinoma and urothelial carcinoma of the prostate gland:A case report

BACKGROUND Adenocarcinoma is the most common subtype of prostate cancer.Prostatic urothelial carcinoma(UC)typically originates from the prostatic urethra.The concurrent occurrence of adenocarcinoma and UC of the prostate gland is uncommon.CASE SUMMARY We present the case of an 82-year-old male patient with simultaneous adenocarcinoma and UC of the prostate gland.The patient underwent a transrectal ultrasound-guided biopsy,and the pathology test revealed UC.Subsequently,transurethral laser prostatectomy was performed,and the pathology test indicated adenocarcinoma of the prostate with a Gleason score of 3+4 and highgrade UC.Therefore,the patient was treated with androgen deprivation therapy,systemic chemotherapy,and immunotherapy.Magnetic resonance imaging performed during follow-up revealed a prostate tumor classified as cT2cN1M0,stage IVA.Therefore,the patient underwent robotic-assisted radical prostatectomy and bilateral pelvic lymph node dissection.The final pathology test of the prostate gland revealed acinar-type adenocarcinoma,Gleason pattern 4+3,pT2N0M0,and high-grade UC.The patient regularly presented to the clinic for postoperative follow-up evaluations.He did not experience any urinary discomfort.CONCLUSION According to our literature review,this is the first reported case of coexisting adenocarcinoma and UC of the prostate gland.

The effect of interleukin 6 on the growth of LNCaP and PC-3 prostatic carcinoma cells

Objective To investigate the effect of IL-6 on prostatic carcinoma cell lines, and differential effects on androgen-dependent and androgen-independent prostatic carcinoma cells. Methods The IL-6 producing capacities of LNCaP and PC-3 cells were determined, and effects of exogenous IL-6 and anti-IL - 6 antibodies on LNCaP and PC - 3 cells were examined. Results LNCaP produced a very small amount of IL-6, but PC-3 produced more, the concentraion of IL-6 being 190 pg/48 h per ml(1 × 106). The exogenous IL-6 inhibited LNCaP growth significantly,but had no obvious effect on PC -3 cells. Anti-IL-6 antibodies lowered PC-3 cells growth rate but had neutral effect on LNCaP. Conclusion PC-3 cells produces IL-6 massively in autocrine manner. IL-6 could be antagonized by anti-IL-6 antibodies,resulting in slowing PC-3 cells growth, and LNCaP cells growth could be inhibited by exogenous IL-6.7 refs,2 tabs.

Treatment-induced neuroendocrine prostate cancer and de novo neuroendocrine prostate cancer:Identification,prognosis and survival,genetic and epigenetic factors

Neuroendocrine prostate cancer(NEPC)shows an aggressive behavior compared to prostate cancer(PCa),also known as prostate adenocarcinoma.Scanty foci in PCa can harbor genetic alternation that can arise in a heterogeneity of prostate cancer.NEPC may arise de novo or develop following androgen deprivation therapy(ADT).NEPC that arise following ADT has the nomenclature“treatmentemerging/induced NEPC(t-NEPC)”.t-NEPC would be anticipated in castration resistant prostate cancer(CRPC)and metastatic PCa.t-NEPC is characterized by low or absent androgen receptor(AR)expression,independence of AR signaling,and gain of neuroendocrine phenotype.t-NEPC is an aggressive metastatic tumor,develops from PCa in response to drug induced ADT,and shows very short response to conventional therapy.t-NEPC occurs in 10%-17%of patients with CRPC.De novo NEPC is rare and is accounting for less than 2%of all PCa.The molecular mechanisms underlying the trans-differentiation from CRPC to t-NEPC are not fully elucidated.Sphingosine kinase 1 plays a significant role in t-NEPC development.Although neuroendocrine markers:Synaptophysin,chromogranin A,and insulinoma associated protein 1(INSM1)are expressed in t-NEPC,they are non-specific for diagnosis,prognosis,and follow-up of therapy.t-NEPC shows enriched genomic alteration in tumor protein P53(TP53)and retinoblastoma 1(RB1).There are evidences suggest that t-NEPC might develop through epigenetic evolution.There are genomic,epigenetic,and transcriptional alterations that are reported to be involved in development of t-NEPC.Knock-outs of TP53 and RB1 were found to contribute in development of t-NEPC.PCa is resistant to immunotherapy,and at present there are running trials to approach immunotherapy for PCa,CRPC,and t-NEPC.

Diagnosis of prostatic neuroendocrine carcinoma: Two cases report and literature review

Two cases of prostatic neuroendocrine carcinoma(PNEC) imaged by computed tomography(CT) and magnetic resonance imaging(MRI), and literature review are presented. Early enhanced CT, MRI, especially diffusionweighted image were emphasized, the complementary roles of ultrasound, CT, MRI, clinical and laboratory characteristic's features in achieving accurate diagnosis were valued in the preoperative diagnosis of PNEC.

The Inhibitory Effects of an Antisense u-PAR Vector on Invasion of Highly Invasive Human Prostate Carcinoma PC-3M Cell Subclones

To observe the inhibitory effects of an antisense u-PAR vector on invasion of highly invasive PC-3M cell subclones, the effects of the antisense u-PAR on activity of MMP-9 in those highly invasive cell subclones were detected by a quantitative RT-PCR and zymography. The monolayer invasion assay and colony formation assay in soft agar were used. And tumorigenesis rate and invasions by the cell subclones with or without the antisense u-PAR were observed in nude mice. It was found that in vitro growth of highly invasive PC-3M cell subclones transfected with the antisense u-PAR was declined, and the ability of anchorage-independent growth of those cell subclones was found decreased sharply, with the inhibiting rate becoming 79%and 60% , respectively. Although the anti-sense u-PAR didn't change MMP-9 gene transcription, they could inhibit the activation of MMP-9 of highly invasive PC-3M cell subclones. Moreover, the tumorigenesis rate of the cell subclones with the antisense u-PAR decreased and the growth of a neoplasm also slowed down. The t tests showed the difference between experimental and control groups was statistically significant (P<0.01). The anti-sense u-PAR vector could not only inhibit the invasion ability of highly invasive PC-3M cell subclones in vitro but also restrain the growth of those cell subclones in vivo.

Prostatic Small Cell Carcinoma: Diagnosis and Management

Prostatic small cell carcinoma (PSCC) is a distinct clinical phenotype of prostate cancer. Although rare, this phenotype is highly aggressive with very high mortality. Due to this, it is imperative for clinicians to be aware of it, diagnose it early and treat it appropriately. In this article we discuss the current literature, outline a plan for its diagnosis and management, and highlight latest research on this topic.

Six transmembrane epithelial antigens of the prostate to illustrate inflammatory response in gastrointestinal cancers

Gastrointestinal cancer(GIC)is a common and widespread form of tumor,with colonoscopy and upper gastrointestinal endoscopy available to detect relevant precancerous polyps and lesions.However,many patients are already in the late stages when first diagnosed with such cancer,resulting in a poor prognosis.Thus,it is necessary to explore new methods and research directions in order to improve the treatment of GIC.Given the specific nature of the gastrointestinal tract,research should focus on the mechanisms of various inflammations and the interactions between food entering and exiting from the gastrointestinal tract and cancer cells.Interestingly,six transmembrane epithelial antigens of the prostates(STEAPs)have been found to be significantly linked to the progression of malignant tumors,associated with intracellular oxidative stress and playing a major role in inflammation with their structure and function.This paper explores the mechanism of STEAPs in the inflammatory response of GIC,providing a theoretical basis for the prevention and early intervention of GIC.The basic properties of the STEAP family as metal reductase are also explained.When it comes to intervention for GIC prevention,STEAPs can affect the activity of Fe^(3+),Cu^(2+) reductase and regulate metal ion uptake in vivo,participating in inflammation-related iron and copper homeostasis.Thus,the mechanism of STEAPs on inflammation is of important value in the prevention of GIC.

爱必妥对前列腺癌PC-3细胞功能学的影响

目的观察不同浓度爱必妥对前列腺癌PC-3细胞的增殖、侵袭及凋亡的作用,并初步探索其可能的作用机制。方法使用不同浓度的(10、20、40、80μg/mL)爱必妥作用于PC-3细胞24 h后,CCK-8检测细胞增殖活力变化;流式检测细胞凋亡变化;transwell检测细胞侵袭能力变化;RT-PCR检测EGFR mRNA表达变化;Western Blot法检测Bax和Bcl-2蛋白表达变化。结果CCK-8结果显示,不同浓度的爱必妥作用24 h后均可以抑制PC-3的细胞增殖活力(P<0.001),且药物抑制作用与浓度呈剂量依赖关系;凋亡检测结果显示,不同浓度的爱必妥均抑制PC-3细胞的侵袭能力(P<0.001),且药物抑制作用与浓度呈剂量依赖关系;凋亡检测结果显示,不同浓度的爱必妥均导致PC-3细胞的总凋亡比例增加(P<0.01),且这种促凋亡能力与与浓度呈剂量依赖关系;Western Blot结果显示,不同浓度的爱必妥均可以抑制Bc1-2蛋白表达(P<0.05),同时促进Bax蛋白表达(P<0.05),且抑制和促进作用与药物浓度呈剂量依赖关系;RT-PCR结果显示,不同浓度的爱必妥均可以抑制EGFR mRNA表达(P<0.05),且抑制作用与药物浓度同样呈剂量依赖关系。结论爱必妥可以抑制前列腺癌细胞PC-3的增殖和侵袭,促进细胞凋亡,且这种作用可能是通过抑制EGFR信号通路导致细胞凋亡而实现。

Nephrotic Sydrome Can Be a Marker for Prostatic Carcinoma

Paraneoplastic syndromes (PS) represent a large spectrum of symptoms, associated with malignant diseases. PS can be diagnosed in asymptomatic patients with occult carcinoma, clinically active cancer, and during clinical remission, suggesting a recurrence of the neoplasm. The underlying mechanisms of PS are not completely understood but several authors have suggested that the increased production of biologically active immune factors and cytokines from the neoplastic cells may underlie the etiology of PS. Although rare, the renal involvement of patients with prostatic carcinoma has been reported. The most common paraneoplastic-associated glomerulopathy in prostatic cancer is the membranoproliferative glomerulonephritis with nephrotic syndrome (NS). In this review, we aimed to discuss the incidence of nephrotic syndrome secondary to prostatic carcinoma, its challenging diagnosis, clinical manifestation, and treatment.

Inhibitory effects of apogossypolone on subcutaneous implants of human LNCaP prostatic carcinoma cells

Objective:The aim of this study was to investigate the inhibitory effect of apogossypolone (ApoG2) on subcutaneous implants of human LNCaP prostatic carcinoma cells, and explore its mechanism. Methods:To establish human LNCaP prostatic carcinoma cell line subcutaneous xenograft models and observe the inhibitory effect of ApoG2 on the tumor model. Immunohistochemistry was employed to observe the expression of Bcl-2, PCNA, CD31, caspase-3 and-8 in tumor tissues. The microvessel density was calculated. Results:ApoG2 could obviously inhibit the growth of subcutaneous prostatic carcinoma implant. ApoG2 decreased the expression of PCNA and CD31, and increased the expression of caspases-3,-8 in tumor tissues. Conclusion:ApoG2 has an inhibitory effect on prostatic carcinoma implants.

Prostatic carcinosarcoma seven years after radical prostatectomy and hormonal therapy for prostatic adenocarcinoma:A case report

BACKGROUND Prostatic carcinosarcoma is a very rare and highly aggressive tumor.It may occur after androgen deprivation therapy(ADT)for adenocarcinoma even after a 7-year interval.CASE SUMMARY A 66-year-old man presented with recurrent symptoms of gross hematuria and urinary retention.The patient had a previous history of combined radical prostatectomy and ADT for prostate cancer 7 years prior.He received total pelvic exenteration for a recurrent pelvic carcinosarcoma.Pathology and immunostaining revealed a carcinosarcoma of prostatic origin with focal spindled cells and bizarre giant cells.The patient subsequently underwent transverse colostomy for carcinosarcoma recurrence and bowel obstruction 3 mo later.Five months after the diagnosis of prostatic carcinosarcoma,the patient died of multiple organ metastases.CONCLUSION Prostatic carcinosarcoma after adenocarcinoma is exceedingly rare.ADT mediated transformation and dedifferentiation of the epithelial components may be the origin of this malignancy.

A Case Report of an Inverted Papilloma of the Prostatic Urethra and a Synchronous Low-Grade Papillary Carcinoma of the Bladder

Inverted urothelial papilloma is a rare benign tumour and represents one of the urothelial lesions with inverted morphology. Accurate diagnosis and differentiation from other inverted lesions is important because its proper clinical management and expected clinical outcomes are distinctly different. Here we describe a case of a large inverted urothelial papilloma of the prostatic urethra and a synchronous non-invasive low-grade papillary urothelial carcinoma of the bladder in a 60 year-old man. We focus on the differential diagnosis of inverted urothelial papilloma.

Management about intravesical histological transformation of prostatic mucinous carcinoma after radical prostatectomy:A case report

BACKGROUND Prostatic mucinous carcinoma(MC)and prostatic signet ring cell carcinoma are two variants of prostate cancer.MC has a higher overall survival time among all variants,while signet ring cell carcinoma is associated with lower survival time relative to other carcinomas.Only a small proportion of prostatic MC may contain signet ring cells.Over the last several decades there were only 12 patients that were documented in two studies.CASE SUMMARY We report on a 64-year-old man who was diagnosed with prostatic MC after he received a robotic-assisted laparoscopic radical prostatectomy in the West China Hospital.After robotic-assisted laparoscopic radical prostatectomy,the patient underwent three successive transurethral resections of bladder tumors.Pathological examination of the first transurethral resection of bladder tumors specimen indicated that the neoplasm was prostatic MC that had metastasized to the urinary bladder.The subsequent two transurethral resections of bladder tumors indicated the presence of prostatic mucinous carcinoma with signet ring cells.CONCLUSION This case report aimed to share the management experience,raise awareness,and highlight the importance of multidisciplinary cooperation of prostatic mucinous carcinoma with signet ring cells.

Preliminary Study of Selenium (Se) Toxicity in Human Prostate Carcinoma (PC3) Cells with the Overexpression of Selenocysteine Synthase (SecS) Gene

Selenium (Se) is a trace element required for normal body function. Its supplementation of human diet at standard optimum amount prevents oxidative damages in cells and could be a viable method in the prevention of diseases related to DNA damage, including cancer, neurodegenerative diseases and aging. While Se anticancer properties have been linked to its ability to remove excess Reactive Oxygen Species (ROS) in cells, the underlying molecular mechanism remains unknown. Recent studies have shown that the removal of ROS alone cannot account for Se anticancer properties. To really comprehend the molecular basis of Se anticancer properties, current researches now focus on the metabolism of Se in the cell, especially Se-containing amino acids. Selenocysteine (Sec) is a novel amino acid and one of the selenium-containing compounds in the cell. It is essential in the maintenance of the integrity of its parent proteins, some of which include enzymes such as Glutathione Peroxidases (GPXs) and Thioredoxin Reductases (TrXs). We propose in this study that the overproduction of Sec via the overexpression of Selenocysteine synthase (SecS) gene and Se supplementation induced cell death in Prostate Carcinoma (PC-3) cells. Although the mechanism underlying the cell death induction is unknown, we propose it could be due to the random incorporation of Sec into proteins at high concentration, causing premature protein degradation and cell death. The outcome of this study showed that increasing the concentration of intracellular Se-containing amino acids may provide important clinical implications for the treatment of cancer.

Abrogation of heat-shock protein (HSP)70 expression induced cell growth inhibition and apoptosis in human androgen-independent prostate cancer cell line PC-3m

Aim: To investigate the effect of abrogating heat shock protein (HSP) 70 expression by antisense HSP70 oligonucleotides treatment on human androgen-independent prostate cancer cell line PC-3m growth. Methods: PC-3m cells were treated with 0-16 μmol/L antisense HSP70 oligomers for 0-100 hr. Cell growth inhibition was analyzed using a trypan blue dye exclusion test. Apoptotic cells were detected and confirmed by flow cytometric analysis and DNA fragmentation analysis. The protein expression of HSP70 and bcl-2 affected by antisense HSP70 oligomers were determined using Western blot. Results: Antisense HSP70 oligomer induced apoptosis and then inhibited proliferation of PC-3m cells in a dose- and time-dependent manner. Ladder-like patterns of DNA fragments were observed in PC-3m cells treated with 10 μmol/L antisense HSP70 oligomer for 48 hr or 8 μmol/L for 72 hr on agarose gel electrophoresis. Antisense HSP70 oligomer pretreatment enhanced the subsequent induction of apoptosis by heat shock in PC-3m cells. In addition, undetectable HSP70 expression was observed at a concentration of 10 μmol/L antisense HSP70 oligomer treatment for 48 hr or 8 μmol/L for 72 hr in Western blot, which was paralleled by decreased expression levels of anti-apoptotic protein bcl-2. Conclusion: HSP70 antisense oligomer treatment abrogates the expression of HSP70, which may disrupt HSP70-bcl-2-interactions and further down-regulate bcl-2 expression, in turn inducing apoptosis and inhibiting cell growth in PC-3m cells.

Manganese antagonizes iron blocking mitochondrial aconitase expression in human prostate carcinoma cells

Aim： To investigate the possible role of manganese in the regulation of mitochondrial aconitase （mACON） activity human prostate carcinoma cell line PC-3 cells. Methods： The mACON enzymatic activities of human prostate carcinoma cell line PC-3 cells were determined using a reduced nicotinamide adenine dinucleotide-coupled assay. Immunoblot and transient gene expression assays were used to study gene expression of the mACON. The putative response element for gene expression was identified using reporter assays with site-directed mutagenesis and electrophoretic mobility-shift assays. Results： In vitro study revealed that manganese chloride （MnCI2） treatment for 16 h inhibited the enzymatic activity of mACON, which induced the inhibition of citrate utility and cell proliferation of PC- 3 cells. Although results from transient gene expression assays showed that MnCI2 treatment upregulated gene translation by approximately 5-fold through the iron response element pathway, immunoblot and reporter assays showed that MnCl2 treatments inhibited protein and gene expression of mACON. This effect was reversed by cotreatment with ferric ammonium citrate. Additional reporter assays with site-directed mutagenesis and electrophoretic mobility-shift assays suggested that a putative metal response element in the promoter of the mACON gene was involved in the regulation of MnCh on the gene expression of mACON. Conclusion： These findings suggest that manganese acts as an antagonist of iron, disrupting the enzymatic activity and gene expression of mACON and citrate metabolism in the prostate.

Synchronous primary carcinomas of the bladder and prostate

Aim： To determine the incidence of adenocarcinoma of the prostate for patients undergoing radical cystoprostatectomy for bladder cancer in Taiwan. Methods： A total of 248 patients in Taiwan who were histologically confirmed for transitional cell carcinoma of the bladder underwent cystoprostatectomy. Histopathologic evaluation of the prostate specimens sectioned at 5 mm intervals was performed. Results： Of the 248 patients, 10 （4.03%） were found to have prostate cancer. Of the 10 cases of unsuspected prostate cancer, eight proved to be at stage T1 or T2, and two at T3 and T4, respectively. This rate of incidentally found prostate cancer amongst our bladder cancer patients appeared to be lower than that found in bladder cancer patients in similar studies in USA. Conclusion： Although the incidence of incidental prostate cancer in patients in Taiwan with bladder cancer is not high compared with that in Western countries, we suggest that digital rectal examination and prostate-specific antigen （PSA） are important screening tools for men with bladder cancer, especially for those aged 60 years and older in Taiwan.

Small-cell neuroendocrine carcinoma of the prostate： are heterotransplants a better experimental model？

Small-cell neuroendocrine carcinoma of the prostate （SCNCP） is an uncommon type of prostate cancer. However, it is of clinical importance because it is one of the most aggressive tumors of the prostate with a very poor prognosis. There exist few artificially cultured tumor cell lines to study SCNCE Then, another approach to that study consists in the use of fresh tumor tissue obtained from patients and its heterotransplantation into host mice. The purpose of this review is to integrate data from more than 20 years of heterotransplantation research in the study of small-cell neuroendocrine carcinoma of the prostate （SCNCP）. Heterotransplantation has provided data regarding the histopathology, karyotype, DNA content, cell cycle frequency, tumor markers, androgen receptor expression, metastasis and take rate of this prostate disease. When possible, comparisons between original in situ specimens removed from patients and heterotransplanted tissue from host mice have been made. There are advantages, as well as limitations, that have been identified for SCNCP heterotransplants versus xenotransplantation of cultured cells. Overall, heterotransplanted tumors are better than conventional tumor xenografts at retaining tumor morphology, pathology, secretory activity and expression of tumor markers of the patient＇s original specimen. Furthermore, heterotransplanted tissue preserves the three-dimensional tumor architecture of the prostate to maintain critical stromal-epithelial cell interactions.