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Modern Pathology : An Official Journal... Jan 2018Benign mimics present either as common challenges in daily routine practice or may cause diagnostic dilemmas because some are less commonly seen and one may be less... (Review)
Review
Benign mimics present either as common challenges in daily routine practice or may cause diagnostic dilemmas because some are less commonly seen and one may be less familiar in recognizing them. There are a multitude of mimics of prostatic adenocarcinoma, which may represent normal gland structures, benign proliferations, atrophic lesions, hyperplastic or metaplastic changes, and inflammatory processes. Some of them are preferentially found in certain anatomic areas of the prostate, either confined to the prostate, or outside of the gland. Various benign mimics of prostatic carcinoma may be also evaluated based on their morphologic similarity to Gleason patterns 3-5 of prostatic adenocarcinoma. Most of the mimics are easily recognizable in larger specimens, such as TUR of the prostate or radical prostatectomy specimens, but they may pose diagnostic problems when the evaluation is done on limited tissue, such as needle-core biopsies or if prostate specimens are infrequently encountered in practice. Therefore, before signing out a report with a diagnosis of prostatic carcinoma, pathologists should carefully consider and rule out the various benign lesions that may mimic carcinoma. This is particularly relevant in the current prostate biopsy practice which relies on using extended biopsy core templates. The awareness and familiarity with the characteristic features of the mimics and judicial use of additional ancillary tests, including immunohistochemistry can prevent overdiagnosis and false-positive interpretation. This review provides a contemporary update on the broad spectrum of the benign prostatic lesions that can mimic prostate adenocarcinoma, outlines their key morphologic and immunohistochemical diagnostic features, and provides a diagnostic, pattern-based approach in establishing a correct diagnosis and distinguishing them reliably from prostatic adenocarcinoma.
Topics: Adenocarcinoma; Atrophy; Biopsy, Large-Core Needle; Consensus; Diagnosis, Differential; Humans; Hyperplasia; Immunohistochemistry; Male; Metaplasia; Neoplasm Grading; Prostate; Prostatic Neoplasms
PubMed: 29297489
DOI: 10.1038/modpathol.2017.136 -
Pathology Jan 2021The histopathological diagnosis of prostatic adenocarcinoma is challenged by the existence of numerous benign mimics. Most of these lesions have no clinical significance... (Review)
Review
The histopathological diagnosis of prostatic adenocarcinoma is challenged by the existence of numerous benign mimics. Most of these lesions have no clinical significance and many do not need to be reported. Their clinical relevance lies in the risk that they are misinterpreted as cancer. This review presents the histopathological features of benign mimics and discusses their distinction from cancer. The lesions that are most often misdiagnosed as cancer are atrophy and its variants, including simple atrophy, partial atrophy and post-atrophic hyperplasia. Benign proliferations are a group of lesions with crowded small glands with no or little nuclear atypia. The most problematic entity of this group is adenosis, which may have a more alarming architecture than some cancers. A diagnostic problem with atrophy and several of the benign proliferations is that the glands often have a discontinuous or absent basal cell layer. Hyperplastic and metaplastic lesions include basal cell hyperplasia. Basal cell hyperplasia may especially mimic prostate cancer with its small dark glands, variable nuclear atypia and a pseudoinfiltrative pattern, which may be present. The anatomical structure that most often causes diagnostic problems is the seminal vesicle. The mucosa of the seminal vesicle contains small acini, often with very pronounced nuclear atypia that may be misinterpreted as cancer. Pathologists need to be familiar with these mimics, as a false positive diagnosis of prostate cancer may lead to unnecessary radical treatment.
Topics: Adenocarcinoma; Atrophy; Diagnosis, Differential; Humans; Male; Prostate; Prostatic Hyperplasia; Prostatic Neoplasms
PubMed: 33070957
DOI: 10.1016/j.pathol.2020.08.006 -
Archives of Pathology & Laboratory... Oct 2015The differential diagnosis for atypical cribriform lesions of the prostate has become increasingly complex and includes intraductal carcinoma of the prostate, high-grade... (Review)
Review
The differential diagnosis for atypical cribriform lesions of the prostate has become increasingly complex and includes intraductal carcinoma of the prostate, high-grade prostatic intraepithelial neoplasia, and atypical intraductal proliferations. In this review, we summarize the morphologic and molecular features and significance of intraductal carcinoma of the prostate. We also summarize our institution's strategy for reporting and treatment recommendations for intraductal carcinoma of the prostate.
Topics: Adenocarcinoma; Biomarkers, Tumor; Carcinoma, Intraductal, Noninfiltrating; Diagnosis, Differential; Humans; Male; Prostate; Prostatectomy; Prostatic Intraepithelial Neoplasia; Prostatic Neoplasms
PubMed: 26414467
DOI: 10.5858/arpa.2015-0206-RA -
Journal of Cancer Research and... 2023In India, prostate carcinoma is the fifth most common cause of carcinoma in men, and the fourth in cancer mortality. Incidence of prostate malignancy is increasing in...
INTRODUCTION
In India, prostate carcinoma is the fifth most common cause of carcinoma in men, and the fourth in cancer mortality. Incidence of prostate malignancy is increasing in India by one percent every year. Prostate carcinoma is graded using the Gleason scoring system. The Gleason score is very useful for predicting the prognosis of prostate carcinoma. The collaborative use of clinical features, combined with the size of the prostate, prostate-specific antigen levels, and histopathological features helps in making an accurate and early diagnosis of the patients.
MATERIAL AND METHOD
This present prospective study included all histologically proven cases of prostate carcinoma in the Department of Pathology, Guru Gobind Singh Medical Hospital over a period of one year. A detailed histopathological examination of the H and E stained sections is carried out under light microscope including histological typing, Gleason scoring and grading. The Gleason grade was correlated with serum PSA levels.
RESULTS
Out of 80 cases, 28 (35%) were reported as Gleason grade group 3 with a Gleason score of 7 (4 + 3). 12 cases (15%) showed a Gleason grade group 2 with a Gleason score of 7 (3 + 4). Grade group 4 (Gleason score 8) and grade group 5 were observed in 22 cases (27.5%) and 18 cases (22.5%), respectively. Whereas, no case of Gleason grade group 1 with Gleason score of 6 (3 + 3) was seen.
CONCLUSION
Gleason's Group Grade 3 outnumbered all the group grades, contributing 35% (28 cases) of the total cases of prostatic adenocarcinoma. Serum PSA levels were raised (>10 ng/ml) in 100% of cases. Henceforth, it signifies the importance of serum PSA levels in prostate carcinoma. Lymphovascular invasion was associated with higher group grade of prostatic adenocarcinoma.
Topics: Male; Humans; Prostate-Specific Antigen; Prostate; Neoplasm Grading; Tertiary Care Centers; Prospective Studies; Prostatic Neoplasms; Carcinoma; Adenocarcinoma
PubMed: 37787299
DOI: 10.4103/jcrt.jcrt_1719_21 -
The Prostate Jan 2022Metabolic reprograming is now a recognized hallmark of cancer. The prostate-specific phosphatase and tensin homolog deleted on chromosome 10 (Pten) gene-conditional...
BACKGROUND
Metabolic reprograming is now a recognized hallmark of cancer. The prostate-specific phosphatase and tensin homolog deleted on chromosome 10 (Pten) gene-conditional knockout (KO) mouse carcinogenesis model is highly desirable for studying prostate cancer biology and prevention due to its close resemblance of primary molecular defects and histopathological features of human prostate cancer. We have recently published macromolecular profiling of this model by proteomics and transcriptomics, denoting a preeminence of inflammation and myeloid suppressive immune cell features. Here, we performed metabolomic analyses of Pten-KO prostate versus wild type (WT) counterpart for discernable changes in the aqueous metabolites and contrasted to those in the TRAMP neuroendocrine carcinoma (NECa).
METHODS
Three matched pairs of tissue-specific conditional Pten-KO mouse prostate and WT prostate of litter/cage-mates at 20-22 weeks of age and three pairs of TRAMP NECa versus WT (28-31 weeks) were profiled for their global aqueous metabolite changes, using hydrophilic interaction liquid chromatography-tandem mass spectrometry.
RESULTS
The Pten-KO prostate increased purine nucleotide pools, cystathionine, and both reduced and oxidized glutathione (GSH, GSSG), and gluconate/glucuronate species in addition to cholesteryl sulfate and polyamine precursor ornithine. On the contrary, Pten-KO prostate contained diminished pools of glycolytic intermediates and phosphorylcholine derivatives, select amino acids, and their metabolites. Bioinformatic integration revealed a significant shunting of glucose away from glycolysis-citrate cycle and glycerol-lipid genesis to pentose phosphate cycle for NADPH/GSH/GSSG redox and pentose moieties for purine and pyrimidine nucleotides, and glycosylation/glucuronidation. Implicit arginine catabolism to ornithine was consistent with immunosuppression in Pten-KO model. While also increased in cystathionine-GSH/GSSG, purine, and pyrimidine nucleotide pools and glucuronidation at the expense of glycolysis-citrate cycle, the TRAMP NECa increased abundance of many amino acids, methyl donor S-adenosyl-methionine, and intermediates for phospholipids without increasing cholesteryl sulfate or ornithine.
CONCLUSIONS
The aqueous metabolomic patterns in Pten-KO prostate and TRAMP NECa shared similarities in the greater pools of cystathionine, GSH/GSSG redox pair, and nucleotides and shunting away from glycolysis-citrate cycle in both models. Remarkable metabolic distinctions between them included metabolisms of many amino acids (protein synthesis; arginine-ornithine/immune suppression) and cholesteryl sulfate and methylation donor for epigenetic regulations.
Topics: Animals; Biomarkers; Carcinoma, Neuroendocrine; Chromatography, Liquid; Disease Models, Animal; Male; Metabolomics; Mice; Mice, Knockout; PTEN Phosphohydrolase; Prostate; Prostatic Neoplasms; Receptors, Tumor Necrosis Factor, Member 25; Tandem Mass Spectrometry
PubMed: 34662447
DOI: 10.1002/pros.24256 -
American Journal of Men's Health 2022The tRNA-derived fragments (tRFs) are a new class of regulatory noncoding RNAs and have different biological functions in cancer. This article investigated the...
The tRNA-derived fragments (tRFs) are a new class of regulatory noncoding RNAs and have different biological functions in cancer. This article investigated the expression and clinicopathological significance of tRF-Glu-TTC-2 in prostate carcinoma (PCa), and its effect on tumor growth. Expression profiles of tRFs and tiRNAs were analyzed by tRF and tiRNAs microarray in PCa samples, and then the expression was confirmed by qRT-PCR; RNA in situ hybridization was used to detect the positive expression of tRF-Glu-TTC-2 and to analyze the correlation between the expression level of tRF-Glu-TTC-2 and clinicopathological parameters. CCK-8 experiment was used to detect the effect of tRF-Glu-TTC-2 on the proliferation of PCa cells, and nude mice subcutaneous tumor model was used to detect the effect of tRF-Glu-TTC-2 on the growth of PCa cells. The results showed that tRF-Glu-TTC-2 was mainly positive and its expression level increased in PCa. The high expression was closely related to the tumor size ( < .05). Overexpression of tRF-Glu-TTC-2 promoted the proliferation of PCa cells, and decreased expression of tRF-Glu-TTC-2 inhibited the proliferation of PCa cells ( < .05). The results of subcutaneous tumor transplantation in nude mice showed that the tumor volume and weight of the knockdown group were smaller than those of the control group(all s < .05). Ki-67 staining showed that the proportion of Ki-67-positive cells in the reduced tRF-Glu-TTC-2 group was lower than that in the control group ( < .05). The tRF-Glu-TTC-2 may be a new oncogene that can promote growth and proliferation of PCa. It provides a new idea for the treatment of PCa.
Topics: Male; Mice; Animals; Humans; Mice, Nude; Prostate; Ki-67 Antigen; Prostatic Neoplasms; Carcinoma
PubMed: 36377736
DOI: 10.1177/15579883221135970 -
Pathology Oct 2023The presence of intraductal carcinoma of the prostate (IDCP) correlates with late-stage disease and poor outcomes for patients with prostatic adenocarcinoma, but the...
The presence of intraductal carcinoma of the prostate (IDCP) correlates with late-stage disease and poor outcomes for patients with prostatic adenocarcinoma, but the accurate and reliable staging of disease severity remains challenging. Immunohistochemistry (IHC) has been utilised to overcome problems in assessing IDCP morphology, but the current markers have only demonstrated limited utility in characterising the complex biology of this lesion. In a retrospective study of a cohort of patients who had been diagnosed with IDCP, we utilised IHC on radical prostatectomy sections with a biomarker panel of Appl1, Sortilin and Syndecan-1, to interpret different architectural patterns and to explore the theory that IDCP occurs from retrograde spread of high-grade invasive prostatic adenocarcinoma. Cribriform IDCP displayed strong Appl1, Sortilin and Syndecan-1 labelling patterns, while solid IDCP architecture had high intensity Appl1 and Syndecan-1 labelling, but minimal Sortilin labelling. Notably, the expression pattern of the biomarker panel in regions of IDCP was similar to that of adjacent invasive prostatic adenocarcinoma, and also comparable to prostate cancer showing perineural and vascular invasion. The Appl1, Sortilin, and Syndecan-1 biomarker panel in IDCP provides evidence for the model of retrograde spread of invasive prostatic carcinoma into ducts/acini, and supports the inclusion of IDCP into the five-tier Gleason grading system.
Topics: Male; Humans; Prostate; Carcinoma, Intraductal, Noninfiltrating; Retrospective Studies; Immunohistochemistry; Syndecan-1; Prostatic Neoplasms; Neoplasm Grading
PubMed: 37422404
DOI: 10.1016/j.pathol.2023.05.004 -
Archivos Espanoles de Urologia Aug 2022To report the treatment and clinical monitoring in patients with prostatic evanescent carcinoma at Hospital Carlos Andrade Marin.
OBJECTIVE
To report the treatment and clinical monitoring in patients with prostatic evanescent carcinoma at Hospital Carlos Andrade Marin.
METHODS
We reviewed the medical records of 148 patients undergoing by robot-assisted radical prostatectomy in Carlos Andrade Marin hospital. The cases reported between January 2016 to December 2018. The diagnosis was carried by taking a transrectal prostate biopsy with 12 cylinders. This samples are studied by the pathologist who reviews the radical prostatectomy surgery.
RESULTS
Three patients had prostatic evanescent carcinoma, which those cases showed Gleason 6 (3+3) prostate cancer. Two received neoadjuvant hormone therapy and the other patient presented minor tumor invasion in 1 out of 12 cylinders used during the biopsy. In the three cases, after the sample analysis, there was no residual tumor evidence. Therefore, they were classified as pT10.
CONCLUSIONS
In this study, the results obtained from the patients studied presents the incidence of prostatic evanescent carcinoma is 2%. The combination of these different factors such as clinical status, preoperative PSA, number of positive cylinders and the invasion percentage, additionally to the usage of neoadjuvant hormone therapy prior the radical prostatectomy can help to predict evanescent carcinoma of the prostate.
Topics: Carcinoma; Hormones; Humans; Male; Neoplasm Staging; Prostate; Prostate-Specific Antigen; Prostatectomy; Prostatic Neoplasms; Retrospective Studies
PubMed: 36138509
DOI: 10.56434/j.arch.esp.urol.20227506.85 -
Asian Journal of Surgery Oct 2022
Topics: Adenocarcinoma; Colon; Humans; Male; Prostate; Prostatic Neoplasms
PubMed: 35523607
DOI: 10.1016/j.asjsur.2022.04.106 -
Virchows Archiv : An International... May 2019Intraductal carcinoma of the prostate gland (IDCP), which is now categorised as a distinct entity by WHO 2016, includes two biologically distinct diseases. IDCP... (Review)
Review
Intraductal carcinoma of the prostate gland (IDCP), which is now categorised as a distinct entity by WHO 2016, includes two biologically distinct diseases. IDCP associated with invasive carcinoma (IDCP-inv) generally represents a growth pattern of invasive prostatic adenocarcinoma while the rarely encountered pure IDCP is a precursor of prostate cancer. This review highlights issues that require further discussion and clarification. The diagnostic criterion "nuclear size at least 6 times normal" is ambiguous as "size" could refer to either nuclear area or diameter. If area, then this criterion could be re-defined as nuclear diameter at least three times normal as it is difficult to visually compare area of nuclei. It is also unclear whether IDCP could also include tumours with ductal morphology. There is no consensus whether pure IDCP in needle biopsies should be managed with re-biopsy or radical therapy. A pragmatic approach would be to recommend radical therapy only for extensive pure IDCP that is morphologically unequivocal for high-grade prostate cancer. Active surveillance is not appropriate when low-grade invasive cancer is associated with IDCP, as such patients usually have unsampled high-grade prostatic adenocarcinoma. It is generally recommended that IDCP component of IDCP-inv should be included in tumour extent but not grade. However, there are good arguments in favour of grading IDCP associated with invasive cancer. All historical as well as contemporary Gleason outcome data are based on morphology and would have included an associated IDCP component in the tumour grade. WHO 2016 recommends that IDCP should not be graded, but it is unclear whether this applies to both pure IDCP and IDCP-inv.
Topics: Adenocarcinoma; Biopsy, Needle; Carcinoma, Intraductal, Noninfiltrating; Humans; Male; Neoplasm Grading; Prostate; Prostatic Neoplasms
PubMed: 30825003
DOI: 10.1007/s00428-019-02544-6