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.
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http://dx.doi.org/10.1038/modpathol.2017.136 | DOI Listing |
Medicina (Kaunas)
December 2024
Department of Pathology and Cytology, University Hospital Center Rijeka, 51000 Rijeka, Croatia.
: Prostate cancer is one of the most commonly diagnosed cancers in the male population and the fifth leading cause of cancer death worldwide in men as of 2022. One of the potential biomarkers that can predict the progression of the disease is the transmembrane adhesion molecule CD44s. The aims of this study were to determine the expression of CD44s in prostate cancer in the central tumor mass and in the tumor periphery of the disease and to compare it with the clinicopathological parameters (PSA, Gleason score, surgical margins, and biochemical recurrence of the disease) in patients treated with radical prostatectomy.
View Article and Find Full Text PDFCancers (Basel)
December 2024
Cancer Research Program, Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, NC 27707, USA.
Background: Chemokines, along with their receptors, exert critical roles in tumor development and progression. In prostate cancer (PCa), interleukin-8 (IL-8/CXCL8) was shown to enhance angiogenesis, proliferation, and metastasis. CXCL8 activates two receptors, CXCR1 and CXCR2.
View Article and Find Full Text PDFFront Immunol
January 2025
Yi-Huan Genitourinary Cancer Group, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Primary small cell neuroendocrine carcinoma of the prostate is extremely rare, highly aggressive, and has a very poor prognosis, with an overall survival typically not exceeding one year. Standard treatment is generally based on the regimen for small cell lung cancer (SCLC), with guidelines recommending etoposide combined with cisplatin (EP regimen) as the first-line treatment. However, their therapeutic effects are limited.
View Article and Find Full Text PDFInt Cancer Conf J
January 2025
Department of Urology, The Second Affiliated Hospital of Xi'an Jiaotong University, No. 157 Xiwu Road, Xi'an, 710004 China.
Mismatch repair deficiency (MMRd) or microsatellite instability high (MSI-H) is rare in prostate cancer and more frequently observed in cases with ductal histology. MLH1 copy number loss is extremely rare in MMRd tumors. Herein, we describe a case of prostate ductal adenocarcinoma with MLH1 copy number loss, microsatellite instability high and BRCA2 mutation could derive benefit from immunotherapy plus ADT.
View Article and Find Full Text PDFMayo Clin Proc
January 2025
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN.
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