Carcinome intracanalaire de la prostate

Pathologie (Heidelb). 2025 Jul 30. doi: 10.1007/s00292-025-01450-w. Online ahead of print.ABSTRACTThe Gleason grading system is the cornerstone of risk stratification and clinical decision-making in prostate cancer patients. In the last decade, new insights on quantitative grading and the importance of particular growth patterns have further optimized pathological tumor grading. This review provides an update on the latest grading recommendations and discusses contemporary research directions.PMID:40736715 | DOI:10.1007/s00292-025-01450-w

Pathologie (Heidelb). 2025 Aug 1. doi: 10.1007/s00292-025-01453-7. Online ahead of print.ABSTRACTLarge gland lesions of the prostate encompass a spectrum of entities from benign histoanatomic variation to invasive high-grade carcinoma. Despite overlapping morphologic features, accurate diagnosis is critical because the clinical management of these lesions varies from no additional follow-up to possible definitive resection or radiotherapy. This manuscript provides a concise overview of large gland lesions with a focus on practical diagnostic features and clinical significance. Where necessary, a brief historical perspective is included as many of these entities have diagnostic and molecular criteria which are still being established. Unfortunately, controversies and lack of consensus within urologic subspecialty groups have made this a challenging topic for the broader pathologist community. This paper serves as a snapshot of our current understanding of the spectrum of intraductal lesions of the prostate and their mimics.PMID:40748479 | DOI:10.1007/s00292-025-01453-7

Pathologie (Heidelb). 2025 Aug 5. doi: 10.1007/s00292-025-01455-5. Online ahead of print.ABSTRACTDespite advances in imaging diagnostics, the histological confirmation of suspected carcinoma through prostate core needle biopsy remains essential for treatment planning. Diagnosis is based on established morphological criteria such as architectural disturbances, cellular atypia, and loss of the basal cell layer. In addition to the most common acinar prostate carcinoma, various subtypes and rare histological patterns exist, which must be differentiated from benign mimickers. Immunohistochemical methods support diagnostic accuracy but should be carefully interpreted in the context of morphology. Tumor extent in core biopsy specimens should preferably be reported in millimeters. Diagnostic uncertainties can be coded as atypical small acinar proliferation (ASAP) or atypical intraductal proliferation (AIP) to facilitate appropriate clinical interpretation.PMID:40762717 | DOI:10.1007/s00292-025-01455-5

J Histochem Cytochem. 2025 Jul 19:221554251349873. doi: 10.1369/00221554251349873. Online ahead of print.ABSTRACTProstate cancer (PC) is the second leading cause of cancer-related death in men worldwide. Its progression is marked by significant phenotypic changes in stromal cells and alterations in extracellular matrix (ECM) composition, including variations in collagen fibers, proteoglycans (PGs), and glycosaminoglycans. Tumor cells also modulate ECM secretion through adenosine A3 receptor (A3AR) activity. This study aimed to evaluate stromal cells, ECM components, and A3AR expression in prostate biopsies and explore their association with clinicopathological variables. We analyzed tissue samples from 96 patients diagnosed with PC or benign prostatic hyperplasia (BPH), using immunohistochemistry for alpha-smooth muscle actin and A3AR, and histochemical methods for ECM components. PC samples showed reduced stromal cell content and increased PGs, collagen fibers, and A3AR levels compared with BPH. While we found associations with histological classification, no significant correlations were observed with preoperative prostate-specific antigen levels or clinical risk categories. Our findings suggest that ECM components and A3AR may be involved in PCr progression and hold potential as biomarkers. However, due to the limited number of high-grade cases, further studies are needed to confirm these associations.PMID:40682346 | DOI:10.1369/00221554251349873

Radiology. 2025 Jul;316(1):e241710. doi: 10.1148/radiol.241710.ABSTRACTBackground MRI-targeted biopsies are recommended for prostate cancer diagnosis. In-bore MRI-targeted biopsy enables high-precision needle placement; however, the factors affecting prostate cancer detection rates and the potential for grade and patient risk migration require further investigation. Purpose To evaluate factors affecting the detection rate of prostate cancer in patients who underwent in-bore MRI-targeted biopsy and their influence on histologic concordance between biopsy (bGG) and surgical grade group (sGG). Materials and Methods This retrospective study evaluated in-bore MRI-targeted biopsies performed between March 2015 and January 2023. The agreement between bGG and sGG was assessed using Cohen weighted κ. The detection rate of prostate cancer and the concordance rates between bGG and sGG in patients undergoing prostatectomy were compared between biopsy systems (manual and robotic) and by patient biopsy status, lesion size (≤10 mm vs >10 mm), and Prostate Imaging Reporting and Data System (PI-RADS) category. Results In total, 780 lesions (patient median age, 65 years [IQR, 59-70 years]) were included. Among patients with previous negative biopsy and biopsy-naive patients, the detection rates of grade group (GG) 2 or higher cancer were higher in patients with PI-RADS category 4 or higher lesions (42.5% and 46.5%) and lesions larger than 10 mm (45.1% and 43.4%) (P < .05). Surgical upgrading was higher in lesions with bGG 1 than in those with bGG 2-4 cancers (66.1% vs 16.0% [P < .001]). In the 216 patients undergoing radical prostatectomy, bGG and sGG showed moderate to substantial agreement (weighted κ correlation coefficient, 0.61 [95% CI: 0.51, 0.71]). A downgrade of two or more grades between bGG and sGG was rare (5.7%). Histopathologic concordance did not depend on the PI-RADS category, target lesion size, biopsy system, or patient biopsy status (P = .90). Conclusion The in-bore MRI-targeted biopsy detection rates for GG 2 or higher prostate cancer depend on the target lesion size and PI-RADS category, and there is a substantial risk of histologic upgrades in men with GG 1 lesions at MRI-targeted biopsy. © RSNA, 2025 Supplemental material is available for this article. See also the editorial by Milot in this issue.PMID:40728405 | DOI:10.1148/radiol.241710

J Neuroendocrinol. 2025 Jul 31:e70074. doi: 10.1111/jne.70074. Online ahead of print.ABSTRACTThe specific human leukocyte antigen (HLA) alleles in individuals with tumors that ectopically express adrenocorticotropic hormone (ACTH), resulting in paraneoplastic isolated ACTH deficiency (IAD), remain elusive, primarily because of the scarcity of reported cases. In this study, we endeavored to elucidate the pathogenic mechanisms underlying paraneoplastic IAD, a novel subtype of autoimmune hypophysitis. We specifically examined the histological characteristics of ACTH-expressing cells in cancer tissues of one patient and investigated the prevalence of shared HLA alleles across three patients diagnosed with paraneoplastic IAD. We analyzed the histological features of prostate-cancer tissues, including ectopic ACTH expression, in a patient with paraneoplastic IAD. In addition, we investigated common HLA alleles and estimated haplotypes among this patient and two others with paraneoplastic IAD on which we previously reported. Immunohistochemical analyses revealed ACTH-positive cells in only one of four tissue samples. Ectopic ACTH expression was limited to areas of relatively high-grade prostate cancer, with cellular cords and cribriform glands that exhibited nuclear hyperchromatism. HLA typing revealed shared class II alleles and haplotypes, including DRB4*01:03, among the three cases. This study provides novel histological insights and highlights the commonality of HLA class II alleles in the diagnosis and pathogenesis of paraneoplastic IAD, potentially aiding the identification of new cases and our understanding of the underlying mechanisms of the disease.PMID:40745446 | DOI:10.1111/jne.70074