American Journal of Surgical Pathology最新文献

{"title":"Hepatocellular Carcinoma With JAK1 Mutations Harbors Distinct Histologic Features and Specific Mutational Hotspots in an Asian Cohort.","authors":"Jia-Huei Tsai, Yung-Ming Jeng, Yen-Yi Lin, Jau-Yu Liau","doi":"10.1097/PAS.0000000000002619","DOIUrl":"https://doi.org/10.1097/PAS.0000000000002619","url":null,"abstract":"<p><p>The pathogenesis and clinicopathological features of hepatocellular carcinoma (HCC) harboring JAK1 mutation have not been reported. Sixty inflammatory hepatocellular adenoma-like HCCs (IHA-like HCCs) and 16 IHAs were analyzed using targeted next-generation sequencing. Nearly all IHA-like HCCs (n=59, 98%) showed positive SAA/CRP expression. Genetic alterations of the JAK/STAT pathway were detected in 35 (58%) IHA-like HCCs, encompassing mutations in JAK1 (n=22), STAT3 (n=8), and IL6ST (n=5). Nine (56%) IHAs harbored mutations in STAT3 (n=3), IL6ST (n=4), GNAS (n=1), and FRK (n=1). All the mutations occurred in a mutually exclusive manner. JAK1 mutations were frequent (22/60, 37%) in IHA-like HCCs. JAK1-mutated IHA-like HCCs displayed distinctive cytologic characteristics, including abundant eosinophilic cytoplasm, vesicular chromatin, and prominent central nucleoli. Recurrent hotspot JAK1 mutations were identified at S703, S729, and L910. Surveillance for JAK1 mutations in the HCC genomics of other cohorts also revealed recurrent mutations at S703, S729, and L910. In particular, the S703 and S729 mutations were strongly associated with the features of Asian ethnicity, presence of chronic viral hepatitis, and hepatic fibrosis/cirrhosis. In conclusion, JAK1 mutations were frequent in HCC with IHA-like morphology in an Asian cohort. JAK1 mutation exhibited recurrent and specific hotspot mutations at S703, S729, and L910 in HCC. Patients diagnosed with JAK1-mutated HCC may be eligible for JAK-targeted molecular therapy.</p>","PeriodicalId":7772,"journal":{"name":"American Journal of Surgical Pathology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adult Mixed Epithelial and Stromal Tumor of the Kidney Harbors Recurrent Whole Chromosome 12 Gain.","authors":"Benjamin L Coiner, Busra Y Bayrak, Ozlem T Isikci, Stephanie E Siegmund, Michelle S Hirsch, Mahmut Akgul","doi":"10.1097/PAS.0000000000002620","DOIUrl":"https://doi.org/10.1097/PAS.0000000000002620","url":null,"abstract":"<p><p>Mixed epithelial and stromal tumor (MEST), including adult cystic nephroma (CN), is an uncommon benign renal neoplasm that mostly occurs in middle-aged women. To date, a comprehensive molecular genetic investigation of MEST and/or adult CN has not been performed. Fourteen archival cases of MEST were identified, and comprehensive clinicopathologic and molecular characterization was performed. Tumors arose only in female patients (median: 49 y, range: 35 to 82 y) and showed variable admixtures of bland epithelial glands, tubules, and cysts within an ovarian-type spindle cell stroma. In total, copy number alterations (CNAs) were detected in 6/14 (42.9%) MEST by next-generation sequencing (N=5) and karyotype (N=1). Relative whole-chromosome gains of chromosome 12 were identified in 5/14 (35.7%) MESTs. Two cases showed gains on chromosome 12 alone. Three cases with chromosome 12 gains harbored additional nonrecurrent CNAs. A single case without chromosome 12 gain harbored a relative whole-chromosome gain of chromosome 8 and loss of chromosome 21. No clinically actionable alterations were identified, and there were no alterations in renal neoplasia-related genes (eg, VHL, FH, SDHA/B/D, ELOC, TFEB, TFE3, DICER1, MET, MTOR, and TSC1/2). Of 13 cases with follow-up (median: 81.2 mo), no recurrences were identified after surgery. Although not entirely sensitive nor specific, chromosome 12 gain is the first evidence of recurrent alterations in MEST, supporting its classification as a neoplasm.</p>","PeriodicalId":7772,"journal":{"name":"American Journal of Surgical Pathology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Widespread Loss of Heterozygosity and Endoreduplication in Odontogenic Myxoma: Expanding the Clinicopathologic Spectrum of An Enigmatic Odontogenic Neoplasm.","authors":"Ivan J Stojanov, Melad N Dababneh, Vincent Cracolici, Sana Qureshi, Travis Hattery, Mark Chen, Benjamin F Smith, Diane O'Neill, Matthew Wolbert, Keith M Schneider, Sheila Shurtleff, Caroline Astbury, Katherine B Geiersbach, Sook-Bin Woo, Karen Fritchie, Grace E Weber, Josephine K Dermawan","doi":"10.1097/PAS.0000000000002616","DOIUrl":"https://doi.org/10.1097/PAS.0000000000002616","url":null,"abstract":"<p><p>Odontogenic myxoma (OM) is an uncommon, locally aggressive odontogenic neoplasm with characteristic histologic and clinico-radiographic features but with potential for histologic overlap with other odontogenic and non-odontogenic entities and a non-specific immunoprofile. Widespread loss of heterozygosity (LOH) has been recently described in rare cases of OM. The aim of this study was to determine whether widespread LOH represents a recurrent molecular signature that can be leveraged for clinical decision-making. Allele-specific copy number variation data from chromosomal microarray were generated from 7 OM, comprising a combined prospective and retrospective cohort. Four tumors arose in the mandible and 3 in the maxilla in patients ranging in age from 18 to 94 years (median: 44), with tumor size ranging from 2.2 to 13.0 cm. Variable amounts of fibrous stroma (odontogenic \"fibromyxoma\") were present in 4/7 OM, and hypercellularity not typically appreciated in conventional OM was present in 3/7 cases. All OM (7/7) demonstrated widespread LOH, with 5 cases showing a near-haploid/low hypodiploid genomes (multiple monosomies) and 2 cases showing evidence of pseudo-hyperdiploidy due to probable endoreduplication. Both pseudo-hyperdiploid cases were ≥10 cm in size; 1 represented local recurrence. Chromosomes 1 to 3, 6, 9, 11, 13, 15, and 22 demonstrated LOH in ≥75% of cases (chromosomes 1 to 3, 6, and 9 in 100% of cases), while chromosomes 5, 12, 19, and 20 universally retained heterozygosity. Altogether, widespread LOH is a recurrent event in OM and a novel finding in odontogenic pathology, and allele-specific copy number variation analysis can serve as a diagnostic adjunct in challenging cases.</p>","PeriodicalId":7772,"journal":{"name":"American Journal of Surgical Pathology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Placental Enterovirus Infection Is Not Evident in Chronic Histiocytic Intervillositis.","authors":"Emily F Cornish, Alexander Lennon, Julianne R Brown, James Burton, Olumide Ogunbiyi, Theodoros Xenakis, Yara Sanchez Corrales, J C Hutchinson, David J Williams","doi":"10.1097/PAS.0000000000002621","DOIUrl":"https://doi.org/10.1097/PAS.0000000000002621","url":null,"abstract":"","PeriodicalId":7772,"journal":{"name":"American Journal of Surgical Pathology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinicopathologic Spectrum and Intraprostatic Heterogeneity of Primary Mismatch Repair-Deficient Prostate Cancer.","authors":"Darrell Martin, Carol C Cheung, Chen Yang, Léonie Beauchamp, Mehdi Mansoor, Sophia M Green, Shamini Selvarajah, Susan Prendeville","doi":"10.1097/PAS.0000000000002623","DOIUrl":"https://doi.org/10.1097/PAS.0000000000002623","url":null,"abstract":"<p><p>Mismatch repair deficiency (MMRd) is identified in a small subset of prostate cancers and has implications for therapy selection and germline testing. The clinicopathologic spectrum of primary MMRd prostate cancer remains incompletely characterized. We evaluated 32 primary treatment-naive MMRd prostatic adenocarcinomas identified at a single institution. Grade group distribution included GG5 (n=12, 38%), GG4 (n=4, 13%), GG3 (n=7, 22%), and GG2 (n=9, 28%). Intraductal and/or invasive cribriform carcinoma was identified in 78% of cases overall and in 78% of GG2 tumors. MMR protein loss predominantly involved MSH2/MSH6 (78%), with isolated MSH6 loss in 16% and MLH1/PMS2 loss in 6%. Concordant pathogenic MMR gene alterations were identified on targeted NGS in all cases, while concurrent Tier 1/2 HRR gene alterations were present in 11 cases (35%), including ATM, BRCA1, and BRCA2. Germline testing performed in 15 cases identified Lynch syndrome in 5 (33%). MMR immunohistochemistry performed on multiple tissue blocks in 14 cases revealed discordant MMR status between tumor foci in 8 cases (57%), with MMR deficiency consistently restricted to the highest-grade focus and retained expression in spatially separate lower-grade foci. One additional case demonstrated apparent intratumoral heterogeneity within a single biopsy core, with MMR deficiency restricted to a higher-grade component and retained expression in the adjacent lower-grade tumor. These findings demonstrate a broader clinicopathologic spectrum of primary MMRd prostate cancer than previously recognized. Frequent discordance of MMR status between tumor foci highlights the importance of evaluating the highest-grade tumor focus when assessing multifocal primary prostate cancer.</p>","PeriodicalId":7772,"journal":{"name":"American Journal of Surgical Pathology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Subtyping of Biliary Tract Neuroendocrine Carcinomas: Clinicopathological Features and Prognostic Implications.","authors":"Yumi Asai, Minoru Esaki, Satoshi Nara, Chigusa Morizane, Takuji Okusaka, Nobuyoshi Hiraoka","doi":"10.1097/PAS.0000000000002618","DOIUrl":"https://doi.org/10.1097/PAS.0000000000002618","url":null,"abstract":"<p><p>Neuroendocrine carcinoma (NEC) of the biliary tract is an exceptionally rare and highly aggressive malignancy, and its molecular subtype landscape and diagnostic boundaries remain poorly defined. We retrospectively analyzed 42 biliary tract NECs, including 22 surgically resected cases, arising in the intrahepatic bile duct (n=8), extrahepatic bile duct (n=6), gallbladder (n=23), and ampulla of Vater (n=5). Using immunohistochemistry, NECs were classified into ASCL1 (A), NEUROD1 (N), POU2F3 (P), and null subtypes, and their clinicopathological features and disease-specific survival (DSS) were assessed. In the surgical cohort, the incidence of NEC ranged from 0.5% to 2.8% across anatomic sites. Most surgically resected tumors were combined with adenocarcinoma and classified as mixed neuroendocrine-non-neuroendocrine neoplasms, and metastatic lesions were predominantly composed of NEC regardless of the proportion of the NEC component in the primary tumor. Four cases arose in association with intraductal papillary neoplasms. Molecular subtyping identified 21% A-type, 40% N-type, 26% P-type, and 12% null-type tumors. The P type was enriched in gallbladder NECs (39%). The N type was more frequently associated with resectable disease, whereas the P type tended to be associated with unresectable disease. DSS differed significantly among the molecular subtypes, and the null type independently predicted shorter DSS (hazard ratio=3.48; P=0.034). Notably, several P-type tumors lacked expression of conventional neuroendocrine markers, including chromogranin A, synaptophysin, and INSM1. These findings indicate that biliary tract NECs exhibit a distinct, site-dependent molecular subtype distribution and suggest that molecular subtyping may serve as a practical adjunct to diagnosis and prognostic stratification.</p>","PeriodicalId":7772,"journal":{"name":"American Journal of Surgical Pathology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FOG1: A Highly Sensitive and Specific Diagnostic Marker for Gastroesophageal Adenocarcinoma.","authors":"Yaohong Wang, Feng Yin, Jun Yao, Dongfeng Tan, Lei Huo, Hongxia Sun, Wei Lu, Khaja B Khan, Luisa M Solis Soto, Larisa V Kostousov, Qiong Gan, Shilin Zhao, Rand Shakhtour, Yan Peng, Jianping Zhao, Dongwei Zhang, Jinsong Liu, Hui Chen, Constance T Albarracin, Yun Wu, Aysegul A Sahin, Huamin Wang, Qingqing Ding","doi":"10.1097/PAS.0000000000002617","DOIUrl":"https://doi.org/10.1097/PAS.0000000000002617","url":null,"abstract":"<p><p>Currently, there is no sensitive and specific diagnostic immunohistochemistry (IHC) marker to identify gastric and esophageal adenocarcinomas (GEAs). CDX2 is the most widely used tumor marker to determine gastrointestinal (GI) origin and has been shown to be an excellent marker for lower GI adenocarcinomas, including both small and large bowel adenocarcinomas. However, it has limited utility in upper GI adenocarcinomas, as CDX2 is a key marker for intestinal differentiation and is expressed in fewer than 50% of all gastric adenocarcinomas. In this study, through TCGA data mining, we identified friend of GATA1 (FOG1) as a potential sensitive and specific marker for GEAs, as high mRNA expression levels of FOG1 were found exclusively in GEAs across 29 solid tumor types. We then analyzed FOG1 and CDX2 protein expressions by IHC in 187 cases of GEA and esophageal squamous cell carcinomas (eSCC) and found that neither FOG1 nor CDX2 was expressed in eSCC. In contrast, the majority (91.1%) of GEAs showed moderate to high FOG1 expression, whereas 51.3% of GEAs demonstrated negative to low CDX2 expression. Only 4 (2.5%) GEAs showed moderate to high CDX2 expression with negative to low FOG1 expression. Conversely, among 168 cases of colonic adenocarcinoma, most (71.4%) exhibited intermediate-to-high CDX2 expression, whereas 92.9% showed negative-to-low FOG1 expression. Only 5 (3%) colonic adenocarcinomas demonstrated moderate-to-high FOG1 expression with negative-to-low CDX2 expression. Moderate to high FOG1 expression was detected in a small proportion of pancreatic (15.5%) and ampullary (11.2%) adenocarcinomas, but was rare (1.6% to 3.3%) in adenocarcinomas of the breast, lung, and ovary. In addition, there were no FOG1 expressions detected in lung squamous cell carcinoma, hepatocellular carcinoma, melanoma, and carcinomas of the salivary gland, thyroid, bladder, kidney, prostate, and uterus. Our data indicate that FOG1 is not only a sensitive, but also a specific marker for gastroesophageal adenocarcinoma.</p>","PeriodicalId":7772,"journal":{"name":"American Journal of Surgical Pathology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Renal Synovial Sarcoma Revisited: Clinicopathologic and Molecular Insights From 70 Cases With Report of a Rare SS18::NEDD4 Fusion.","authors":"Hui Min Tan, Busra Yaprak Bayrak, Katrina Collins, Ziying Ye, Rumeal D Whaley, Ming Liang Oon, Geethanjali Gude, Wai-Tung Lee, Fei Chen, Wendong Yu, Mahmut Akgul, Pedram Argani, Fang-Ming Deng, Michelle R Downes, Nancy Greenland, Sounak Gupta, Huiying He, Jiaoti Huang, Timothy D Jones, Selva Kabul, Seema Kaushal, Kemal Kosemehmetoglu, Antonio Lopez-Beltran, Fiona Maclean, Rohit Mehra, Ankur R Sangoi, Rajal B Shah, Stephanie E Siegmund, Puay Hoon Tan, Toyonori Tsuzuki, Bangchen Wang, Sean R Williamson, Chin-Lee Wu, Douglas Jian-Xian Wu, Ting Zhao, Qiu Rao, Liang Cheng","doi":"10.1097/PAS.0000000000002610","DOIUrl":"https://doi.org/10.1097/PAS.0000000000002610","url":null,"abstract":"<p><p>Synovial sarcoma is a rare malignant mesenchymal neoplasm that typically occurs in soft tissue sites, and the kidney is an uncommon primary location. Previous studies of primary renal synovial sarcoma are limited by small sample sizes, and our understanding remains incomplete. Here, we present the largest multi-institutional case series to date of primary renal synovial sarcoma, with a focus on novel and molecular findings. A total of 70 cases were contributed by multiple institutions. Comprehensive clinical and histopathologic data were collected and analyzed. The mean patient age was 40 years, with a male-to-female ratio of 1.9:1. The most common presenting signs and symptoms were pain and hematuria. The mean tumor size was 11.6 cm (range: 2.3 to 26 cm), with frequent cystic change and necrosis. The mean follow-up was 29 months (range: 2 to 129 mo), and the rates of metastasis, recurrence, and death due to disease were 62.7%, 33.3%, and 50.0%, respectively. Histologically, 56.1% were monophasic synovial sarcoma, 15.1% were biphasic, and 28.8% were poorly differentiated or showed round cell features. Molecularly, SS18::SSX2 fusion was detected in the majority of cases assessed (n=19), followed by SS18::SSX1 fusion (n=6) and a rare SS18::NEDD4 fusion (n=1). Given the morphologic and immunohistochemical overlaps with many other neoplasms, accurate diagnosis with preferably molecular techniques is crucial for appropriate prognostication and treatment of this aggressive tumor.</p>","PeriodicalId":7772,"journal":{"name":"American Journal of Surgical Pathology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148878884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expanding the Morphologic, Clinical, and Molecular Spectrum of Succinate Dehydrogenase A (SDHA)-Deficient Renal Cell Carcinoma: A Case Series With Review of Literature.","authors":"Shivani Kandukuri, Anandi Lobo, Harrison Tsai, Manju Aron, Shilpy Jha, Michelle S Hirsch, Sambit Mohanty","doi":"10.1097/PAS.0000000000002611","DOIUrl":"https://doi.org/10.1097/PAS.0000000000002611","url":null,"abstract":"<p><p>Succinate dehydrogenase (SDH)-deficient renal cell carcinoma (RCC) is defined by mutations in SDH subunits (A, B, C, or D) and is associated with hereditary paraganglioma-pheochromocytoma syndrome and gastrointestinal stromal tumors (GISTs) in some patients. This multi-institutional study analyzed 5 SDHA-deficient RCCs using morphology, immunohistochemistry (IHC), and next-generation sequencing (NGS). Patients had a median age of 40 years with male predominance (4:1). Initially, tumors were diagnosed as SDHA-deficient RCC (1), collecting duct carcinoma (1), or high-grade RCC, NOS (3). NGS subsequently identified 4 tumors as SDHA-deficient RCC. Common histologic features included papillary (100%) and nested (100%) architecture, solid growth (80%), eosinophilic/flocculent cytoplasm (100%), cytoplasmic vacuoles with inclusions (80%), and nuclear grooves (20%). Four of 5 tumors were high-grade (ISUP/WHO grade 3) with desmoplastic stroma and occasional inflammation. All tumors showed loss of SDHB expression (5/5), while SDHA expression was lost in 4/5, demonstrating that SDHA IHC may be preserved despite SDHA mutation. NGS identified SDHA mutations in four tumors. During follow-up, 2 of 4 patients developed metastases within 14 to 34 months, whereas the remaining 2 had no spread after 11 to 19 months. SDHA-deficient RCC displays a spectrum from classic SDHB-deficient RCC morphology to heterogeneous high-grade tumors. It should be considered in high-grade RCCs, particularly RCC NOS with papillary or collecting duct carcinoma-like morphology and vacuolated tumor cells. NGS is recommended, especially when SDHB loss is detected, as SDHA IHC may be retained. Unlike most SDHB-deficient RCCs, SDHA-deficient RCC appears more aggressive, with increased metastatic risk and poorer prognosis.</p>","PeriodicalId":7772,"journal":{"name":"American Journal of Surgical Pathology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148878931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"International Society of Urological Pathology Multidisciplinary Expert Consultation Conference on Evaluation of Treatment Effects in Prostate and Bladder Cancer: Working Group 2: The Urinary Bladder.","authors":"Michelle R Downes, Sara E Wobker, Steven C Smith, Markus Eckstein, Mahmut Akgul, Dilek E Baydar, Fadi Brimo, Eva Compérat, Arndt Hartmann, Ashish M Kamat, Anandi Lobo, Maria R Raspollini, Ankur R Sangoi, Shahrokh F Shariat, Toyonori Tsuzuki, Bas W G van Rhijn, Sean R Williamson, Geert J L H van Leenders, Liang Cheng, Antonio Lopez-Beltran","doi":"10.1097/PAS.0000000000002613","DOIUrl":"https://doi.org/10.1097/PAS.0000000000002613","url":null,"abstract":"<p><p>Treatment effects in the urinary bladder are variable and range from localized post-transurethral resection changes to widespread systemic therapy effects. The International Society of Urological Pathology (ISUP) organized a consensus meeting in Vienna, Austria, in September 2025, focused on the evaluation of treatment effects in both the prostate and bladder. Working Group 2 was assigned the topic of the urinary bladder, and a group of pathologists and clinicians was convened. They worked cooperatively to develop a 30-question, premeeting survey for the ISUP membership, which covered the following topics: systemic therapy-related changes, intravesical therapy and radiotherapy-related changes, macroscopic examination and reporting of treated bladder specimens, and relevant ancillary testing methods for grossly residual and/or minimal residual disease. The premeeting survey results highlighted uncertainty about tumor regression grading (TRG), variability in reporting practices for post-resection and intravesical therapy cases, and divergent opinions on the potential utility of molecular testing. Based on findings from this crowd-sourced experience, the Working Group researched the primary medical literature to study the problematic premeeting survey topics, curated focused presentations of published experience for the consensus meeting participants and developed refined consensus questions for consensus voting. Consensus was achieved in 18/19 polling statements. Use of molecular tests to distinguish benign mimickers from carcinoma did not reach consensus. Overall, the surveys and in-person consensus voting supported standardized reporting practices and terminology for post-therapy cases, interdisciplinary development of a bladder TRG scheme, and the utility of select molecular and immunohistochemical testing in the post-treatment setting.</p>","PeriodicalId":7772,"journal":{"name":"American Journal of Surgical Pathology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}