Initial Biopsy Research Articles

Chaotic blastocysts in preimplantation genetic testing for aneuploidy: prevalence, characterization, and re-biopsy results.

Chaotic blastocysts in preimplantation genetic testing for aneuploidy: prevalence, characterization, and re-biopsy results.

The Role of Repeat Skeletal Muscle Biopsy: Indications, Yield and Outcomes

ABSTRACTIntroduction/AimsMuscle biopsy performed to investigate weakness and/or pain may be nondiagnostic and prompt repeat biopsy. We determined the indications and yield of rebiopsy.MethodsPatients who underwent > 1 muscle biopsy (South Australia, 2000–2023) were identified. Biopsy indication and histological diagnosis at initial (B1) and subsequent (B2) biopsy were documented. Two histological outcomes were defined: change from non‐specific (B1) to specific diagnosis (B2) (Outcome 1) or change in specific diagnosis (Outcome 2). Clinical records were reviewed to determine if rebiopsy affected clinical decision making.ResultsRepeat biopsies accounted for 112/3089 (3.6%) of biopsies. The main indications for repeating a biopsy were specific diagnostic query (36/112, 32.1%), most commonly inclusion body myositis (IBM) or genetic myopathy, and unexpected clinical trajectory (74/112, 66.1%).Almost half of rebiopsies (48/112, 42.9%) met Outcome 1 (31/48) or 2 (17/48). Altered histological diagnosis impacted clinical decision‐making in 17/22 (77.3%) patients. 21/34 (61.8%) with an initial non‐specific myopathy achieved Outcome 1. B2 showed prominent atrophy in seven patients; 3/7 had non‐specific myopathy on B1.Open biopsy method for repeat biopsy was associated with Outcome 1 or 2 (OR 4.3 [IQR 1.6–11.5], p = 0.004).DiscussionRepeat muscle biopsy achieved a specific diagnosis in 43% of cases and frequently impacted clinical decision‐making. The highest yield was when IBM was suspected clinically, or when B1 showed non‐specific myopathy. Non‐specific myopathy may progress to histological atrophy; the role of untreated inflammation in driving this is unclear.

High-grade Endometrial Carcinoma With Serous and Colorectal Carcinoma-like Components: Unique Morphology in Correlation With Immunohistochemical and Molecular Findings.

Endometrial carcinoma with intestinal differentiation/colorectal carcinoma-like (CRC-like) features is rare with few cases reported to date. Those described are mainly endometrioid carcinomas with intestinal differentiation. We report a case of high-grade endometrial carcinoma with serous and intestinal/CRC-like components. The gross, histologic, immunohistochemical, and molecular features are described for both components of the tumor in the initial diagnostic biopsy and subsequent resection specimen. The diagnosis of primary endometrial carcinoma with serous and CRC-like components is supported by immunohistochemical and molecular findings, as well as clinical workup. The rarity of this phenomenon poses diagnostic challenges. In addition, the literature is reviewed with specific emphasis on the molecular and pathologic features of mixed endometrial carcinomas, including those with intestinal/CRC-like features.

Localization procedure for breast lesions at time of biopsy - Which patients would benefit?

Localization procedure for breast lesions at time of biopsy - Which patients would benefit?

Bilateral Wilms Tumour: Is Neoadjuvant Doxorubicin Necessary?

Approximately 5% to 8% of patients with Wilms tumour have bilateral disease. The prevalence of bilateral Wilms tumour (BWT) is higher in individuals with genetic predisposition syndromes than in those without. The goal of therapy is to preserve as much renal tissue as possible without compromising the overall oncological outcomes, utilising neoadjuvant chemotherapy followed by nephron sparing surgery (NSS) if possible. The Children’s Oncology Group (COG) in North America and the International Society of Paediatric Oncology (SIOP) in Europe have developed the main protocols for the treatment of BWT. Both protocols are similar: initial biopsies are not indicated, and they both recommend surgical resection at week 6 or no later than week 12. Chemotherapy includes the use of vincristine and actinomycin-D in both protocols, but the COG approach also includes the use of doxorubicin, which is a cardiotoxic drug with important long-term effects on the cardiac function of childhood cancer survivors. What doxorubicin adds to patients with BWT in terms of radiological tumour response, resectability, long-term renal function and overall survival, is still not very well described and it may be variable depending on the tumour biology. This article describes the current approach for BWT in North America and Europe, focusing on the potential effect that doxorubicin may have on patient outcomes.

Leniolisib Treatment of Childhood-Onset Lupus Nephritis in Activated PI3K-Delta Syndrome Illustrates Precision Medicine in Pediatric Autoimmunity

Background Constitutively active PI3Kδ, as occurs in patients with activated PI3K-delta syndrome (APDS) 1, results in disturbed immune cell development and function leading to microbial susceptibility and immune dysregulation. Leniolisib, a novel, orally FDA-approved bioavailable small molecule inhibitor, was engineered to selectively target PI3Kδ signaling. Leniolisib was shown to partially reconstitute lymphocyte subsets and decrease lymphoproliferation as measured by reduced spleen size and lymphadenopathy. However, its effect in other immune dysregulation manifestations has not been studied. Methods We evaluated the patient’s peripheral blood by flow cytometry and kidney biopsies by spatial single-cell transcriptomics and proteomics to track LN progression during treatment with leniolisib. Results The patient presented at age 10 yo with recurrent sinopulmonary infections and significant bronchiectasis. She developed class IV LN at age 14 yo with autoantibodies to dsDNA, RNP, SSA, and Smith. She was treated with corticosteroids, cyclophosphamide, mycophenolate, hydroxychloroquine, and tacrolimus with suboptimal renal response and infectious complications. She was also treated with rituximab, but early B cell repopulation (with plasmablast skewing) persisted with LN flares. The frequency of her peripheral CD21lo B cells, plasmablasts, CD8 T effector memory, exhausted (PD1+), and senescent (CD57hi) cell subpopulations decreased after three doses of rituximab, with some clinical improvement in renal function, but remained clinically tenuous. She started leniolisib in April 2023, three years after her initial renal biopsy, with marked improvement and weaning of immunomodulation. Multiplexed ion beam imaging (MIBI) demonstrated that the CD45+ leukocytes in the patient’s kidney biopsy had a significant increase in the CD8 T cells and M1 macrophages compared with other 30 cLN patients’ biopsies, based on single-cell antibody panel in situ immune profiling. These data were further confirmed by spatial transcriptomic data. These tissue-specific findings are consistent with the genetic immunopathology of the patient, particularly the increased CD8 T cellular effector phenotype, which drives the immune infiltrate and renal disease in the APDS patient. Conclusions This report illustrates the criticality of understanding the underlying disease mechanism to guide pathway and patient specific therapy in autoimmunity. Further, it demonstrates the therapeutic effect leniolisib for the treatment of APDS-related immune dysregulation complications beyond splenomegaly and lymphadenopathy. Figure 1.

Residual disease volume and prognosis in endometrioid precancer after progestin therapy.

Progestin therapy is a conservative treatment option for atypical hyperplasia/endometrioid intraepithelial neoplasia (AEH/EIN), particularly for patients seeking fertility preservation or for whom surgery is not feasible. However, approximately 30% of patients exhibit resistance to therapy, underscoring the need for early identification of responders and non-responders. We conducted a retrospective study of 252 AEH/EIN patients who underwent progestin therapy, with serial follow-up endometrial biopsies yielding 892 samples with quantifiable residual disease (RD). The amount of RD was evaluated as a predictor of therapeutic response, with a focus on its prognostic significance. Among the 252 patients, 194 (77%) were classified as responders, while 58 (23%) were non-responders. Responders exhibited a progressive reduction in RD across follow-up biopsies, with all achieving complete decidualization by the final biopsy. In contrast, non-responders consistently demonstrated persistent RD, with more RD in initial biopsies post progestin therapy significantly correlating with non-response. An amount of RD exceeding 20% in the initial biopsy or a less than 50% reduction in subsequent biopsies strongly predicted therapeutic failure (p < 0.001). The amount of RD is a valuable predictive marker for progestin therapy outcomes in AEH/EIN patients. Incorporating RD volume assessment in pathology reports can enhance clinical decision-making, facilitating more personalized and effective treatment strategies. Early identification of non-responders may prevent prolonged ineffective therapy and enable timely alternative interventions.

Multisystem Langerhans cell histiocytosis in a pediatric patient: a rare case report with literature review and future directions.

Langerhans cell histiocytosis (LCH) is a rare disorder characterized by the proliferation of Langerhans cells that affects multiple organs. It presents variably in children, complicating diagnosis and treatment strategies. Understanding its genetic and clinical characteristics is crucial for its effective management. We report the case of a 13-year-old male with multisystem LCH involving the temporal bone, parotid gland, and lymph nodes, who presented with auricular pain and swelling. Despite the initial non-specific treatment, advanced imaging and biopsy confirmed the diagnosis. The patient underwent a treatment regimen according to the LCH4 protocol, which included Prednisolone and Vinblastine, and showed significant improvement. This case highlights the necessity of a multidisciplinary approach for diagnosing and managing LCH and illustrates the potential of genetic research and targeted therapies to improve outcomes. Future studies should explore the genetic basis of LCH and the potential links between immunization and disease onset, aiming to refine treatment protocols and enhance patient prognosis.

Abstract 72: A case of immune therapy-refractory composite lymphoma: The complex interplay between two distinct tumors within a single spatial microenvironment

Abstract Immune checkpoint (IC) therapy with anti-PD1 agents is typically used in treatment-refractory classic Hodgkin lymphoma (CHL). However, we present a rare case of composite classic Follicular lymphoma (cFL) and CHL whereby frontline use of anti-PD1 therapy (Nivolumab) in combination with standard AVD (Doxorubicin, Vinblastine, Dacarbazine) was clinically justified. We performed the Visium spatial transcriptomics assay to gain insight into the unique tumor cell characteristics and immune cell composition of the tumor microenvironment both pre- and post-IC therapy. Our case is a of a 44-year-old female who presented with fever, night sweats, and cervical lymphadenopathy. The patient underwent frontline IC combination therapy with single-agent Nivolumab and standard AVD. She showed nearly complete treatment response after 6 cycles. However, three months post-therapy, she developed new symptoms of fatigue, fever, and inguinal lymphadenopathy. Excisional biopsy of the inguinal lymph node showed recurrence of the cFL with no evidence of the previous CHL. The clinicopathologic findings suggest a primary treatment response of the CHL to IC combination therapy, but refractory response of the cFL. To understand the complex immune cell composition of this rare lymphoma, we performed the 10X Genomics Visium CytAssist assay on a representative tumor area from the formalin-fixed paraffin-embedded tissue block of the initial diagnostic biopsy. The data were analyzed using a bioinformatics workflow for cell deconvolution to identify cellular composition, ligand-receptor interaction analysis to study cell-cell communication, and spatial gene expression analysis to understand the disease context. Pathologic diagnosis of the lymph node excision showed a composite lymphoma comprised of cFL and CHL. Cytogenetic fluorescence in situ hybridization (FISH) study for BCL2 rearrangement was negative. Our analysis revealed distinct transcriptomic profiles associated with cFL and CHL regions within the lymph node excision. We identified unique immune cell infiltration patterns with pronounced CD4(+) T-cell memory signatures in both cFL and CHL regions. We observed transitional zones between the two lymphomas characterized by a mixed expression profile with increased stromal and stem cell markers. Furthermore, we uncovered T-cell immunoregulatory and trafficking signals localized to the CHL and transitional zones, potentially influencing the surrounding tumor microenvironment. In conclusion, this study provides an unprecedented investigation into a rare case of composite lymphoma treated with frontline IC combination therapy through molecular and spatial profiling. Further analysis using the Visium assay is pending on the subsequent post-therapy tissue biopsy which may undoubtedly reveal underlying unique biologic relationships. Citation Format: Ashley K. Volaric, James Gerson, Karamatullah Danyal, Rangsinee Nusapan, Seth Frietze. A case of immune therapy-refractory composite lymphoma: The complex interplay between two distinct tumors within a single spatial microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 72.

Abstract 4659: AI-powered assessment of morphologic likeness to small cell lung cancer (SCLC) predicts progression to SCLC and TKI response in EGFR-mutant NSCLC

Abstract Background: A subset of EGFR-mutant non-small cell lung cancers (NSCLC) progresses to small cell lung carcinoma (SCLC) during tyrosine kinase inhibitor (TKI) therapy, particularly in cases with inactivating RB1 mutations. As RB1 mutations are likely foundational events in SCLC transformation, we hypothesize that tumors susceptible to this transformation exhibit morphologic features resembling SCLC even at the time of the initial diagnostic biopsy. Methods: We developed a predictive model for identifying the SCLC phenotype using H&amp;E-stained slides from cases with confirmed SCLC histological diagnosis. Morphological features of individual cells were extracted through a grid-based image retrieval method, enhanced by subcellular compartmental analysis with an emphasis on nuclear and cytoplasmic characteristics. These features were used to quantify the morphological SCLC-likeness for each case. The SCLC-like phenotype was defined as the top 25% of cases exhibiting the highest SCLC-likeness scores. The model was then applied to 106 real-world advanced-stage EGFR-mutant NSCLC cases to validate the extracted features and assess clinical correlations. The primary endpoints were progression-free survival (PFS) after TKI therapy according to SCLC-like phenotype versus others, along with the rate of SCLC transformation. Secondary endpoints were RB1 mutations confirmed by targeted panel sequencing or whole exome sequencing. Results: The SCLC-like phenotype case images correlated with pathologist-interpretable features of SCLC, including a significantly smaller nuclear area (56 μm2 vs. 102 μm2) and increased nuclear optical density (18.01 vs. 15.68) reflecting hyperchromasia, consistent with typical SCLC morphology. Among the 106 patients with EGFR-mutant NSCLC, 26 were classified as having the SCLC-like phenotype. Patients with the SCLC-like phenotype demonstrated significantly worse PFS after TKI treatment (HR 1.71, CI 1.08-2.71, P = 0.02). Among the cases with secondary tissue biopsies (n = 68), SCLC transformation was observed in 4 cases, with a numerically higher frequency in the SCLC-like phenotype group compared to others (15.8% [3/19] vs. 2.0% [1/49], P = 0.06). No significant difference in RB1 mutation frequency was found via panel or whole exome sequencing. Conclusion: This is the first study to demonstrate the potential of morphologic assessment in identifying features pertinent to SCLC transformation and in optimizing prognostication in EGFR-mutant NSCLC treated with TKI. Given the heterogeneity in advanced-stage EGFR-mutant NSCLCs and the need to optimize therapeutic regimens, further and prospective studies are warranted. Citation Format: Soohyun Hwang, Hyukjung Kim, Yeong Hak Bang, Jun-Gi Jeong, Chang Ho Ahn, Seungeun Lee, Sanghoon Song, Aaron Valero Puche, JaeWoong Shin, Sehhoon Park, Hyun Ae Jung, Jong-Mu Sun, Yoon-La Choi, Jin Seok Ahn, Myung-Ju Ahn, Siraj Ali, Chan-Young Ock, Se-Hoon Lee. AI-powered assessment of morphologic likeness to small cell lung cancer (SCLC) predicts progression to SCLC and TKI response in EGFR-mutant NSCLC [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 4659.

De-escalation of Monitoring in Active Surveillance for Prostate Cancer: Results from the GAP3 Consortium

De-escalation of Monitoring in Active Surveillance for Prostate Cancer: Results from the GAP3 Consortium

Canadian Recommendations on Optimal Breast Biopsy Practices Developed Using a Modified Delphi Panel.

Canadian Recommendations on Optimal Breast Biopsy Practices Developed Using a Modified Delphi Panel.

CT-guided biopsy of 18F-piflufolastat radiotracer avid lesions in osseous metastatic prostate disease: Initial experience, technical factors and biopsy yield.

CT-guided biopsy of 18F-piflufolastat radiotracer avid lesions in osseous metastatic prostate disease: Initial experience, technical factors and biopsy yield.

Deciphering Deception: Pancreatic Mass Presenting as Post-Transplant Lymphoproliferative Disorder

ABSTRACT Post-transplant lymphoproliferative disorder (PTLD) represents a spectrum of lymphoid proliferations occurring in immunocompromised transplant recipients, often associated with Epstein-Barr virus (EBV). PTLD frequently manifests at extranodal sites, posing diagnostic challenges due to its variable clinical presentation and potential mimicry of other malignancies. Here, we report a rare case of PTLD presenting as a pancreatic mass in a 68-year-old renal transplant recipient, who exhibited progressive gastrointestinal symptoms including nausea, vomiting, and jaundice. Initial imaging revealed a pancreatic head mass and extensive lymphadenopathy. Although an initial lymph node biopsy was inconclusive, endoscopic ultrasound-guided biopsy of the pancreatic mass confirmed diffuse large B-cell lymphoma, specifically activated B-cell type, indicating monomorphic PTLD. The patient's management included immunosuppression reduction and initiation of mini-R-CHOP chemotherapy. This case highlights the atypical PTLD presentation involving atypical sites such as the pancreas, emphasizing the need for persistent clinical suspicion and comprehensive diagnostic evaluation in post-transplant patients. Early recognition and a multidisciplinary approach to treatment are vital to optimizing outcomes in patients with PTLD presenting with atypical gastrointestinal manifestations.

Small Intestinal Neurofibroma With Atypical 17q11.2 Microdeletions: A Rare Cause of Abdominal Distension.

Neurofibromatosis Type 1 (NF1) is a rare autosomal dominant disorder caused by mutations or deletions in the NF1 gene, with approximately 5% to 11% of cases specifically attributed to the 17q11.2 microdeletion. While cutaneous manifestations are common, gastrointestinal involvement occurs in 10%-25% of cases, with symptomatic presentations being exceptionally rare. This report describes an unusual case of NF1 presenting with small intestinal neurofibroma, emphasizing diagnostic challenges and management strategies. A 22-year-old male with a 1-year history of recurrent abdominal distension was admitted. Physical examination revealed pathognomonic features of NF1, including axillary freckling and café-au-lait macules. Laboratory tests demonstrated anemia and hypoalbuminemia. Imaging and enteroscopy identified a stenotic ileal lesion with mesenteric lymphadenopathy. Initial biopsy suggested neurofibroma, confirmed by whole-exome sequencing revealing a 17q11.2 microdeletion involving the NF1 gene. Following palliative ileostomy, definitive surgical resection achieved complete remission. Histopathology confirmed small intestinal neurofibroma in NF1. This case underscores that gastrointestinal neurofibromas, though uncommon, should be considered in NF1 patients with persistent abdominal symptoms. A combination of clinical assessment, imaging, endoscopy, and genetic testing is essential for accurate diagnosis. Surgical intervention remains the definitive treatment for symptomatic lesions. The report expands the phenotypic spectrum of NF1 and highlights the importance of multidisciplinary management in rare gastrointestinal manifestations.

P088 IgG4-related disease: not losing sight of the diagnosis

Abstract Background/Aims We present a case of IgG4-related disease with ocular manifestations, negative serum IgG4 and a borderline initial biopsy, whose diagnosis was confirmed on repeat biopsy. Methods N/A Results The patient presented initially in December 2022 to ophthalmology with a 2-year history of intermittent bilateral painful lacrimal gland enlargement. All investigations were unremarkable including normal ANCA and IgG4 levels. Furthermore, the lacrimal gland biopsy showed chronic non-specific inflammation. She was referred from the GP with Raynaud’s, joint pain, fatigue, sicca symptoms and photosensitivity. She was under the care of the ophthalmology team for dacryoadenitis. She had a positive ANA 1:1600 titre, but otherwise negative serology and unremarkable urinalysis. There was no synovitis, no lymphadenopathy, but ongoing fullness of the upper eyelids. Her symptoms progressed. Extended myositis panel was normal, as was a CT-TAP. An ultrasound of her salivary glands was suggestive of bilateral sialadenitis affecting the submandibular glands. Her symptoms responded to a course of steroids given in primary care. An MRI orbit which showed lacrimal gland inflammation. A PET-CT was then requested which confirmed bilateral sialadenitis. A repeat lacrimal biopsy was performed, and this biopsy showed &amp;gt;50% positivity of IgG4 plasma cells. A PM/Scl-75 antibody has developed on repeat myositis screening She was diagnosed with IgG4-related disease, then started on 15mg of prednisolone and azathioprine. Glucocorticoid therapy was cautiously given in view of her PM/Scl-75 positivity. Conclusion IgG4-related disease is an immune mediated fibrosing and inflammatory disease, which affects multiple systems and commonly mimics certain vasculitidies such as GPA. It most commonly causes type one autoimmune pancreatitis, sclerosing cholangitis, periorbital swelling, bilateral sialadenitis or retroperitoneal fibrosis; however, it can affect any organ. The inflammation and fibrosis can cause the formation of tumour-like mass lesions, which often require biopsy. Due to the very non-specific presentations of IgG4-related disease, there are very detailed ACR/EULAR diagnostic criteria. Ocular manifestations occur in 17-23% of patients with IgG4-related disease. It can affect periorbital and orbital tissues, as well as extraocular muscles. Clinically, it presents with proptosis and dacryoadenitis. Whilst IgG4-related disease has a male preponderance, ocular disease specifically is more common in females. Once IgG4-related disease is diagnosed, therapy initially involves glucocorticoids. Following this, disease-modifying therapy such as methotrexate, azathioprine, cyclophosphamide or mycophenolate can be started. IgG4-related disease often mimics a variety of other conditions, and there are no perfect diagnostic tests. Early therapy helps suppress the inflammatory component of the disease and prevent more extensive fibrosis from forming. By maintaining a reasonable index of suspicion, patients can be diagnosed and started on effective treatment early. Disclosure T. Bond: None. N. Abdullah: None. S. Shaffu: None.

Incomplete concordance between laboratory and pathologic findings on post-induction kidney biopsy in pediatric patients with proliferative lupus nephritis.

Proliferative lupus nephritis (LN) is associated with increased risk of progression to kidney failure. After initial kidney biopsy, the utility and timing of subsequent biopsies is unknown. There is known discordance between the laboratory parameters used to diagnose LN and the histopathologic classification. We explore the utility of a subsequent kidney biopsy in guiding treatment of LN to determine the factors that warrant follow-up kidney biopsy. We conducted a single center retrospective cohort study of 30 SLE patients who underwent serial kidney biopsy for LN. Subjects were stratified based on their Childhood Arthritis and Rheumatology Research Alliance (CARRA) renal response into complete renal response (CRR) and incomplete renal response (IRR) groups at the time of second biopsy. Among 30 patients with LN, 11/18 in CRR group and 11/12 in IRR group had persistent proliferative nephritis at 1 ± 0.3years after initial biopsy. Only SLEDAI score was associated with an increased risk of persistent proliferative nephritis (p = 0.03). Initial CARRA response category was associated with outcome at last follow-up (mean 4.5years), with 11/18 CRR and 3/12 IRR achieving CRR at last follow-up at mean 4.5years (p < 0.001). Kidney biopsy directly impacted clinical decision in 7/18 CRR patients in the CRR group who had therapy escalated or reduction withheld due to biopsy findings. Available laboratory markers in LN are insufficient to identify children with ongoing proliferative nephritis. Follow-up kidney biopsy may be warranted for children with CRR at 1year after initial biopsy.

Expression of Epithelial-Mesenchymal Transition-Related Protein Claudin-10 in Oral Lichen Planus.

Oral lichen planus (OLP) is a common skin disease of indeterminate etiology that can affect the oral mucosa.Epithelial-mesenchymal transition (EMT) is a critical biological event that plays an essential rolein several functions, such as development, tissue repair, and stem cell dynamics, but also in cancer progression. Claudin-10, an EMT-related protein, is encoded by the CLDN10 gene in humans. In the present work, we studied the immunohistological expression of Claudin-10in OLP compared to normal oral mucosa. Fifty-one formalin-fixed, paraffin-embedded samples diagnosed as OLP from patients who did not receive any medications for the treatment ofOLP until the initial biopsy and ten formalin-fixed, paraffin-embedded samples diagnosed as comprising histologically normal oral mucosa tissue from resection margins of fibromas were immunohistochemically stained and analyzed for Claudin-10. The expression of Claudin-10 was evaluatedas significantly enhanced in OLP epithelium compared to controls (p<0.001).In the superficial epithelial layer, the staining was markedly higher in OLP than in the controls (p=0.008), and in the stroma, the staining was significantly stronger in OLP (p=0.027). In the intermediate epithelial layer, the staining was significantly weaker in OLP than in the controls (p=0.001), and in the basal layer, the staining was markedly reduced in OLP (p<0.001). The immunohistological expression of Claudin-10 has been described and analyzed in oral mucosal disease for the first time. Our findings indicate that the expression of Claudin-10 is dysregulated in OLP, possibly showing an interaction between the epithelium and the underlying tissue.

Surgical Practices in the Management of Pediatric Renal Tumors in Low- and Middle-Income Countries in the Asia Pacific Region.

To profile the surgical management of pediatric renal tumors rendered in low- and middle-income countries (LMICs) of the Asia Pacific region, which are not currently affiliated to any pediatric renal tumor cooperative group. An online survey was conducted among surgeons and urologists identified through the St. Jude Global Online Community Asia Pacific Pediatric Surgical Collaborations Group and participants of the St. Jude-VIVA Pediatric Surgical Oncology Symposium 2024. Ninety-six of 99 respondents provided replies, together representing 11 countries and 51 institutions. The majority (n = 90, 93.8%) were pediatric surgeons, with 26.7% having had subspecialty training in urology or oncology; 60% had experience managing Wilms tumors for more than 5years, though 64% performed less than three nephrectomies per year. A chemotherapy-first approach was specified by 31% of institutions, but employed by 40% of respondents in actual practice. Of those who practiced a chemotherapy-first approach, 44.8% did so without an initial biopsy. Notably, 38% of respondents and 55% of institutions did not adhere to a consistent protocol. Lymph node biopsy practices varied widely, with only 40.6% sampling routinely and 56.3% had ever experienced a tumor rupture during nephrectomy. Most (90%) perceived that Wilms tumors comprised 90% of all renal tumors in Asian children-contrary to known demographic data. There is substantial variation in the upfront surgical management of renal tumors in Asia Pacific LMICs. Considering the unique epidemiology of renal tumors in Asians and limited surgical capabilities, there is a great need for regional collaboration to better standardize the initial surgical management approach.

The presence of prostate MRI-visible lesions at follow-up biopsy as a risk factor for histopathological upgrading during active surveillance.

To prospectively determine the ability of visible lesions on multiparametric MRI (PI-RADS 4-5) and commonly used biomarkers to predict disease upgrading on rebiopsy in men with low-risk prostate cancer (PCa) enrolled in active surveillance (AS). For this prospective study, approved by the Institutional Review Board (IRB), we selected consecutive patients with low-risk, low-grade, and localized prostate cancer (PCa) from our active surveillance (AS) program, who were enrolled between March 2014 and December 2020. Patients who had undergone previous prostate surgery, hormonal treatment, had contraindications for mpMRI, or transrectal ultrasound-guided (TRUS) biopsy were excluded from this study. All eligible patients underwent mpMRI at least 3 months after the initial biopsy, followed by MRI-targeted TRUS-guided re-biopsy within 12 months after enrollment. The mpMRI studies were evaluated by an experienced radiologist using the PI-RADS v2 classification. Statistical significance was determined by comparing the results from the MRI with the pathology data from rebiopsy. There were 240 patients included. Overall upgrading rate was 41.2% (99/240), higher among patients classified as PIRADS 4 or 5 (77%). MRI sensitivity was 77.7% and specificity was 83.6% on re-biopsy. Visible lesion on mpMRI, PSA density and 3 + /12 positive cores at the first biopsy were good predictors of disease upgrade on rebiopsy. On our predictive model, patients with PI-RADS 4 or 5, PSA density > 0.15ng/mL/cm3, and 3 + /12 positive cores at first biopsy had 92.4% chance of having clinically significant PCa. Patients in AS with PI-RADS 4 or 5 lesions, PSA density > 0.15ng/mL/cm3 and 3 + /12 positive cores at first biopsy have a high probability of having significant PCa on re-biopsy.