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Related articles to: NKX3-1 antibody
- Esophageal squamous cell carcinoma (ESCC) classically presents with progressive dysphagia and weight loss, but atypical presentations may redirect the diagnostic workup before the esophageal primary is identified. We report a case illustrating the simultaneous convergence of three diagnostic pitfalls: absence of dysphagia, bone-predominant metastatic presentation initially managed as carcinoma of unknown primary (CUP), and negative p40 staining in a vertebral biopsy in a patient subsequently confirmed to have invasive mid-esophageal squamous cell carcinoma. A 66-year-old African American man with dementia, active tobacco exposure, and prior alcohol use disorder presented with constipation, abdominal pain, melena, fever, nausea, vomiting, and progressive back pain. Dysphagia or odynophagia was not documented. CT of the abdomen and pelvis demonstrated diffuse lytic osseous metastases. During evaluation and palliation of symptomatic L2 disease, kyphoplasty and radiofrequency ablation were performed, and bilateral core biopsies showed poorly differentiated carcinoma that was AE1/AE3-positive but negative for p40, CK7, CK20, TTF-1, S100, GATA-3, PAX8, and NKX3.1, yielding an initial diagnosis of CUP. Subsequent chest CT revealed esophageal wall thickening with intraluminal debris. Esophagogastroduodenoscopy (EGD) identified a non-obstructive ulcerated mid-esophageal lesion, and biopsy confirmed invasive squamous cell carcinoma. Poor performance status precluded systemic therapy; palliative external-beam radiation was initiated after diagnosis but discontinued because of clinical deterioration, and the patient transitioned to hospice before passing several weeks after diagnosis. Melena is a gastrointestinal alarm feature, and the combination of gastrointestinal bleeding and an esophageal imaging abnormality warrants timely endoscopic evaluation even when dysphagia is not reported or the symptom history is unreliable. Negative p40 staining in a poorly differentiated, potentially decalcified bone specimen may reflect loss of lineage-marker expression, technical antigen degradation, or both. Tissue or plasma genomic profiling and emerging cell-free DNA methylation classifiers could complement the workup but would not replace direct biopsy of a radiographically suspicious esophageal lesion. In metastatic poorly differentiated carcinoma, lack of documented dysphagia should not exclude an esophageal primary, particularly in patients with cognitive impairment. A p40-negative bone biopsy does not rule out squamous lineage. Timely EGD and integrated clinicopathologic assessment are essential when clinical or imaging findings suggest esophageal involvement. - Source: PubMed
Publication date: 2026/08/21
Brim HassanBajwa WardahBrim AnasAduli FarshadAbdelLatief AmroZafar RabiaLaiyemo Adeyinka OAshktorab Hassan - Lung adenocarcinoma rarely presents as a grossly or bronchoscopically visible tumor protruding into the bronchial lumen. This multicenter retrospective study aimed to reappraise this unusual growth pattern, termed endobronchial polypoid adenocarcinoma, and to examine its clinicopathological characteristics. We retrospectively reviewed 2261 surgically resected primary lung adenocarcinomas from 4 institutions and identified 11 cases of endobronchial polypoid adenocarcinoma, accounting for ∼0.5% of the included cases. All tumors showed both pulmonary parenchymal and endobronchial components, and direct continuity between the 2 components through the bronchial wall was identified in 8 cases. A lepidic pattern was observed in the pulmonary parenchymal component in 8 cases. In the involved endobronchial mucosa, abrupt transitions between non-neoplastic ciliated epithelium and adenocarcinoma were identified in all cases. Spread through air spaces was observed in 10 of the 11 cases. EGFR mutations were detected in 3 of 9 examined cases. TTF-1 positivity and NKX3.1 negativity supported a terminal respiratory unit-type rather than bronchial gland-type origin. Postoperative recurrence was observed in 5 patients, with a median time to recurrence of 6 months. Two patients died of the disease. These findings suggest that endobronchial polypoid growth may represent a rare, macroscopically recognizable manifestation of airway-associated progression in lung adenocarcinoma, conceptually related to STAS and endobronchial spreading of adenocarcinoma (EBSA). - Source: PubMed
Publication date: 2026/08/25
Shimazu MiyukiTakahara TaishiOishi RisaSeki MasanoriSatou AkiraYamamoto YukiMaeda NagakoHinokimoto AkanaKurita NaokiTaniguchi NatsukiOhashi AkikoTakahashi EmikoIto SatoruTsuzuki Toyonori - Prostate cancer (PCa) is one of the most prevalent malignancies affecting male health globally, ranking as the fifth leading cause of cancer-related mortality in men. Post-translational modifications (PTMs), encompassing a diverse array of biochemical alterations such as methylation, acetylation, phosphorylation, ubiquitination, SUMOylation, glycosylation, and lactylation, constitute a critical category of epigenetic regulatory mechanisms that modulate numerous cellular processes in both physiological and pathological contexts. Despite their fundamental importance, the precise functional implications of PTMs in PCa pathogenesis remain incompletely elucidated. Current evidence has established that multiple oncogenic signaling pathways (including AR, PTEN/PI3K/AKT, CDK4/6-RB, Wnt/β-catenin, and JAK/STAT3), key transcription factors (such as AR, p53, ERG, NKX3.1, FOXA1, HOXB13, KLF, and MYC), and specific histone modification patterns are intimately associated with PCa progression. Furthermore, emerging studies have implicated PTMs in mediating drug resistance and immune suppression in PCa, representing two major clinical challenges in contemporary PCa management. Beyond these canonical regulatory mechanisms, metabolism-associated and emerging PTMs further connect metabolic reprogramming with AR variant splicing, lineage plasticity, immune modulation, and therapeutic resistance. We also discuss the clinical implications of PTMs in PCa, including PTM-directed clinical trials, targeted protein degradation strategies, and diagnostic or prognostic biomarker development. In light of these critical findings, this review systematically synthesizes current research elucidating the mechanistic roles of PTMs in regulating these molecular determinants of PCa progression, with the aim of providing a comprehensive understanding of PTM-mediated regulatory networks and offering translational insights for potential clinical applications. - Source: PubMed
Publication date: 2026/08/24
Ren HuanLi XuanjiJiang ZhiliangBai YunjinAi Jianzhong - Allergic rhinitis (AR) is a common airway disease characterized by epithelial barrier dysfunction and Type 2 inflammation. Although the aryl hydrocarbon receptor (AhR) regulates mucosal immunity and epithelial homeostasis, its role in epithelial pathology in AR remains poorly defined. We sought to determine the contribution of AhR signaling to AR pathogenesis and to identify downstream mechanisms linking barrier dysfunction to Type 2 inflammation. - Source: PubMed
Publication date: 2026/08/24
Yuan XuanZeng YixiangXie ShaobingZhong WeiGu WenjingHu MinxuanZhang HuaXu AngelJiang WeihongXie ZhihaiGao Peisong - Decompensated heart failure (DHF) may occasionally conceal an underlying systemic malignancy. Persistent hematological abnormalities, particularly thrombocytopenia and markedly elevated alkaline phosphatase (ALP), extending beyond the acute phase of illness warrant systematic evaluation for bone marrow pathology or infiltrative disease, irrespective of the presenting diagnosis. A 53-year-old man with no prior comorbidities presented with DHF, bicytopenia (anemia and thrombocytopenia), and markedly elevated ALP. He developed disseminated intravascular coagulation (DIC) during hospitalization, managed with fresh frozen plasma (FFP), platelet concentrates, and cryoprecipitate, with subsequent resolution; however, thrombocytopenia and ALP elevation persisted. Bone marrow examination revealed infiltration by metastatic adenocarcinoma. Despite comprehensive evaluation including gastrointestinal endoscopies, contrast-enhanced computed tomography (CT), and 18-fluorodeoxyglucose positron emission tomography-CT (18-FDG PET-CT), the primary site remained elusive in the setting of multiple elevated tumor markers: prostate-specific antigen (PSA), carcinoembryonic antigen (CEA), and carbohydrate antigen (CA) 19-9. Immunohistochemistry of the bone marrow biopsy demonstrated positivity for cytokeratin (CK) and NKX3.1, establishing prostatic origin. Subsequent prostate biopsy confirmed left-lobe prostatic adenocarcinoma with a Gleason score of 4+3=7 (Grade Group 3), tumor comprising 70% of the biopsy core, and perineural invasion, consistent with high-risk locally advanced disease. The patient was commenced on androgen deprivation therapy (ADT). Persistent thrombocytopenia and markedly elevated ALP may represent the sole initial manifestation of occult metastatic prostate cancer, even in young patients with no urological symptoms. Immunohistochemistry, particularly NKX3.1, is indispensable in establishing prostatic origin when the primary site remains radiologically occult after comprehensive investigation. - Source: PubMed
Publication date: 2026/07/13
Krishnegowda RaviRao V R SrinidhiMalipatil Ramangouda