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- Primary carcinoma of the seminal vesicle is an exceptionally rare genitourinary malignancy, with evidence limited largely to case reports and small retrospective series. Diagnosis requires exclusion of more common secondary involvement from prostate, bladder, or rectal carcinoma through integration of clinical findings, imaging, histomorphology, and immunohistochemistry. Patients typically present with nonspecific symptoms and often have locally advanced disease. Computed tomography identifies retrovesical masses, while magnetic resonance imaging provides superior local staging. Core biopsy may establish the diagnosis, although definitive classification may require resection. The typical immunophenotype is CK7-positive, often with CA-125 expression, and negative for PSA, PAP, and NKX3.1; however, no marker profile is invariable. A contemporary panel including GATA3, p63/p40, uroplakin markers, CK20, p53, CD44, CDX2, and SATB2 is important for excluding urothelial and intestinal primaries. Conventional papillary adenocarcinoma is the predominant histological type, with mucinous, clear cell, squamous, and neuroendocrine variants also reported. Non-carcinomatous primary seminal vesicle neoplasms, including germ-cell tumours, sarcomas, solitary fibrous tumour, and mixed epithelial and stromal tumour, form an important differential diagnosis. Complete surgical excision with negative margins is the treatment most consistently associated with prolonged survival in the reported cases and is generally regarded as the only potentially curative option, whereas radiotherapy, chemotherapy, and hormonal therapy are selectively used for advanced or recurrent disease. International registries and collaborative molecular studies are needed to improve diagnosis, treatment, and follow-up. - Source: PubMed
Publication date: 2026/09/11
Zachariou AthanasiosDaligkaros GrigoriosFiliponi Maria - - Source: PubMed
Publication date: 2026/09/15
Leiva-Murillo Enmanuel AJerónimo Carles Cebrián ISingh-Kaur KaramjotMatas-García Ana - Prostatic involvement by bladder urothelial carcinoma is uncommon, and prostatic stromal invasion usually indicates aggressive tumor biology and poor prognosis. Such patients may present with prostatic enlargement or a mass at the bladder neck-prostate junction, while serum prostate-specific antigen (PSA) may remain within the normal range. This diagnostic overlap may lead to clinical confusion with benign prostatic hyperplasia or primary prostatic tumors. - Source: PubMed
Publication date: 2026/08/21
Wang ChengWang MengyunHe Yue - 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