Secondary hemophagocytic lymphohistiocytosis (sHLH) is a life-threatening hyperinflammatory syndrome characterized by diverse triggers and clinical manifestations. Early recognition and precise classification of sHLH are prerequisites for effective treatment. In recent years, significant progress has been made in the diagnosis and treatment of sHLH. This study systematically reviews the advances in the diagnosis and treatment of sHLH by integrating existing guidelines, expert consensus, and evidence from clinical research. In terms of diagnosis, in addition to the classic HLH-2004 criteria, emerging diagnostic tools such as the HScore scoring system and the optimized HLH inflammatory index (OHI) have improved the accuracy of early detection of sHLH. sHLH can be triggered by various endogenous and exogenous factors. Common etiological classifications include infection-associated HLH, malignant-tumor-associated HLH, macrophage activation syndrome, immunotherapy-associated HLH, and transplantation-associated HLH. Their clinical features and laboratory indicators differ, and understanding these characteristic differences is essential for classification, differential diagnosis, and treatment guidance. The treatment principles for sHLH include actively addressing the underlying condition suspected of inducing HLH, as well as implementing targeted treatment to control abnormal immune activation and excessive inflammatory responses. If the patient is stable and the trigger is clearly identified, systemic treatment of the underlying disease along with adequate support is sufficient. If the patient's condition deteriorates, specific treatment should be initiated immediately. In terms of specific treatment schemes, in addition to conventional chemotherapy, targeted therapies, particularly those against cytokines, have demonstrated favorable efficacy and have become crucial strategies for improving the prognosis of sHLH patients.

In clinical practice, for patients with thrombocytopenia or morphological and functional abnormalities, it is necessary to differentiate between hereditary thrombocytopenia (HT) and acquired (secondary) thrombocytopenia, which is crucial for patient management and the selection of treatment strategies. The symptoms of HT patients are heterogeneous. Based on the inheritance patterns of their gene mutations, including autosomal dominant inheritance, autosomal recessive inheritance, and X-linked inheritance, patients can be classified accordingly. The diagnosis and classification management of HT remain highly challenging. Although genetic testing is the gold standard for confirming HT, without prior evidence of the patient suspected of having HT, the probability of discovering diagnostic and pathogenic mutations through disease gene testing is much lower. In clinical practice, it is possible to narrow down the suspicion based on positive family history, typical clinical manifestations, laboratory tests, etc., thereby providing a rapid and definitive diagnosis for patients. Understanding the mutated genes and types in HT patients, and analyzing the sources of mutations, can help reveal the pathogenic mechanisms of gene mutations. This further predicts the impact of mutations and facilitates the development of patient-specific treatment and management strategies, as well as genetic counseling for patients.

With the widespread adoption of whole-slide scanning and the advancement of digital pathology techno-logy, the use of artificial intelligence (AI) for the analysis of peripheral blood and bone marrow smears has achieved notable breakthroughs, including the application of object detection (You Only Look Once, YOLO), weakly supervised contrastive learning, and multiple instance learning (MIL) in addressing cell recognition and domain shifts. Among them, MIL has been successfully applied in the auxiliary diagnosis of acute promyelocytic leukemia (M₃), effectively providing early warning of critical cases through global feature aggregation of the entire smear. Studies indicate that the accuracy of AI in determining subtypes of myeloproliferative neoplasm (MPN) is as high as 93.1%. The area under the receiver operating characteristic curve for AI predicting the risk of transformation to AML in patients with myelodysplastic syndrome (MDS) based on morphological features is 0.81. The correlation coefficient between AI-based automated quantification of hematopoietic tissue and pathologist assessment results reaches 0.78, confirming the value of AI in bone marrow biopsy pathological analysis, especially highlighting the potential of whole-slide-level models for clinical application. In terms of clinical practice application, a standardized model of AI pre-classification combined with manual review has been established for peripheral blood smear analysis. In bone marrow biopsy pathological analysis, although AI has achieved digital scanning, its current applications remain limited to cell counting and preliminary screening due to the complexity of cell lineages and the heterogeneity of dysplastic hematopoiesis. Furthermore, digital remote consultation plays an important role in alleviating the uneven distribution of medical resources. In the future, with the maturation of multi-modal fusion and large language model (LLM)-based report generation technology, AI is expected to evolve from a simple counting and classification tool into a comprehensive model integrating diagnosis, subtyping, and prognosis assessment.

VEXAS (Vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is a recently recognized autoinflammatory disease involving multiple systems, caused by somatic mutations in the ubiquitin-like modifier activating enzyme 1 (UBA1) gene. Since the disease was first reported in 2020, the number of cases has increased rapidly worldwide, and single case and case series have also been reported in China. VEXAS syndrome predominantly occurs in middle-aged and elderly males, with complex and diverse clinical manifestations that often involve multiple systems, including fever, skin lesions, chondritis, pulmonary infiltrates, vasculitis, and macrocytic anemia, making it prone to misdiagnosis as other rheumatic or hematologic diseases. Diagnosis of VEXAS syndrome highly relies on UBA1 gene sequencing, which should be performed in patients with characteristic clinical presentations mentioned above and vacuolization of myeloid and erythroid precursor cells observed in bone marrow biopsy. The treatment of VEXAS syndrome is highly challenging, and there is currently no comprehensive standardized treatment guideline. Glucocorticoids are the first-line treatment for controlling acute inflammation, but most patients exhibit steroid dependence. Traditional immunosuppressants are mostly ineffective or difficult to sustain, while Janus kinase (JAK) inhibitors, interleukin-6 (IL-6) inhibitors, and hypomethylating agents have shown good efficacy in some patients. Allogeneic hematopoietic stem cell transplantation is currently the only method that can cure VEXAS syndrome, but the benefits and risks for patients must be strictly evaluated. Targeted precision therapy against UBA1-mutant clones may become a future research direction.

The disease burden of multiple myeloma (MM) has been continuously increasing globally and in China. In 2021, the number of newly-diagnosed MM cases globally reached 148 754.63, and the number of deaths was 116 359.63. In China, the number of newly-diagnosed cases was 17 250, and the number of deaths was 12 984. The burden is heavier in males, elderly populations, and economically developed regions, while the rising prevalence in younger populations also deserves attention. The disease burden of MM is expected to continue to increase in the future, with high body mass index being an important associated risk factor. In 2025, the "Clinical Practice Guidelines in Oncology: Multiple Myeloma" issued by the National Comprehensive Cancer Network (NCCN) underwent rapid iterations from Version 1.2026 (hereafter referred to as 2026.V1) to Version 3.2026 (2026.V3), covering the entire process of MM diagnosis and treatment. This study compares and interprets the 2026.V1 guideline with the 2025.V2 version, and supplements the interpretation of updates in 2026.V2 and 2026.V3, aiming to help clinicians improve MM diagnosis and treatment, optimize the management of high-risk MM patients, and further enhance the prognosis of MM patients in China. The core content of this study can be summarized as "three additions, four optimizations, two focuses, and one emphasis". The "three additions" include the incorporation of individualized treatment for special populations, diagnostic and therapeutic pathways for MM with central nervous system (CNS) involvement, and management of monoclonal immunoglobulin deposition disease (MIDD). The "four optimizations" include strengthening the application of next-generation sequencing (NGS) and renal biopsy in diagnostic examination, incorporating International Myeloma Society/International Myeloma Working Group (IMS-IMWG) criteria in high-risk stratification for precise identification of high-risk patients, emphasizing four-drug combination priority for newly diagnosed patients and earlier use of immunotherapy for relapsed patients in treatment regimens, and clarifying the timing of PET/CT application in follow-up monitoring. The "two focuses" refer to focusing on infection prevention (refining infection control for treatments such as chimeric antigen receptor T cell therapy [CAR-T]) and renal function protection (clarif-ying preferred drugs and doses of bone-modifying agents). The "one emphasis" refers to giving attention to the management of solitary plasmacytoma and smoldering myeloma subtypes. The 2026.V1 guideline focuses on "precision, diversity, and whole-course management", highlighting multidisciplinary collaboration and individualized treatment, while the 2026.V2 and 2026.V3 further optimize drug recommendations for relapsed/refractory patients.

In 2022, there were approximately 2.5 million newly-diagnosed cases of lung cancer and 1.8 million deaths worldwide. In China, there were about 1.060 6 million newly-diagnosed cases and 733 300 deaths from lung cancer. The incidence and mortality of lung cancer ranked first among malignant tumors in China and globally. Non-small cell lung cancer (NSCLC) accounts for about 85% of lung cancer cases. Biomarker testing is crucial for its treatment selection. From December 2024 to January 2025, the National Comprehensive Cancer Network (NCCN) successively released the 2025 first (V1), second (V2) and third (V3) versions of clinical practice guidelines for NSCLC. Some of the updates are of great significance in the field of lung cancer diagnosis and treatment. The main updates in V1 include initial treatment evaluation, biomarker tes-ting, optimization of treatment pathways for specific gene mutations, and the addition of emerging targeted therapeutic drugs. Major newly added drugs include erdafitinib for the fibroblast growth factor receptor (FGFR) gene, zenocutuzumab for neuroregulatory protein 1 (NRG1) gene fusions, and trastuzumab deruxtecan for human epidermal growth factor receptor 2 (HER2) overexpression, providing patients with more treatment options. V2 adds ensartinib as the first-line preferred regimen for anaplastic lymphoma kinase (ALK) - rearranged NSCLC. V3 recommends nivolumab subcutaneous injection as an alternative to intravenous infusion for neoadjuvant system treatment. Despite the continuous emergence of new targets and therapies, how to achieve precise, accessible, and standardized testing and treatment remains the core challenge and optimization direction in future clinical practice.

Objective To construct a causal artificial intelligence (AI) framework model embedded with medical knowledge for AI-assisted diagnosis of bone marrow morphology in acute leukemia based on medical diagnostic logic. Methods A stage-by-stage causal AI diagnostic framework guided by medical knowledge was constructed using a dataset of 20 089 microscopic images of bone marrow and peripheral blood smears of 93 cases(69 patients with other diseases exhibiting normal bone marrow and peripheral blood; 24 patients with hematological diseases, including 14 cases of acute leukemia ) from Ruijin Hospital (2020-2023). Multiple specialized modules including bone marrow hyperplasia assessment module(M1), bone marrow cell classification module(M2), AKP score calculation module(M3), POX-stained leukaemic cell feature extraction module(M4), and CE -stained leukaemic cell feature extraction module(M5), were trained and tested in a 7∶3 ratio to extract key morphological features, including bone marrow hyperplasia status, the constituent ratio of bone marrow cells, and cytochemical staining patterns in both bone marrow and peripheral blood. Based on morphological characteristics of the peripheral blood and bone marrow of hematological diseases, the aforementioned specific AI recognition models were combined step by step according to medical diagnostic logic, integrating multi-dimensional morphological characteristics of bone marrow cells, and a two-stage process sequential diagnosis and prediction was carried(stage 1: integrating M1, M2, and M3;stage2: integrating modules 4 and 5). The first stage involved distinguishing between normal and abnormal bone marrow cases, while simultaneously identifying chronic myeloid leukemia. The second stage focused on the diagnosis of acute leukemia and the differentiation of its subtypes. An end-to-end AI diagnostic framework model was also established as a control and compared with the medical knowledge-embedded causal AI diagnostic framework model in real-case diagnostic testing. Results The medical knowledge-embedded causal AI diagnostic framework model achieved higher accuracy than the end-to-end AI framework model in real-case diagnostic testing at both stages (Stage 1 accuracy: 90.00% vs. 70.00%; Stage 2 accuracy: 83.33% vs. 66.67%). Conclusions Medical expertise and diagnostic logic play a crucial role in AI-assisted diagnosis of bone marrow cell morphology for hematological diseases. The application of the medical knowledge-embedded causal AI diagnostic framework model improves the accuracy and interpretability of AI-assisted diagnosis, providing a novel and generalizable paradigm for intelligent diagnosis of hematological diseases.

Objective To investigate the distribution of targetable mutations and clinical benefits of targeted therapy in Chinese patients with pulmonary large cell neuroendocrine carcinoma (LCNEC). Methods Retrospective data were collected from 44 consecutive treatment-naive LCNEC patients at the North Campus of Ruijin Hospital, Shanghai Jiao Tong University School of Medicine between January 2021 and December 2023. PD-L1 expression in pathological tissues was detected by immunohistochemistry, and mutations in 11 driver genes (ALK, ROS1, RET, NTRK1-3, MET, EGFR, BRAF, KRAS, HER2) were detected by quantitative real-time PCR. All patients were followed up for a median duration of 24 months. Results Among the 44 LCNEC patients, with a median age of 70.5 years, and males were predominant (93.2%, 41/44). Stage Ⅲ and Ⅳ disease accounted for 77.2% (34/44). The rates of lymph node metastasis and distant metastasis were 68.2% and 47.7%, respectively. Targetable mutations were identified in 11.4% (5/44) of the patients, including EGFR 19Del (1 case), ALK rearrangement (1 case), MET ex14 skipping mutation (1 case), and KRAS G12C mutation (2 cases). In the LCNEC pathological tissues, programmed death-ligand 1 (PD-L1) was negative in 79.5% (35/44) of the patients, while only 6.8% (3/44) demonstrated high PD-L1 expression (≥ 50%). Among the 34 Ⅲ-Ⅳ patients, the median progression-free survival (PFS) was 6.6 months in the three patients who received targeted therapy, which was significantly longer than the 4.8 months in the 31 patients who received non-targeted therapy (P < 0.05). The PFS reached 7 months and 11 months in patients with EGFR mutations and ALK rearrangements, respectively, whereas the patient with MET ex14 mutation responded poorly to targeted therapy, with a PFS of 2 months. Conclusions In the real-world Chinese population, LCNEC is highly aggressive, with over 70% of patients presenting at stage Ⅲ or Ⅳ. The low PD-L1 expression (negative rate of 79.5%) in pathological tissues indicates a limited population that may potentially benefit from immunotherapy. Additionally, 11.4% of patients have targetable mutations, among whom those with EGFR mutations or ALK rearrangements show favorable responses to targeted therapy. Molecular subtyping may have important guiding value for identifying the patient population who benefit from treatment for LCNEC.

Objective To investigate the expression of arginine and glutamate rich protein 1 (ARGLU1) in cervical cancer tissues and its relationship with clinicopathological characteristics and prognosis in cervical cancer patients, and to provide new clues for exploring the molecular mechanisms of cervical cancer development. Methods Fresh tissue samples of cancer tissues and adjacent tissues were collected from 32 consecutive cervical cancer patients diagnosed and treated at our hospital from January 2024 to November 2024. Additionally, paraffin-embedded samples of cancer tissue were collected from 152 cervical cancer patients, including 63 cases from our hospital (collected from June 2020 to March 2023, with postoperative follow-up until June 2025, follow-up duration ranging from 2.33 to 5.08 years) and 89 cases from a tissue microarray (collected from January 2010 to October 2011, with postoperative follow-up until March 2017, follow-up duration ranging from 5.50 to 7.25 years). Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry were used to detect the differences in ARGLU1 mRNA and protein expression between cervical cancer tissues and corresponding adjacent tissues. The relationship between the expression of ARGLU1 and the clinicopathological characteristics of cervical cancer patients was further analyzed, and prognosis was assessed using the Kaplan-Meier method. Results The relative expression of ARGLU1 mRNA in cervical cancer tissues was significantly higher than that in adjacent tissues [(2.72±0.52) vs. (1.33±0.44), (P<0.05)], and the high expression rate of ARGLU1 protein in cervical cancer tissues was also significantly higher than that in adjacent tissues (68.75% vs. 28.13%, χ²=10.573, P<0.05). The high expression rate of ARGLU1 and the relative expression level of ARGLU1 mRNA in cervical cancer patients with lymph node metastasis were higher than those in patients without lymph node metastasis [86.49% (32/37) vs. 66.09% (76/115), χ²=5.664, P<0.05; (3.177±0.255) vs. (2.539±0.482), t=-3.748, P<0.05]. Moreover, the differences in the high expression rate of ARGLU1 and the relative expression level of ARGLU1 mRNA among cervical cancer patients at different clinical stages were statistically significant [Stage Ⅰ 58.18% (32/55), Stage Ⅱ 69.23% (27/39), Stage Ⅲ 77.78% (28/36), Stage Ⅳ 95.45% (21/22), χ²=11.654, P<0.05; Stage Ⅰ (2.489±0.518), Stage Ⅱ (2.919±0.426), Stage Ⅲ (2.930±0.257), Stage Ⅳ (3.340±0.071), t=3.393, P<0.05]. Univariate survival analysis showed that the age of cervical cancer patients, the stage of cervical cancer, lymph node metastasis status, and the level of ARGLU1 expression were the factors affecting the prognosis of cervical cancer patients (P<0.05). The results of multivariate Cox risk model analysis showed that age, tumor stage, lymph node metastasis status, and ARGLU1 expression level were independent factors influencing the prognosis of cervical cancer patients (P<0.05). Prognostic analysis using the Kaplan-Meier method showed that patients with high ARGLU1 expression had significantly lower 5-year overall survival rate and 5-year disease-free survival rate compared to patients with low expression (44% vs. 84%, Log-rank χ²=14.580, P<0.05; 43% vs. 83%, Log-rank χ²=14.736, P<0.05). Conclusions ARGLU1 is highly expressed in cervical cancer tissues and is closely associated with adverse pathological features and poor prognosis, suggesting that ARGLU1 may play a significant role in the development and progression of cervical cancer, and it may serve as a potential prognostic biomarker and therapeutic target.

Objective To investigate the pathological and immunohistochemical features, diagnosis, and key points of differential diagnosis of calcifying fibrous tumors (CFT) occurring in the gastrointestinal tract. Methods The clinical and pathological data of 5 consecutive patients with gastrointestinal CFT admitted to Huangshan People's Hospital from October 2023 to November 2024 were retrospectively collected. The clinical and pathological features of gastrointestinal CFT were analyzed by HE staining and immunohistochemical staining, and relevant literature was reviewed. Results Among the 5 patients, there were 2 males and 3 females, aged between 49 and 68 years old. Four cases with single lesion occurred in the gastric body (3 cases) and fundus (1 cases), and one case involved multiple masses in the gastric body, ileum, and pelvic abdominal wall. Microscopically, the tumors exhibited abundant hyalinized collagen fibers mixed with a small number of fibroblasts and blood vessels. The cells showed no atypia, and mitotic figures were rare. Three cases were accompanied by psammoma bodies or dystrophic calcifications. Immunohistochemical staining showed that tumor cells expressed Vimentin (5/5), SMA (2/5), CD34 (1/5), and CD117 (2/5), but no DOG-1, Desmin, and S-100. The Ki-67 proliferation index was approximately 1%. All 5 patients were followed up for 6-18 months, and no tumor recurrence or metastasis was observed. Conclusions Gastrointestinal CFT is a relatively rare benign tumor that needs to be differentiated from other mesenchymal tumors, such as gastrointestinal stromal tumors and inflammatory myofibroblastic tumors. Characteristic histomorphological features, such as hyaline degeneration and dystrophic calcification, are helpful for diagnosis.

Objective To construct Candida glabrata epithelial adhesin EPA1 and EPA6 gene knockout strains and analyze the effects of gene knockout on the biofilm formation of Candida glabrata. Methods Using fusion PCR and homologous recombination techniques, EPA1 and EPA6 gene knockout constructs were generated, with genomic DNA of Candida glabrata strain ATCC 2001 and plasmid DNA carrying the selectable marker hygromycin resistance gene (HyR) as templates. The knockout constructs were transfected into ATCC 2001 using the lithium acetate transfection method to obtain Δepa1 and Δepa6 knockout strains. The virulence phenotypes of the knockout strains were observed through hydrophobicity tests and biofilm formation experiments. Results Compared with the standard strain ATCC 2001, whose hydrophobicity was 91.5%, the hydrophobicity of Δepa1 and Δepa6 obtained in this study decreased to 61.6% and 75.5%, respectively (P<0.05). After incubation at 30℃ for 4, 16, and 24 hours, the biofilm formation abilities of Δepa1 and Δepa6 were significantly lower than those of the standard strain ATCC 2001 (P<0.05). Conclusions The Candida glabrata EPA1 and EPA6 gene knockout strains are successfully constructed, and it is confirmed that the EPA1 and EPA6 genes can enhance strain virulence biofilm formation.

This study reports a case of a 44-year-old female patient with multiple myeloma (MM). Her condition was initially relieved after treatment with bortezomib combined with dexamethasone. However, due to the patient's failure to adhere to the treatment schedule, the disease progressed. After switching to CD38 monoclonal antibody therapy, the di-sease again achieved remission. After 5 months of treatment, the patient suddenly experienced abdominal distension accompanied by cessation of anal gas and stool passage. Abdominal CT indicated intestinal obstruction. The patient underwent exploratory laparotomy, intestinal resection and anastomosis, and abdominal drainage. Postoperative T-cell spot test (T-SPOT) and pathological results confirmed the diagnosis of isolated intestinal tuberculosis complicated by incomplete intestinal obstruction. The patient received six months of quadruple anti-tuberculosis therapy (rifampicin 450 mg once daily orally, isoniazid 300 mg once daily orally, pyrazinamide 500 mg three times daily orally, streptomycin 750 mg once daily intramuscularly), after which her tuberculosis condition improved. However, due to the suspension of anti-tumor therapy, the MM progressed. The patient discontinued treatment for financial reasons and ultimately passed away 19 months after surgery due to MM progression. A review of relevant cases in the database shows that one patient who developed intestinal tuberculosis after heart transplantation was diagnosed with MM during anti-tuberculosis treatment, which later progressed to aggressive plasma cell leukemia. Although induction chemotherapy was administered, the patient experienced retroperitoneal hemorrhage and pancytopenia, and ultimately transitioned to palliative care. This case highlights that patients in an immunosuppressed state (such as MM) have a significantly increased risk of tuberculosis infection, among which extrapulmonary manifestations, such as intestinal tuberculosis, are relatively rare. Due to its atypical clinical manifestations, it is prone to being missed or misdiagnosed. Such infections may interfere with the course of antitumor therapy and affect patient prognosis. Clinicians should remain vigilant and strengthen differential diagnosis.

Mutations in the ATP13A2 gene are associated with various neurodegenerative diseases, including Kufor-Rakeb syndrome (KRS), hereditary spastic paraplegia type 78 (SPG78), neuronal ceroid lipofuscinosis type 12 (CLN12), and amyotrophic lateral sclerosis (ALS). This study reports a case of a rare homozygous mutation in the ATP13A2 gene (Exon12 c.1062G>T: p.Lys354Asn). The patient, a 35-year-old female, initially presented with involuntary tremors in both upper limbs, which were considered posture- and action-induced myoclonus. The symptoms progressively involved both lower limbs, accompanied by bradykinesia, spastic gait in the lower limbs, cognitive impairment, and psychiatric behavioral abnormalities. Electromyography (EMG) revealed paroxysmal EMG discharges in both lower limbs when the patient was in the standing and semi-recumbent positions, with irregular discharge frequencies. Somatosensory evoked potential testing indicated a significant increase in P25 amplitude, suggesting a cortical origin of the myoclonus. The patient was treated with levetiracetam combined with clonazepam to alleviate the myoclonus and levodopa/benserazide combined with pramipexole for parkinsonian symptoms. Significant improvements were observed in myoclonus, muscle rigidity, and bradykinesia, and the patient regained independent ambulation. This mutation site in this patient has not been previously reported in the PubMed database, the Chinese Medical Journal (CMJ) Full-Text Database, Wanfang Database, or the China National Knowledge Infrastructure (CNKI). Amino acid conservation analysis indicated that this site was highly conserved among six vertebrate species, including humans, rats, mice, cattle, chimpanzees, and pigs. According to the genetic mutation classification standards and guidelines of the American College of Medical Genetics and Genomics (ACMGG), this mutation is considered likely pathogenic, exhibiting overlapping phenotypic features of KRS and SPG78. The phenotype of coarse limb myoclonus of cortical origin represents the first reported case associated with this gene, thereby expanding its clinical phenotypic spectrum.

Lung cancer is one of the most common malignancies worldwide. In 2022, there were approximately 1 060 600 newly-diagnosed cases globally. Uncommon metastatic sites of lung cancer include the pancreas (5%-10%), gastrointestinal tract, kidneys, heart, skin (more common in small cell lung cancer). Among these, lung cancer metastasis to the seminal vesicle is extremely rare and prone to being missed or misdiagnosed. This paper reports a case of a patient presen-ting with dysuria and prostate enlargement: Ultrasonography and enhanced CT of the abdomen and pelvis showed a mass in the right seminal vesicle, and enhanced CT of the chest showed a space-occupying lesion in the upper lobe of the right lung. Pathological examination of a puncture biopsy of the right lung lesion confirmed adenocarcinoma. Based on positive immunohistochemical markers (TIF-1 and Napsin), it was diagnosed as primary lung adenocarcinoma. Pathological examination of a puncture biopsy of the seminal vesicle mass confirmed poorly differentiated adenocarcinoma,and immunohistochemical markers were negative for CA125, CK7, PSA, and CK20, but positive for TIF-1 and Napsin, suggesting lung cancer metastasis to the seminal vesicle. Based on comprehensive examinations, the patient was finally diagnosed with stage Ⅳ lung adenocarcinoma. Molecular targeted therapy with 125 mg of icotinib tablets was administered, and ¹²⁵I seeds were implanted in both the lung and seminal vesicle lesions under CT guidance for radiotherapy. Follow-up of two months showed no progression of the lesions. This case report enriches the spectrum of metastatic sites of lung cancer and highlights the need to further summarize the clinical characteristics and prognosis of patients with seminal vesicle metastasis from lung cancer.