BackgroundBody mass index (BMI) has been associated with improved outcomes in several malignancies, including prostate cancer. However, the impact of BMI on treatment efficacy, particularly with androgen receptor pathway inhibitors (ARPIs), in metastatic hormone-sensitive prostate cancer (mHSPC) remains insufficiently characterized. This study aimed to evaluate the association between BMI and radiographic progression-free survival (rPFS) in patients with mHSPC receiving first-line therapies.MethodsWe retrospectively analyzed 330 patients with newly diagnosed mHSPC. Patients were stratified by their treatment regime and baseline BMI. rPFS was assessed using Kaplan-Meier analysis and Cox proportional hazards models. Multivariate analyses included clinically relevant covariates and factors significant in univariate analyses.ResultsWith a median follow-up of 47 months, median rPFS for the entire cohort was 34 months. Patients with BMI≥25 kg/m[2] demonstrated significantly longer median rPFS. Higher BMI was associated with favorable baseline characteristics, including better ECOG performance status and higher hemoglobin levels. In multivariate analysis, liver metastases, high-volume disease, low hemoglobin, elevated alkaline phosphatase, and treatment modality remained independent predictors of rPFS, whereas BMI did not retain independent significance. Among overweight patients receiving ARPIs, enzalutamide showed a numerically longer rPFS compared with abiraterone, although this difference was not statistically significant.ConclusionHigher BMI was associated with prolonged rPFS in patients with mHSPC, supporting a potential obesity paradox in this population. While BMI was not an independent predictor in multivariate analysis, it may reflect underlying patient fitness and disease biology. These findings warrant prospective validation into metabolic factors influencing ARPI efficacy.

Liver metastases (LM) in small cell lung cancer (SCLC) are associated with a limited response to immune checkpoint inhibitors (ICIs). In this trial, we evaluated the efficacy of first-line envafolimab plus chemotherapy in SCLC patients with LM and explored potential predictive biomarkers. Patients received envafolimab in combination with chemotherapy for four cycles, followed by envafolimab monotherapy until disease progression or unacceptable toxicity. The primary endpoint was progression-free survival (PFS). Secondary endpoints included safety, objective response, overall survival, and identification of predictive biomarkers. Whole-exome sequencing (WES), transcriptome sequencing, DNA methylation sequencing, circulating tumor DNA (ctDNA) analysis, and cell-free DNA (cfDNA) methylation sequencing were performed on tumor tissues and peripheral blood samples. The objective response rate (ORR) was 75.9%, the disease control rate (DCR) was 100%, and the median PFS was 4.3 months. Granulocyte turnover and TNFRSF9 expression emerged as key indicators across transcriptomic and epigenomic analyses, and were associated with prognosis and liver dysfunction. cfDNA-based assessment of granulocyte turnover reflected both liver damage and tumor dynamics, suggesting its potential for real-time monitoring. These findings suggest that granulocyte activity may contribute to an immunosuppressive tumor microenvironment and serve as a predictive marker for treatment stratification in SCLC with LM.

Metastatic pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis, and survival beyond a decade is exceptional. We report a 59-year-old man with stage IV PDAC presenting with oligometastatic disease involving a pancreatic head/uncinate primary tumor, clustered right posterior hepatic metastases, and left supraclavicular nodal metastasis. Endoscopic ultrasound-guided biopsy of the pancreatic primary lesion confirmed poorly differentiated adenocarcinoma; metastatic involvement was diagnosed radiographically. Baseline disease was limited to three locally treatable sites, and CA19-9 remained within the normal range throughout follow-up. The patient received four courses of high-dose hypofractionated, high-BED lesion-directed radiotherapy with limited systemic therapy. RT1 treated the three baseline disease sites with concurrent oral S-1. Post-RT1 MRI showed partial response of the pancreatic primary tumor and right posterior hepatic metastases according to RECIST 1.1, and PET/CT showed resolution of abnormal pancreatic hypermetabolism in the pancreatic lesion, with a post-treatment SUVmax of 1.1. Metachronous oligoprogression subsequently occurred in the liver and lung: RT2 and RT3 each treated one new hepatic lesion with concurrent S-1, and RT4 treated three clinically progressive pulmonary metastatic targets without concurrent systemic therapy. No grade ≥3 treatment-related toxicity was documented. After RT4, no further systemic antitumor therapy was administered. Radiographic non-progression was documented for approximately 5 years and 5 months after the final thoracic radiotherapy, until February 2023. At telephone follow-up on May 27, 2026, the patient remained alive, independent in daily living, and had an ECOG performance status of 0-1. Overall survival exceeded 11 years and 8 months from diagnosis. This case highlights exceptional long-term survival in oligometastatic and oligoprogressive metastatic PDAC after repeated high-BED lesion-directed radiotherapy. This observation is hypothesis-generating and should not be interpreted as evidence that radiotherapy can replace systemic therapy.

Gastroblastoma is an extremely rare tumor. We report a case of an 8-year-and-10-month-old boy presented with abdominal pain. Ultrasound examination found a solid lesion at the greater curvature of the stomach, and nodules were also discovered at the right adrenal gland and the splenic hilum simultaneously. Pathology confirmed a diagnosis of gastroblastoma with metastases. After 2 years of follow-up, multifocal metastatic gastroblastoma in the liver and the left iliac fossa was detected and confirmed. To the best of our knowledge, this is the first report in the English literature of a pediatric gastroblastoma with metastasis and recurrence.

68Gallium NODAGA-JR11, a somatostatin receptor (SSTR) antagonist, exhibits superior sensitivity in detecting hepatic metastases of neuroendocrine tumors compared with the agonist tracer 68Ga-DOTANOC PET/CT. In the presented case of rectal neuroendocrine tumor, both tracers identified the primary lesion and regional lymph node involvement; however, NODAGA-JR11 PET/CT revealed multiple hepatic metastases not visualized on DOTANOC imaging, resulting in disease upstaging. The enhanced lesion detection is attributed to the antagonist's ability to bind a greater number of receptor sites and reduced hepatic background uptake. These findings highlight the potential impact of NODAGA-JR11 PET/CT on clinical staging and therapeutic decision-making in metastatic neuroendocrine tumors.

Adenoid cystic carcinoma (ACC) with intracranial metastasis and sixth cranial nerve (CN VI) palsy, spinal metastases, and malignant spinal cord compression is an uncommon clinical entity. We present a case of a patient exhibiting this constellation of findings secondary to the parotid ACC. A 55-year-old man with no identifiable risk factors for ACC presented with a 10-year history of a left parotid tumor. He underwent two surgical resections and received one cycle of chemotherapy. Subsequently, his disease progressed locoregionally and systemically. He developed diplopia due to left sixth cranial nerve palsy caused by an intracranial metastatic lesion, together with complete spinal cord syndrome secondary to thoracic spinal metastases with malignant spinal cord compression. The patient was treated with whole-brain radiotherapy for intracranial metastasis and palliative spinal radiotherapy for spinal cord compression, achieving neurological stabilization without further deterioration. Systemic therapy with a tyrosine kinase inhibitor was subsequently initiated (lenvatinib 24 mg QD). The lungs are the most common site of distant metastasis in ACC, followed by bone and liver involvement. However, intracranial dissemination may occur rarely and should be considered in the clinical evaluation of these patients.

Lung metastases are the second most common visceral metastatic site in gallbladder cancer (GBC); however, population-based evidence regarding this metastatic pattern remains limited. In this study, we sought to define the incidence trend of lung metastasis in GBC, identify risk factors associated with its occurrence, and comprehensively assess survival outcomes in this patient population. Data on GBC patients diagnosed 2010-2022 were retrieved from the Surveillance, Epidemiology, and End Results (SEER) database. Joinpoint regression was used to evaluate temporal trends. Multivariate logistic regression was performed to identify independent risk factors. Overall survival (OS) was analyzed via Kaplan-Meier, multivariate Cox regression, and propensity score matching (PSM). The incidence of lung metastasis in GBC patients showed a modest but statistically significant increasing trend from 2010 to 2022, with an average annual percent change of 3.6% (95% CI 1.4%-5.8%, P<0.05). Independent risk factors for lung metastasis included advanced N stage (N1 and N2) and synchronous bone, liver, or brain metastases. GBC patients with lung metastasis exhibited poor prognosis, with a median OS of 5.0 months (95% CI 4.0-6.0). The 1-, 2-, and 3-year OS rates were 18.1%, 4.3%, and 1.0%, respectively. Isolated lung metastasis conferred better survival than concurrent other distant metastases (median OS: 7.0 vs. 4.0 months, P<0.001). Chemotherapy significantly improved survival (HR=0.39, 95% CI 0.32-0.49), whereas primary tumor resection showed no benefit after PSM. Survival rates in this population did not change significantly between 2010 and 2022. In conclusion, this comprehensive, population-based analysis provides contemporary insights into the epidemiology and management of this challenging patient population.