Zhejiang Cancer Hospital is a government-run cancer hospital located in Hangzhou, China.Zhejiang Cancer Hospital became the affiliated Cancer Hospital of university of Chinese Academy of Sciences, and the hosting hospital of Institute of Cancer Research and Basic Medical Science of Chinese Academy of Medical Sciences on May 9, 2019 (Official announcement).The hospital offers medical services to cancer patients from Zhejiang province and nearby regions. The hospital was established in 1963 as one of the four earliest cancer hospitals in China. The hospital also houses the Zhejiang Cancer Research Institute, where scientists and cancer clinicians perform research to find methods for curing cancer..
Mucinous gastric adenocarcinoma (MGC) is a rare, aggressive malignancy. This study aimed to explore whether MGC is associated with poorer survival compared with nonmucinous gastric adenocarcinoma (NMGC) and to further investigate the potential impact of neoadjuvant chemotherapy (NAC) on MGC by assessing overall survival (OS), tumor regression grade (TRG), and histological subtypes. A retrospective analysis was conducted on 492 patients with MGC and 7945 patients with NMGC undergoing resection at Zhejiang Cancer Hospital (2014–2023). Patients were categorized into neoadjuvant and surgery groups. MGC was further classified as pure (≥ 80
Chest X-ray (CXR) plays a pivotal role in clinical diagnosis, and a variety of task-specific and foundation models have been developed for CXR interpretation. However, these models often struggle to adapt to new diagnostic tasks and complex reasoning scenarios. Recently, LLM-based agents have emerged as a promising paradigm for CXR analysis, enhancing model’s capability via tool coordination, multi-step reasoning, and team collaboration, etc. However, existing agents often rely on a single diagnostic pipeline and lack mechanisms for assessing tools’ reliability, limiting their adaptability and credibility. To this end, we propose CXRAgent, a director-orchestrated, multi-stage agent for CXR interpretation, where a central director coordinates the following stages: (1) Tool Invocation: The agent strategically orchestrates a set of CXR-analysis tools, with outputs normalized and verified by the Evidence-driven Validator (EDV), grounding diagnostic outputs with visual evidence to support reliable downstream diagnosis; (2) Diagnostic Planning: Guided by task requirements and intermediate findings, the agent formulates a targeted diagnostic plan, assembles an expert team, defines member roles, and coordinates their interactions to enable adaptive collaborative reasoning; (3) Collaborative Decision-making: The agent integrates insights from the expert team with accumulated contextual memories, synthesizing them into an evidence-backed conclusion. Experiments on diverse tasks show that CXRAgent achieves strong performance with reliable visual grounding, attaining overall accuracies of 67.0% on CheXbench and 75.6% on Medical-CXR-VQA, and a RaTEScore of 0.569 on MIMIC-CXR for report generation. Code and data are available at this link.
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with a poor prognosis, particularly in the presence of liver metastases. The mechanisms by which metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD), influences PDAC progression and metastasis remain poorly understood. This study investigates the role of MASLD in fostering an immunosuppressive microenvironment conducive to PDAC liver metastases and identifies the macrophage migration inhibitory factor (MIF)-CD44 axis as a key mediator of this process. Utilizing data from the UK Biobank (450,754 participants, median follow-up 14.5 years), we observed an overall increased risk of PDAC in the MASLD population (HR: 3.48; 95% CI: 2.69–4.50; P < 0.0001). Clinical cohorts confirmed the strong association between MASLD and hepatic metastases (OR: 7.06; 95% CI: 4.62–10.78; P < 0.0001). Experimental mouse models demonstrated that MASLD enhances tumor cell stemness, immune evasion, and focal adhesion in metastatic liver tissues. Mechanistically, MASLD-induced MIF secretion promotes CD44-positive PDAC cell migration, stemness, and adhesion. Targeting MIF, either genetically or pharmacologically using the MIF tautomerase inhibitor IPG1576 significantly attenuated liver metastasis in preclinical models. Validation in patient samples revealed elevated hepatic MIF and CD44 expression in MASLD-associated PDAC liver metastases. This study highlights the MIF-CD44 axis as a promising therapeutic target and underscores the importance of tailoring treatments for PDAC patients with concurrent MASLD.
Although poly(adenosine diphosphate-ribose) polymerase inhibitors (PARPis) and bevacizumab were approved as first-line maintenance for advanced ovarian cancer (OC), evidence comparing this combination with PARPi monotherapy, especially in BRCA-mutated/homologous recombination-deficient (HRD) patients, is lacking. This study compared combined fuzuloparib (a PARPi) plus apatinib (a vascular endothelial growth factor receptor-2 inhibitor) with either fuzuloparib or placebo as first-line maintenance in patients with advanced OC. Patients who had newly diagnosed, advanced OC and responded to first-line, platinum-based chemotherapy were randomized 2:2:1 to receive combined fuzuloparib (100 mg twice daily) plus apatinib (375 mg daily), fuzuloparib (150 mg twice daily) plus placebo, or double-placebo treatment. The primary end point was blinded independent review committee (BIRC)-assessed progression-free survival (PFS). Six hundred seventy-four patients were randomized to receive fuzuloparib plus apatinib (n = 269), fuzuloparib (n = 269), or placebo (n = 136). At the final analysis (November 1, 2024; 385 BIRC-assessed PFS events; median follow-up, 40 months), the median BIRC-assessed PFS was 26.9 months with the combination versus placebo (hazard ratio [HR], 0.57; 95% confidence interval [CI], 0.44-0.75; one-sided p < .0001) and 29.9 months with fuzuloparib monotherapy versus placebo (HR, 0.58; 95% CI, 0.44-0.75; one-sided p < .0001) compared with 11.1 months with placebo. A PFS benefit was observed regardless of germline BRCA1/2 mutation status. In homologous recombination-deficient patients (including those with BRCA1/2 mutations), combined fuzuloparib and apatinib produced a PFS similar to that of fuzuloparib (34.1 vs. 35.8 months, respectively); in homologous recombination-proficient patients, PFS had a trend favoring the combination (16.6 vs. 11.0 months; HR, 0.73; 95% CI, 0.45-1.19). Both treatments were well tolerated. Overall survival was immature. Both fuzuloparib and combination therapy improved PFS compared with placebo as maintenance therapy for patients who had newly diagnosed, advanced OC. Adding apatinib to fuzuloparib did not prolong PFS among homologous recombination-deficient patients. There was a PFS benefit trend among homologous recombination-proficient patients who received combination therapy compared with those who received monotherapy.
Premature ovarian insufficiency (POI), particularly chemotherapy-induced ovarian failure (CIOF), severely compromises the reproductive and endocrine health of young women. Current fertility-preserving strategies, such as cryopreservation and hormone therapy, fail to restore endogenous ovarian function, underscoring the urgent need for regenerative solutions. Mesenchymal stem cells (MSCs) have emerged as a leading platform to address this challenge. This review synthesizes evidence on MSCs derived from diverse sources—including bone marrow, adipose tissue, umbilical cord, and menstrual blood—and evaluates their therapeutic potential. Preclinical studies consistently demonstrate that MSC transplantation restores follicular reserves and hormonal homeostasis, primarily via paracrine mechanisms. MSCs secrete growth factors and exosomes enriched with regulatory microRNAs (e.g., miR-21, miR-126) that inhibit apoptosis, promote angiogenesis, and activate pro-survival pathways such as PI3K–Akt in injured ovaries. While early clinical data are encouraging, significant translational challenges remain, including inefficient homing, source-dependent variability, and safety concerns such as tumorigenicity. Advanced approaches—such as cell-free exosome-based therapies and engineered biomaterials—are under development to enhance efficacy and safety. A concerted effort to standardize protocols, optimize delivery strategies, and conduct well-designed randomized trials is essential to establish MSC-based therapy as a clinically viable solution for oncofertility preservation.
