Leiomyosarcomas are very rare soft tissue sarcomas originating from smooth muscle cells. This neoplasm can develop in various places around the body, including but not limited to the uterus, retroperitoneum, colon, blood vessels, and bladder. This case report details the discovery of a cecal leiomyosarcoma in a patient who presented to the emergency department after a year of abdominal pain, fatigue, and unexpected weight loss. The report will discuss the available literature on leiomyosarcoma, the surgical approach for management in this patient, and post-operative management.

Desmoid tumors, also known as aggressive fibromatosis, are rare, benign soft tissue neoplasms characterized by local invasiveness and a high recurrence rate. They can mimic malignant tumors, particularly in patients with a history of gastrointestinal stromal tumors (GISTs). We report a case of a 60-year-old male who developed intra-abdominal desmoid tumors five years after undergoing laparoscopy and endoscopy cooperative surgery (LECS) for gastric GIST, followed by adjuvant imatinib therapy. Imaging studies, including contrast-enhanced computed tomography (CT) and positron emission tomography-computed tomography (PET-CT), revealed two mesenteric masses. The larger lesion demonstrated elevated fluorodeoxyglucose (FDG) uptake (SUVmax = 6.7), raising suspicion for recurrent GIST. Surgical resection was performed, and histopathological examination confirmed the diagnosis of desmoid tumors. Immunohistochemical analysis showed positive β-catenin staining, with negative markers for CD34, desmin, and c-kit, distinguishing it from recurrent GIST. This case highlights the diagnostic challenge of differentiating desmoid tumors from GIST recurrence based on imaging alone. Histopathological confirmation remains crucial for accurate diagnosis. Surgical resection is the primary treatment for symptomatic desmoid tumors, but given their high recurrence rate, long-term follow-up and a multidisciplinary approach are essential for optimal management.

Mature cystic teratoma (MCT) is a common benign ovarian neoplasm, but its presentation as bilateral, giant masses in a prepubertal child is rare. Complications like torsion and acute urinary retention pose significant diagnostic and management challenges, where fertility preservation is a primary concern. An 8-year-old premenarchal girl presented with a four-day history of abdominal pain, fever, and acute urinary retention. Examination revealed a large, firm abdominal mass. Imaging suggested bilateral immature teratoma. Emergency laparotomy revealed two massive ovarian masses, with the left torsed, ischemic, and a rudimentary uterus. Bilateral ovarian cystectomy was successfully performed. Histopathology confirmed a right-sided mature cystic teratoma and left-sided hemorrhagic necrosis from torsion, ruling out malignancy. The patient had an uneventful recovery and was commenced on hormone replacement therapy due to compromised ovarian reserve. At two-year follow-up, she remains stable with no complaints. This case underscores that giant ovarian teratomas, though rare in children, can present dramatically. It highlights the critical importance of a fertility-preserving surgical approach even in complex cases and the necessity of long-term, multidisciplinary follow-up to manage subsequent endocrine sequelae.

Thyroid tuberculosis (TB) is a rare form of extrapulmonary infection that can mimic thyroid neoplasms. Diagnosis is challenging due to nonspecific imaging and cytology. We report a case of a 77-year-old female with a history of subtotal gastrectomy for gastric adenocarcinoma. Surveillance CT revealed right-lobe-predominant thyroid enlargement causing tracheal compression. Ultrasound showed a multinodular goitre with a 4.1-cm solid nodule (Thyroid Imaging Reporting and Data System (TI-RADS) 3) and a 1.7-cm hypoechoic nodule (TI-RADS 4). Fine-needle aspiration cytology (FNAC) of the smaller nodule suggested a follicular neoplasm. The right thyroid lobectomy was performed. Histology revealed a follicular adenoma with epithelioid granulomas, and polymerase chain reaction (PCR) confirmed Mycobacterium tuberculosis (M. tuberculosis) complex DNA. The patient completed standard anti-tuberculosis therapy and remained asymptomatic at eight months of follow-up. TB should be considered in patients with nodular thyroid disease, particularly when granulomatous inflammation or compressive symptoms are present. Molecular testing facilitates accurate diagnosis, guides therapy, and helps avoid unnecessary surgery.

Chimeric antigen receptor (CAR) cellular immunotherapy has emerged as a revolutionary modality in cancer treatment. CAR-T cell therapy has demonstrated remarkable efficacy against hematological malignancies; however, its application in solid tumors is significantly constrained by inadequate tumor infiltration, a profoundly immunosuppressive tumor microenvironment (TME), and pervasive antigen heterogeneity. Conversely, macrophages - innate immune cells inherently poised within tissues - exhibit superior tumor-tropic migration, potent phagocytic capability, and a unique capacity to remodel the TME, establishing CAR-engineered macrophages (CAR-M) as a highly promising next-generation therapeutic platform. Despite this considerable promise, the clinical translation of CAR-M faces several critical bottlenecks, including heterogeneity in cell sources, challenges in manufacturing standardization, risks of on-target/off-tumor toxicity, and the dynamic, immunosuppressive nature of the TME. This review offers a systematic and in-depth analysis of the current research landscape and engineering advances in CAR-M therapy. It comprehensively details the molecular evolution of CAR-M designs, spanning from early constructs to sophisticated logic-gated circuits and innovative in vivo generation strategies utilizing lipid nanoparticles (LNPs). We critically evaluate the applicability and limitations of various cellular sources, such as peripheral blood mononuclear cells (PBMCs), induced pluripotent stem cells (iPSCs), and the THP-1 cell line. Furthermore, the review elucidates the multimodal antitumor mechanisms of CAR-M, including the direct "phagocytosis-presentation-activation" cascade, synergistic potential with immune checkpoint blockade, and deep reprogramming of the immunosuppressive TME. By synthesizing the latest preclinical and emerging clinical evidence, this article underscores the distinctive advantages and delineates a translational roadmap for CAR-M development. It is intended to serve as an authoritative reference for the field, providing strategic insights into intelligent receptor design, precision biomanufacturing, and rational combination therapies aimed at overcoming the enduring barriers in solid tumor immunotherapy.

Gastric mucinous adenocarcinoma (GMC) is a rare subtype of gastric cancer characterized by excessive mucus production, aggressive biological behavior, and poor prognosis, with most patients presenting with metastatic disease at initial diagnosis and losing the opportunity for curative resection. Currently, there are no standardized diagnostic and treatment guidelines for metastatic GMC in the conversion therapy setting, and the therapeutic effect of conventional chemotherapy remains unsatisfactory. Herein, we present a 69-year-old male patient diagnosed with HER2-negative, TMB-H advanced GMC, with intraperitoneal and retroperitoneal lymph node metastases. The patient was initially deemed unresectable by the multidisciplinary team (MDT) but opted for conversion therapy due to a strong willingness for treatment and good performance status (ECOG-PS=0). He received 6 cycles of FLOT chemotherapy combined with nivolumab, achieving partial response (PR) per RECIST 1.1. Subsequent laparoscopic distal gastric subtotal resection (D2+ lymphadenectomy) was performed, and postoperative pathology revealed a near pathological complete response (Mandard-TRG1) with no lymph node metastases (0/21), pathologically staged as ypTisN0. Postoperatively, the patient received 4 cycles of XELOX chemotherapy plus nivolumab, followed by consolidative radiotherapy synchronized with capecitabine and nivolumab, and subsequent maintenance therapy with capecitabine and nivolumab until sustained no evidence of disease (NED) was confirmed in January 2023. Regular surveillance, including the latest contrast-enhanced CT in May 2025, showed no recurrence or metastasis, with progression-free survival (PFS) exceeding 5 years. This exceptional and sustained response may be attributed to the synergistic effect of TMB-H and POLD1 mutation, which enhance neoantigen generation and sensitize tumors to immunotherapy. This case highlights the potential of biomarker-driven chemo-immunotherapy combined with MDT-guided multimodal treatment (surgery + adjuvant therapy + consolidative radiotherapy) to achieve curative intent in patients with metastatic GMC, providing valuable insights for personalized treatment strategies in this poor-prognosis population.

Tumor-associated macrophages (TAMs) are central regulators of the metabolic and immunological landscape of solid tumors and are increasingly recognized as key determinants of cancer-cell susceptibility to ferroptosis. Ferroptosis, an iron-dependent form of regulated cell death characterized by lipid peroxidation, is tightly shaped by metabolic cues within the tumor microenvironment (TME). TAMs, through their remarkable metabolic plasticity, modulate iron flux, redox balance, polyunsaturated fatty-acid (PUFA) availability, and glutathione-dependent antioxidant pathways, each of which directly influences ferroptotic vulnerability in neighboring tumor cells. In this review, we synthesize current evidence linking TAM polarization states to the regulation of ferroptosis-related processes, including lipid remodeling, cystokine metabolism, reactive oxygen species (ROS) buffering, and immunometabolic signaling. We further discuss how TAM-derived cytokines, lipid mediators, and iron-handling proteins orchestrate a microenvironment that either promotes or restrains ferroptotic cell death. Finally, we highlight emerging therapeutic strategies aimed at rewiring TAM metabolism or exploiting ferroptosis to overcome immune suppression and therapy resistance. By integrating immunological and metabolic dimensions, this review provides a framework for understanding TAM-ferroptosis crosstalk and its implications for precision immunotherapy in cancer.

Esophageal squamous cell carcinoma (ESCC) remains a major malignancy globally, and long-term survival outcomes remain poor despite advances in multimodal treatment strategies. Neoadjuvant therapy (NAT) has become the standard of care for resectable ESCC; however, substantial interpatient heterogeneity in treatment response persists. Defining malignant cell-intrinsic molecular determinants linked to NAT response is essential for improving prognostic stratification and informing individualized therapeutic decision-making.

To investigate transcriptional alterations in malignant epithelial cells, we analyzed scRNA-seq datasets obtained from ESCC patients both before and after NAT. Overlapping molecular features were identified by integrating differentially expressed genes from pre- and post-treatment malignant cells with bulk RNA-seq data from TCGA and GEO cohorts. Functional enrichment analyses, pseudotime trajectory reconstruction, and transcription factor regulatory network assessments were subsequently performed. Candidate prognostic genes were initially screened through univariate Cox analysis, followed by the development of the NTAMPS model using LASSO-Cox regression. Its prognostic performance was validated in the TCGA-ESCA and GSE53624 cohorts, and clinical applicability was further examined using a nomogram, calibration curves, and decision curve analysis. Immune-related associations, immunotherapy response prediction (IMvigor210 and GSE78220), and drug sensitivity profiling were also conducted. DUXAP8, which carried the largest coefficient in the NTAMPS, was selected for further validation through both in vivo and in vitro assays, including qRT-PCR and evaluations of cell proliferation, migration, invasion, and colony formation.

Malignant epithelial cells exhibited pronounced transcriptional remodeling after NAT, characterized by enrichment of pathways related to the cell cycle, DNA replication, and epithelial-mesenchymal transition. Cell-cell communication analysis revealed substantial reorganization of the MIF signaling pathway, including increased interactions of MIF-ACKR3 and MIF-(CD74+CXCR4/CD44), with fibroblasts acting as major signal senders and macrophages serving as primary receivers. Twenty-one prognosis-related genes were identified, and a ten-gene NTAMPS demonstrated strong prognostic performance. Both NTAMPS and clinical stage emerged as independent prognostic factors and were integrated into a nomogram with favorable calibration and decision curve characteristics. A high NTAMPS was associated with an immunosuppressive microenvironment, reduced predicted response to immunotherapy, and distinct drug sensitivity patterns. DUXAP8, the top positive risk gene within NTAMPS, was highly expressed in ESCC tissues and cell lines, and its silencing suppressed cell proliferation, migration, invasion, and clonogenic potential.

This study establishes NTAMPS as a novel malignant cell-derived prognostic signature for ESCC by integrating single-cell and bulk transcriptomic data. NTAMPS enables effective prognostic stratification, predicts potential immunotherapy benefit, and highlights therapeutic vulnerabilities. DUXAP8 was further identified as a candidate molecular driver that may improve ESCC management in the context of neoadjuvant therapy.

Several PD-1 inhibitors used in first-line treatment of advanced non-squamous non-small cell lung cancer in China, including sintilimab, toripalimab and camrelizumab, have demonstrated significant survival benefits in phase III trials. However, their comparative cost-effectiveness within the Chinese national medical insurance system remains unclear.

A Markov model with progression-free, progressive disease and death states was developed from the Chinese national medical insurance system payer perspective. Clinical efficacy inputs were obtained from three China-based phase III randomized trials. Individual patient data were reconstructed from published Kaplan-Meier curves using the Guyot method, and parametric survival models were fitted for extrapolation. Costs included drug acquisition, administration, adverse event management and post-progression therapy. Outcomes were total costs, quality-adjusted life-years (QALYs) and incremental cost-effectiveness ratios (ICERs). One-way and probabilistic sensitivity analyses were conducted.

Sintilimab incurred the lowest cost (230,813 CNY) and generated 1.1 QALYs. Toripalimab yielded the same QALYs at a higher cost and was strictly dominated. Camrelizumab produced the highest QALYs (1.2) at a total cost of 253,056 CNY. Compared with sintilimab, camrelizumab had an ICER of 164,983 CNY/QALY, below the willingness-to-pay threshold of 287,247 CNY/QALY. Sensitivity analyses confirmed the robustness of these findings.

Among the three domestic PD-1 inhibitors evaluated, camrelizumab is the most cost-effective first-line treatment option for advanced non-squamous NSCLC in China.

Ischemic preconditioning of parathyroid glands (IPCP) is biologically plausible but clinical evidence is limited. In this single-center randomized trial (ChiCTR2000039788), we compared IPCP versus control during total thyroidectomy with central neck dissection.

A total of 135 patients with differentiated thyroid carcinoma were analyzed (IPCP, n = 67; control, n = 68). IPCP consists of three cycles of 60-second occlusion followed by 60-second reperfusion of the ipsilateral superior and inferior thyroid arteries. The baseline characteristics, postoperative hypoparathyroidism (hypoPTH) and hypocalcemia, early parathyroid function recovery (PFR), and surgical complications, were compared between groups.

The incidence of postoperative hypoPTH and protracted hypoPTH was not significantly different between the IPCP and control groups (50.8% vs 41.2%, p = 0.265; 6.0% vs 14.7%, p = 0.096). An exploratory analysis showed a higher rate of early PFR in the IPCP group (88.2% vs 64.3%; p = 0.025). The incidence of postoperative hypocalcemia was similar between groups (79.1% vs 82.4%; p = 0.632). Fewer inadvertent parathyroidectomy occurred in the IPCP group, though this difference was not statistically significant (4.5% vs 8.8%; p = 0.505). Other surgical complications were comparable.

IPCP did not reduce postoperative hypoPTH in this randomized trial. Earlier PFR is exploratory and warrants further investigation in adequately powered trials.