Primary hepatic histiocytic sarcoma (HS) is an exceptionally rare malignancy with nonspecific clinical and morphological features that often mimic other high-grade liver tumors making their diagnosis challenging. We report a 74-year-old man presenting with abdominal and back pain, fatigue, and a solitary right-lobe hepatic mass. Imaging suggested hepatocellular carcinoma, and the patient underwent right posterior sectionectomy. Histopathology revealed a high-grade neoplasm of discohesive large cells with eosinophilic cytoplasm and extensive necrosis. Immunohistochemistry confirmed HS. Given the extreme rarity of primary hepatic HS, we provide a focused literature review highlighting diagnostic challenges, immunophenotypic features, and current insights into the molecular landscape of this aggressive neoplasm.

The interplay between the nervous and immune systems has attracted growing scientific attention due to its implications for tumor progression, immune regulation, and potential therapeutic strategies. Although their primary concentration is on inflammation and homeostasis, this basic information emphasizes the crucial role that neuro-immune interaction plays in disease states, including cancer. Neuro-immune interactions are complex and multifaceted, playing significant effects on the pathophysiology of cancer. These interactions involve both peripheral and central neural pathways, modulating immune cell activity within the tumor microenvironment, and offering promising avenues for innovative therapeutic interventions. This review synthesizes recent advancements in understanding the molecular mechanisms, regulatory pathways, and translational applications of the neuro-immune axis in cancer. We explore the intricate roles of neurotransmitters, cytokines, and neurotrophic factors in mediating this crosstalk, examining how the peripheral, central, and enteric nervous systems regulate tumor immunity. Furthermore, we explore emerging therapeutic strategies that target neural inputs, combine neuroimmune modulation with immunotherapy, and consider the impact of epigenetic regulation on the neuroimmune microenvironment. By synthesizing recent advances, this review aims to provide a comprehensive understanding of this intricate field, identify current challenges, and delineate future research directions to harness neuro-immune modulation for offering promising avenues for innovative therapeutic interventions.

Poly (ADP-ribose) polymerase inhibitors (PARPi) have improved outcomes in ovarian cancer with homologous recombination deficiency (HRD). However, approximately half of high-grade serous ovarian cancers retain intact homologous recombination repair and are classified as homologous recombination-proficient (HRP), limiting the clinical benefit of PARPi in this population. Strategies capable of pharmacologically inducing a functional HRD-like state may expand the therapeutic scope of PARPi.

A drug repurposing screen of 97 FDA-approved targeted agents was conducted in olaparib-insensitive HRP ovarian cancer cell models. Drug interactions were evaluated using cell viability and colony formation assays. Homologous recombination activity was assessed using RAD51 foci formation and DR-GFP reporter assays. DNA damage, cell cycle distribution, and apoptosis were analysed using immunofluorescence and flow cytometry. Antitumour efficacy was evaluated in xenograft models. Immune recognition-related features and susceptibility to CD8⁺ T-cell-mediated killing in vitro were assessed using peripheral blood mononuclear cell (PBMC) coculture assays.

Proteasome inhibitors emerged as the most consistent sensitising drug class. The oral proteasome inhibitor ixazomib citrate demonstrated robust synergy with olaparib across multiple HRP ovarian cancer models. Mechanistically, ixazomib citrate disrupted recruitment of the homologous recombination protein RAD51 to DNA damage sites without reducing its expression, thereby inducing a functional HRD-like state consistent with BRCAness. This disruption increased olaparib-induced DNA damage, resulting in G2/M arrest and apoptosis. In xenograft models, combination therapy significantly suppressed tumour growth compared with either agent alone. Proteasome inhibition also increased tumour-surface MHC class I expression and appeared to enhance susceptibility to CD8⁺ T-cell-mediated tumour cell killing in vitro.

Ixazomib citrate sensitised HRP ovarian cancer models to PARP inhibition by functionally impairing homologous recombination repair. These findings provide preclinical support for proteasome inhibition as a PARPi-sensitising strategy in HRP ovarian cancer. The immune-related observations are based primarily on in vitro coculture experiments and should therefore be considered exploratory. Further validation in additional preclinical and clinically relevant models is warranted.

Pancreatic cancer is a highly lethal gastrointestinal malignancy with chemotherapy resistance as a major obstacle to improving prognosis. Emerging evidence indicates that the intratumoral microbiome is closely implicated in the development, progression, and therapeutic response of pancreatic cancer. The intratumoral microbiome of pancreatic cancer is mainly composed of Proteobacteria and Firmicutes, and its composition is significantly correlated with patient survival. Intratumoral microbes drive tumor progression by remodeling the immune microenvironment, inducing DNA damage, and activating oncogenic signaling pathways. Meanwhile, they exacerbate chemotherapy resistance via multiple mechanisms, including remodeling the extracellular matrix, establishing an immunosuppressive microenvironment, and metabolically inactivating chemotherapeutic agents. This review systematically summarizes the community composition of the intratumoral microbiome in pancreatic cancer, its regulatory effects, and underlying mechanisms on chemotherapy resistance, as well as the latest advances in targeted therapeutic strategies.

Cancer represents a major global health threat, and the development of effective anticancer therapies is urgently needed. Sanguisorba officinalis (DY), a traditional Chinese herbal medicine, possesses properties including cooling blood and promoting blood circulation, detoxifying pathogenic toxins, and astringing sores. Increasing evidence suggests that DY and its bioactive constituents exhibit notable anti-tumor effects, with mechanisms that align with traditional Chinese medical principles of enhancing Zhengqi (fuzheng) and removing Xieqi (quxie). However, a comprehensive review that systematically summarizes the antitumor potential of DY and its bioactive constituents is still lacking. In this review, we summarize the anticancer effects of DY extracts and Ziyuglycosides. In vitro studies demonstrate that DY and its active components can inhibit tumor cell proliferation, induce cell cycle arrest, trigger mitochondria-mediated apoptosis, enhance autophagic flux, and suppress invasion and metastasis by regulating Wnt/β-catenin, PI3K/AKT/mTOR, MAPK, and EGFR/NF-κB signaling pathways, as well as downregulating epithelial-mesenchymal transition-related transcription factors and matrix metalloproteinases. In vivo studies confirms DY and its active components inhibit tumor growth and metastasis, regulate the tumor immune microenvironment, modulate Th17/Treg balance, activate CD8+ T cells, and enhance the anti-tumor immune responses. Notably, clinical application evidence indicates that Diyu Shengbai Pian, a preparation derived from DY, have been proven effective in alleviating leukopenia caused by chemotherapy or radiotherapy, highlighting DY's dual therapeutic potential in tumor suppression and mitigating treatment-related adverse reactions. However, current research mainly focuses on in vitro cellular studies and in vivo animal models, lacking large-scale, standardized clinical trials to validate its long-term efficacy and safety in humans. This review systematically summarizes the mechanisms of the anti-tumor and immunomodulatory effects of DY and its active components, and outlines advancements in improving their in vivo delivery efficiency, providing a theoretical basis and research reference for the translational application of DY in cancer therapy.

Neuroendocrine tumors (NETs) are rare heterogeneous neoplasms that arise in multiple organs of humans and companion animals and can produce diverse hormonal syndromes or remain clinically silent, leading to delayed diagnosis. Given shared environments and conserved neuroendocrine morphology across species, companion animals represent an attractive yet underexplored model for comparative oncology. This literature review searched PubMed through December 2025 and qualitatively synthesized evidence on the epidemiology, macroscopic and histologic features, biomarkers, clinical presentation, imaging modalities, treatment, and prognosis of neuroendocrine tumors in humans, dogs, and cats. Collectively, this review indicates that neuroendocrine tumors in dogs and cats recapitulate many key biological and clinical features of human NETs and therefore hold meaningful translational potential, particularly for functional pancreatic, hepatic, and intestinal tumors. However, substantial gaps in veterinary epidemiologic surveillance, biomarker validation, imaging standardization, and prospective therapeutic evaluation currently limit full comparative integration. Addressing these gaps through coordinated, multicenter comparative studies and harmonized reporting frameworks could enhance diagnosis and management in veterinary patients while advancing spontaneous animal models for human NET research.

Ewing sarcoma is an aggressive neoplasm that is common among children and adolescents, most frequently affecting the pelvis and long bones. Although rare, Ewing sarcoma is known to also occur in extraosseous locations, affecting a broad range of soft tissue structures. The diagnosis of extraosseous Ewing sarcoma is difficult given the nonspecific symptomatology, often related to local tumor burden. Radiological features of this entity overlap with other common malignancies, as Ewing sarcoma typically presents on computed tomography (CT) as a heterogeneous mass containing areas of necrosis and calcification. Imaging plays a central role in the evaluation of this entity, but histologic and molecular analysis remain necessary for definitive diagnosis. We report the case of a 40-year-old female with a primary pancreatic extraosseous Ewing sarcoma. We correlate clinical indicators with imaging findings and pathological analysis to discuss this patient's long-term outcome following multimodal therapy.

Krukenberg tumors are rare metastatic ovarian neoplasms, most commonly originating from gastrointestinal adenocarcinomas, and are histologically characterized by mucin-producing signet-ring cells. Their clinical and radiological presentation is often nonspecific, which may delay diagnosis and complicate differentiation from primary ovarian malignancies. Imaging plays a crucial role in the initial assessment, with ultrasonography typically revealing bilateral or unilateral adnexal masses that are heterogeneous, predominantly solid, and associated with irregular margins and internal necrotic areas. Transvaginal ultrasound further refines lesion characterization by demonstrating a disorganized architecture with mixed solid and cystic components, highly suggestive of malignancy. Definitive diagnosis relies on histopathological examination supported by immunohistochemical profiling to identify the primary origin. Early recognition is essential given the poor prognosis and the need for multidisciplinary management. In this context, we report a case of a metastatic ovarian tumor consistent with a Krukenberg-type lesion.

Colloid adenocarcinoma of the lung is a rare subtype, often difficult to diagnose due to its indolent behavior and atypical imaging. We report a 76-year-old man and former smoker with an incidentally detected right lower lobe mass. Computed tomography (CT) showed a well-defined, lobulated lesion with poor contrast enhancement and internal calcifications and ¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography (¹⁸F-FDG PET/CT) demonstrated low uptake. Multiple percutaneous and surgical biopsies were nondiagnostic. Progressive growth and new onset of mediastinal lymphadenopathy ultimately led to right lower lobectomy, confirming stage IIIA colloid adenocarcinoma. This case highlights imaging limitations, the value of sequential biopsies, and the role of surgical biopsy when less invasive methods repeatedly fail, especially with high clinical suspicion.

Neurofibromatosis type 1 (NF1) is a hereditary tumor predisposition syndrome associated with multiple benign and malignant neoplasms. We report the case of a 55-year-old man with a history of thyroid carcinoma diagnosed 6 years earlier, who was referred for MRI evaluation of a slowly progressive right submandibular mass and a left fronto-temporal brain lesion that had long been considered metastatic disease. Multimodal MRI demonstrated imaging features inconsistent with aggressive metastases. The brain lesion showed no diffusion restriction or hyperperfusion, while MR spectroscopy revealed a prominent myo-inositol peak suggestive of a low-grade glial tumor. The submandibular lesion was well circumscribed and markedly hyperintense on T2-weighted imaging, favoring a neurofibroma. These radiological findings prompted targeted physical examination, which revealed multiple café-au-lait macules, axillary freckling, and diffuse cutaneous neurofibromas, leading to the diagnosis of NF1 according to revised international criteria. This case highlights the important role of multimodal MRI in challenging anchoring bias in oncologic patients and emphasizes the value of correlating imaging findings with clinical examination to identify previously unrecognized genetic syndromes.