Quinoline derivatives are a class of heterocycles featuring a fused benzene‑pyridine scaffold that have attracted notable interest in anticancer drug discovery owing to their favourable physicochemical properties, structural versatility and broad biological activities. Accumulating evidence indicates that quinoline‑based compounds exert antitumour effects through several targets and pathways, including via epigenetic regulation, interference with DNA topology, inhibition of signalling pathways, immune modulation, induction of autophagy and targeting of the cytoskeleton. Structure‑activity relationship (SAR) analyses demonstrate that the electronic effects and steric configurations of substituents on the quinoline ring critically determine potency, selectivity and metabolic stability. In particular, oxygenated, halogenated and strongly electron‑withdrawing groups, as well as nitrogen‑containing heterocyclic substituents, enhance hydrophobic interactions or hydrogen bonding with biological targets, thereby improving inhibitory efficacy. Consequently, the quinoline scaffold has emerged as a rated structural motif in anticancer lead compound discovery. Multidimensional optimisation strategies have been proposed to improve the pharmacokinetic profiles and clinical applicability of quinoline derivatives. Nanocarriers and smart stimuli‑responsive delivery systems markedly enhance solubility, circulation time and tumour targeting, whereas prodrug approaches employing enzyme‑sensitive, pH‑responsive or redox‑activated linkers enable selective activation at tumour sites. Combination therapies also exploit the multi‑pathway activity of quinoline derivatives, enhancing antitumour responses and delaying resistance when combined with immunotherapy, chemotherapy or radiotherapy. Furthermore, artificial intelligence and machine learning approaches have shown increasing utility in virtual screening, quantitative structure‑activity relationship modelling and multi‑objective optimisation, accelerating the identification of potent, low toxicity and synthetically accessible candidates. Overall, quinoline derivatives offer systemic advantages as multi‑target anticancer agents. The present review summarises recent advances in molecular mechanisms, SAR insights and drug design strategies, providing a comprehensive framework for advancing quinoline‑based agents towards next‑generation precision anticancer therapies.

Gastric cancer (GC) is one of the most common malignant tumors worldwide. Metabolic reprogramming and epigenetic dysregulation represent its key pathological characteristics. As a novel lactate‑mediated post‑translational modification, lactylation converts metabolic signals into epigenetic and protein functional regulation, and it is extensively and aberrantly activated in GC. Lactylation drives the malignant progression of GC by promoting cell proliferation, invasion, metastasis and stemness. In addition, lactylation suppresses antitumor immune cell functions, and mediates immune escape and therapeutic resistance. Clinically, global lactylation levels and specific lactylation sites can serve as independent prognostic biomarkers, and corresponding risk models enable prognostic stratification and prediction of immunotherapy response. Intervention strategies targeting lactate production, lactyltransferases and downstream effector axes have emerged as promising directions for GC treatment. The present review summarizes the regulatory mechanisms, biological functions and clinical translational value of lactylation in GC, aiming to provide novel insights for precision diagnostics and therapeutics.

Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer with high brain metastatic (BM) potential. Tumor-derived exosomes are implicated as key modulators during the formation of the pre-metastatic niche (PMN). However, the regulation of TNBC-BM-derived exosomes on brain PMN remains enigmatic.

The morphology and uptake of exosomes were identified using transmission electron microscopy and live-cell imaging, respectively. Differentially secreted miRNAs and mRNA were identified using high-throughput sequencing. The permeability of the blood‒brain barrier (BBB) and tight junction integrity were examined using immunofluorescence staining. Cell viability was examined using the CCK-8 assay. The apoptosis and intracellular ROS were investigated using fluorescence staining. The expression of mRNAs was examined using qPCR.

miR-103b was significantly increased in exosomes derived from TNBC-BM cells. miR-103b compromised the tight junctions of HUVECs and increased BBB permeability in mice. Additionally, miR-103b promoted apoptosis and increased intracellular ROS in HUVECs and U251 cells, two cell lines commonly used as surrogates for brain microvascular endothelial cells and astrocytes, respectively. miR-103b-regulated differentially expressed genes modulated tight junction, apoptosis, oxidative stress, inflammation, and metabolism. Target analysis identified 216 targets of miR-103b, among which hub targets were associated with biological processes involved in maintaining the BBB and the glucose metabolism signaling pathway.

Collectively, our findings for the first time reveal that exosomal miR-103b from TNBC-BM cells potentially regulates the two major cellular constituents of the brain PMN, highlighting its role in the formation of the brain PMN during TNBC-BM and its potential as a promising therapeutic target.

Malignant progression and limited therapeutic response in gastric cancer (GC) cannot be explained solely by increased proliferation or oncogenic alterations. Instead, they reflect how tumor cells regulate their death threshold under sustained damage, metabolic stress and immune pressure. Evidence indicates that GC cells largely retain the capacity for cell death but reduce its effective execution by attenuating signal propagation, weakening key execution steps and altering microenvironmental interactions. As a result, cellular stress persists without effective clearance, promoting survival, resistance and metastasis. The present review synthesized current evidence on the mechanisms and interplay of cell death in GC, with emphasis on their relationships with the tumor microenvironment, host factors and therapeutic stress. It further evaluated their implications for resistance, patient stratification and therapeutic intervention. Reframing GC through the lens of cell death regulation provides a more coherent basis for understanding its biological heterogeneity and for improving therapeutic strategies.

Intradural extramedullary (IDEM) spinal tumors are the most common intradural spinal neoplasms, typically benign and slow-growing. They cause neurological deficits through progressive spinal cord compression. Surgical excision remains the mainstay of treatment, with generally favorable outcomes.

To analyse the clinical profile, surgical management, and functional outcomes of patients with IDEM spinal tumors.

A retrospective study was conducted on 214 patients who underwent microsurgical excision of IDEM tumors between January 2009 and December 2023. Clinical presentation, radiological findings, surgical details, histopathology, complications, and functional outcomes were evaluated. Neurological status was assessed using the Modified McCormick Scale and American Spinal Injury Association impairment scale with a minimum follow-up of 12 months.

The majority of patients were >45 years (40.2%) with a slight female predominance (54.7%). Back pain (80.4%) was the most common presenting symptom, followed by motor deficit (60.3%). The thoracic spine was most frequently involved (45.3%). Gross total resection was achieved in 83.6% of cases. Schwannoma (47.2%) and meningioma (30.8%) were the most common histologies. Mean blood loss and operative time were 172 ± 62 ml and 164 ± 43 min, respectively. Complications were low, with cerebrospinal fluid leak (2.8%) and wound infection (3.3%) being the most frequent. Significant postoperative neurological improvement was observed, with most patients achieving Modified McCormick Grade 1-2 at 2-year follow-up.

IDEM tumors have a favorable prognosis when managed surgically. Microsurgical excision allows high rates of complete resection with low morbidity. Early intervention is associated with better neurological recovery.

Chemotherapy-induced peripheral neuropathy (CIPN), a debilitating dose-limiting toxicity affecting 20-85% of cancer patients, lacks disease-modifying therapies. This review synthesizes evidence supporting acupuncture as a potential multi-target strategy against CIPN. Direct preclinical CIPN studies suggest that electroacupuncture (EA) may modulate selected neuroinflammatory and oxidative pathways, including TLR4/NF-κB signaling, TRPV1 upregulation, and spinal glial activation; proposed effects on Nav1.7-1.9, PGC-1α/AMPK, or HDAC6-related microtubule stabilization remain unconfirmed. Clinically, sham-controlled trials suggest that manual acupuncture and EA may alleviate pain, sensory symptoms, and quality-of-life impairment. High response rates for auricular acupuncture derive from an uncontrolled case series, and ALTENS findings are preliminary. The MC5-A Calmare device delivers Scrambler therapy and is distinct from ALTENS and acupuncture. Combination studies suggest possible additive benefit rather than established synergy. Safety profiles are generally favorable. However, clinical translation is impeded by methodological heterogeneity, subjective "De Qi" assessment, and inadequate patient stratification. Future research should focus on trials with lab markers and cost analyses to determine how well acupuncture helps people complete their treatment.

Cervical carcinosarcoma (CCS), also known as malignant mixed Müllerian tumor (MMMT) of the cervix, is an exceptionally rare and aggressive biphasic neoplasm composed of both epithelial and mesenchymal malignant components. Due to its rarity, optimal management strategies are not well established, particularly in low-resource settings. Most reported cases present at an advanced stage and are associated with poor prognosis. To our knowledge, this represents the first reported metastatic case of CCS from Sub-Saharan Africa. We report a case of advanced CCS in a 33-year-old woman who presented to a tertiary referral center in Northern Tanzania with a five-month history of heavy and prolonged vaginal bleeding, lower abdominal pain, headaches, palpitations, and generalized weakness. Clinical examination revealed a large vaginal mass with restricted uterine mobility and rectal involvement. Imaging demonstrated a heterogeneously enhancing cervical mass measuring 10 × 9 × 14 cm with parametrial invasion, recto-sigmoid infiltration, bilateral ovarian enlargement, peritoneal dissemination, lymphadenopathy, and ascites, consistent with FIGO stage IVB disease. Exploratory laparotomy revealed omental caking, bilateral ovarian masses, liver surface nodules, and extensive pelvic adhesions. A total abdominal hysterectomy (TAH) with bilateral salpingo-oophorectomy (BSO) was performed. Histopathological examination demonstrated a biphasic malignant tumor composed of carcinomatous elements arranged in nests and cords and sarcomatous pleomorphic spindle cells. Immunohistochemistry showed epithelial differentiation with p16 positivity and mesenchymal differentiation highlighted by desmin. Intraoperative findings and imaging confirmed ovarian and peritoneal metastases, consistent with advanced disease. Multidisciplinary review recommended systemic chemotherapy with carboplatin and paclitaxel followed by radiotherapy. Treatment was not initiated, however, due to financial constraints. The patient was subsequently lost to follow-up.

Thyroid carcinoma (TC) is the most common cancer of the endocrine system worldwide, and its incidence has remained stable over the past forty years. Complex hormonal and environmental factors influence TC progression. The gut microbiome, a pivotal mediator in maintaining host physiology and the development of pathology, serves as a biomarker and therapeutic target in cancer immunotherapy. The microbiome-assisted tumor microenvironment (TME) sustains tumors through the modulation of multiple mechanisms. Immune suppression in the TME induces a metastatic phenotype of tumor cells by modulating signaling pathways, cell differentiation, and the innate immune response. Current research has confirmed that gut dysbiosis, bacterial outer membrane components (such as lipopolysaccharides and LPS), and metabolites (such as short-chain fatty acids and SCFAs) have bidirectional regulatory effects on thyroid function. However, the role of the local microbiome in modulating treatment responses and its interactions with the immune TME of TC remains unknown. The literature was searched in PubMed, Web of Science, and Google Scholar using keywords associated with "microbiome" and "thyroid carcinoma". Research articles, clinical trials, letters, and meta-analyses were published by January 2026. This narrative review summarizes the role of the intratumor microbiome in tumor progression, interactions with chemotherapy, radiotherapy, and targeted therapies. The associations between the microbiome and the immune TME of cancers, as well as the characteristics of the immune TME and alterations in the gut/intratumor microbiome in patients with TC receiving different therapies, are discussed. Mediating microbiome and metabolites might be potential strategies for optimizing personalized therapeutic interventions against TC. Future research should focus on defining microbial signatures associated with treatment success and developing targeted strategies to improve patient outcomes on the basis of microbiome modulation.

Triple-negative breast cancer (TNBC) is an aggressive subtype accounting for 10-17% of all breast cancers, characterized by the absence of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 expression. TNBC is associated with high recurrence rates and poor prognosis, particularly after metastatic progression. Current surveillance guidelines rely on clinical evaluation and conventional imaging, which have limited sensitivity for detecting early recurrence. [¹⁸F]fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT) offers the potential to detect metabolic changes indicative of disease activity before anatomical changes become apparent. This review examines the emerging role of FDG PET/CT in the post-treatment evaluation of TNBC in two distinct clinical contexts: (1) surveillance for recurrence after remission, with specific attention to hepatic, pulmonary, osseous, and cerebral metastases, and (2) treatment response assessment in advanced disease following chemotherapy and immunotherapy. Across both contexts, FDG PET/CT offers incremental diagnostic and prognostic value over conventional imaging. However, much of the available evidence is derived from general breast cancer populations and not from TNBC-specific cohorts. Dedicated recurrence-surveillance data in TNBC remain particularly scarce. FDG PET/CT demonstrated 98% sensitivity and 100% specificity for hepatic metastases in a mixed-malignancy cohort, PET Response Criteria in Solid Tumors (PERCIST) criteria showed higher predictive accuracy than Response Evaluation Criteria in Solid Tumors (RECIST) for both progression-free and disease-specific survival, and early interim PET/CT after two cycles of chemotherapy identified metabolic non-responders (<42% SUV_max decrease) who had a 100% rate of residual tumor at surgery in a small TNBC cohort. However, FDG PET/CT remains limited for sub-centimeter pulmonary nodules (due to partial volume effects and respiratory motion) and brain metastases (due to high physiological brain glucose uptake). Additionally, limitations of the current evidence include small study populations, short follow-up periods, cost considerations, and risks of false-positive findings due to post-treatment inflammation and immunotherapy-related pseudoprogression. Beyond FDG, emerging PET tracers, such as radiolabeled fluorothymidine (FLT), fibroblast activation protein inhibitor (FAPI), and prostate-specific membrane antigen (PSMA)-targeted agents, may offer complementary information for TNBC surveillance. Larger, TNBC-specific prospective studies with longer follow-up are needed to establish evidence-based guidelines for incorporating FDG PET/CT into routine TNBC surveillance and response-assessment protocols, alongside formal cost-effectiveness analyses.

Tertiary lymphoid structures (TLSs) are associated with immunotherapy response and survival across solid tumors and are increasingly evaluated as tissue biomarkers. Neoadjuvant treatment provides pretreatment biopsies, on-treatment samples, and surgical resections, but these time points answer different clinical questions. Previous reviews have established TLS biology, maturation, and broad associations with response and survival. Here, we organize the evidence by sampling context, measurement object, and intended use. Pretreatment TLSs are candidate baseline stratification markers; within-patient changes describe pharmacodynamic remodeling only when specimens are comparable; and surgical TLSs describe post-treatment response phenotypes or postoperative prognosis according to the outcome time origin. These roles call for distinct validation designs. Immune cells, stromal organizers, and specialized vasculature can reshape TLSs, but parallel structural and tumor changes do not show that treatment benefit depends on TLSs. TLS-specific loss-and-rescue experiments are still needed to test that causal contribution. Clinical translation should therefore start with the decision being made and align the sample, measurement, missingness rules, and validation design to that decision. This framework explains part of the apparent inconsistency across studies and offers a practical path from descriptive associations to clinically interpretable evidence.