PURPOSE OF REVIEW:Liquid biopsy (LB) is rapidly transforming the management of hormone receptor-positive/HER2-negative (HR+/HER2-) metastatic breast cancer (mBC). In this review, we discuss the most recent findings on circulating tumor DNA (ctDNA) and circulating tumor cells (CTCs), exploring their roles across the treatment continuum, from treatment selection to resistance monitoring. RECENT FINDINGS:ctDNA-based detection of actionable mutations - including ESR1 and PIK3CA - achieved regulatory validation as a primary predictive biomarker for treatment selection, supporting the approval of novel endocrine agents and targeted therapies in HR+/HER2- mBC. Serial ctDNA monitoring demonstrated the ability to intercept emerging resistance mechanisms ahead of radiological progression, opening a window for preemptive therapeutic adaptation. CTCs enumeration maintains robust independent prognostic value, with emerging evidence supporting its role in guiding treatment escalation and de-escalation decisions. Integrated multiparametric LB approaches combining CTCs and ctDNA are crucial to improve prognostic accuracy and clinical decision-making. SUMMARY:LB is progressively shifting from a research tool to a clinical decision-making instrument in HR+/HER2- mBC. Prospective interventional trials, methodological standardization, and integrated strategies are needed to fully translate its potential into improved patient outcomes.
PURPOSE OF REVIEW:Antibody-drug conjugates (ADCs) have rapidly advanced from later-line salvage therapy into first-line metastatic and curative perioperative settings. This review appraises recent practice-changing data that collectively redefined treatment standards across Human epidermal growth factor receptor 2 (HER2)-positive, triple-negative, and hormone receptor-positive/HER2-negative breast cancer. RECENT FINDINGS:Three trials, DESTINY-Breast09, DESTINY-Breast05, and DESTINY-Breast11, established the role of T-DXd across first-line metastatic and perioperative HER2-positive settings, with both early breast cancer indications receiving FDA approval in May 2026. In triple-negative disease, ASCENT-04/KEYNOTE-D19 established sacituzumab govitecan plus pembrolizumab as new first-line option for Programmed cell death ligand 1 (PD-L1)-positive metastatic TNBC. Meanwhile, TROPION-Breast02 had led to the approval of Datopotamab deruxtecan (Dato-DXd) for the first-line treatment of immunotherapy-ineligible patients with metastatic TNBC, whereas ASCENT-03 led to the NCCN incorporation of first-line sacituzumab govitecan for the same population. Multiple further neoadjuvant and adjuvant ADC trials are expected to further reshape treatment algorithms over the coming years. SUMMARY:ADCs now hold regulatory and guideline approval as preferred first-line options across all major breast cancer subtypes, in both the metastatic and curative perioperative settings. Proactive ILD surveillance is essential across all approved agents. Remaining challenges include sequencing among topoisomerase I inhibitor-payload ADCs and awaiting mature survival readouts from perioperative trials.
PURPOSE OF REVIEW:Peripheral neuropathies associated with monoclonal gammopathies and low-grade B-cell lymphomas represent a clinically heterogeneous group of disorders encountered by both neurologists and hematologists. This review provides a practical and updated approach to their diagnosis and management, with a particular focus on IgM-associated neuropathies and anti-MAG neuropathy. RECENT FINDINGS:IgM-related neuropathies encompass immune-mediated disorders - most commonly driven by antibodies against myelin-associated glycoprotein (MAG) - as well as infiltrative mechanisms (neurolymphomatosis, Bing-Neel syndrome) and protein deposition diseases (AL amyloidosis). Anti-MAG neuropathy remains the most common and best-characterized entity. Over the past decade, therapeutic strategies have evolved substantially with the emergence of clone-directed approaches, including anti-CD20-based regimens and covalent Bruton tyrosine kinase inhibitors (cBTKi). However, high-quality evidence remains limited. SUMMARY:Establishing a causal relationship between neuropathy and IgM gammopathy is essential and requires a multidisciplinary approach. Treatment should be individualized and primarily reserved for progressive, functionally impairing disease. Despite therapeutic advances, many patients experience persistent disability, underscoring the need for novel strategies and prospective clinical trials using validated neurological endpoints.
BACKGROUND:Castleman diseases encompass three distinct entities: unicentric Castleman disease, KSHV/HHV-8-associated multicentric Castleman disease (MCD), and idiopathic MCD. HHV-8 MCD is a life-threatening B-cell lymphoproliferative disorder driven by KSHV/HHV-8 infection of B cells, resulting in systemic inflammation and diverse clinical phenotypes. OBJECTIVE:To summarize current knowledge of HHV-8 MCD pathogenesis, clinical presentations, autoimmune complications, and diagnostic advances. METHODS:This review synthesizes existing literature on HHV-8 MCD, with particular attention to emerging diagnostic techniques, including liquid-phase detection of circulating viroblasts. RESULTS:Treatment approaches center on rituximab-based regimens, with outcomes varying between HIV-positive and HIV-negative populations. Novel diagnostic tools combining flow cytometry and viral transcript detection offer rapid identification of disease flares. CONCLUSION:These emerging diagnostic approaches may improve management of HHV-8 MCD, particularly in emergency settings where rapid flare identification is critical.
Purpose of review Haemophagocytic lymphohistiocytosis (HLH), a hyperinflammatory syndrome leading to organ damage and death, may arise as a complication of lymphomas (L-HLH). L-HLH diagnosis is challenging and optimal treatment strategies, influenced by factors such as timing of onset, lymphoma subtype and disease severity, remain ill-defined. This narrative review summarises recent evidence to support clinicians in navigating the competing priorities posed by L-HLH, including the urgent need to control inflammation, establish a diagnosis and initiate lymphoma-directed therapy, while minimising toxicity and avoiding unnecessary immunosuppression. Recent findings While HLH-94 and H-score diagnostic criteria were not specifically designed for L-HLH, the optimised HLH inflammatory index (OHI) was developed in L-HLH patients and predicts the risk of multiorgan failure (MOF) but also benefit from etoposide. Recent evidence also highlights improved survival with early administration of lymphoma targeting drugs while, in critically unwell patients, non-myelosuppressive treatment with anakinra, ruxolitinib and intravenous immunoglobulins (IVIg) might offer a survival advantage. Finally, novel markers such as C-X-C motif chemokine ligand 9 (CXCL-9), recently shown to identify patients responding to interferon γ blockade, might become more widely available in the future. Summary L-HLH encompasses a wide range of clinical presentations that force clinicians to balance competing priorities. Recent evidence improves patients stratification and supports early administration of lymphoma targeting drugs when feasible, etoposide in high risk patients and non-myelosuppressive regimens in critically unwell patients.
Purpose of review Advanced gynecologic cancers are treated broadly, with variable outcomes, even when selected by traditional precision oncology biomarkers. Alternative artificial intelligence (AI)-based biomarkers may improve patient selection, cost efficiency and reduce turnaround times. This review summarizes recent evidence regarding application of AI models for prognostic and predictive biomarker development in gynecological malignancies. Recent findings AI-based biomarker discovery has focused on harnessing computational pathology and radiomics machine and deep learning models to infer molecular subtypes, BRCA 1/2 and homologous recombination status, as well as platinum and maintenance therapy sensitivity. However, small samples sizes, modest discriminative power, lack of explainability and of prospective validation are significant limitations. Summary There is retrospective evidence that AI models potentially constitute useful approaches for precision oncology biomarker detection in advanced gynecological cancers, conditional to prospective validation.
PURPOSE OF REVIEW:Artificial intelligence (AI) is increasingly integrated into robotic-assisted surgery, transforming digital surgical platforms into data-driven environments capable of supporting intraoperative decision-making. In gynecologic oncology, where procedures require high precision and follow relatively standardized workflows, AI technologies may improve surgical quality, reduce variability, and enable safer surgical treatment strategies. This review summarizes recent advances in AI-augmented robotic-assisted surgery, focusing on intraoperative guidance, surgical analytics, and predictive decision support. RECENT FINDINGS:Recent literature demonstrates rapid progress in computer vision models capable of recognizing surgical phases, anatomical landmarks, and procedural steps in real time. Integration of augmented reality, fluorescence imaging, and multimodal imaging platforms is enhancing intraoperative visualization and anatomical orientation. Surgical data science approaches enable objective assessment of technical performance through video-based metrics and machine learning algorithms. Predictive analytics models integrating clinical and imaging data show promising results for risk stratification and outcome prediction, although most applications remain in early stages of validation. SUMMARY:AI-augmented robotic surgery has the potential to improve precision, standardization, and decision-making in gynecologic oncology. However, clinical implementation requires prospective validation, standardized datasets, and integration into routine workflows. Future developments will likely focus on multimodal data integration and context-aware decision support systems.
PURPOSE OF REVIEW:Artificial intelligence (AI) tools for cervical cancer screening have proliferated, but modality-pooled accuracy estimates conflate clinically distinct uses of AI. We re-examine this evidence base through a role-stratified bivariate meta-analysis to clarify where AI is ready for clinical translation and where gaps remain. RECENT FINDINGS:Of 97 eligible studies published between 2019 and 2026, 47 with reconstructible 2 × 2 data were pooled using a bivariate Reitsma model stratified by clinical role. Diagnostic assistance during colposcopy showed the most mature evidence ( k = 21; sensitivity 0.908, specificity 0.844; HSROC AUC 0.94). Primary AI-cytology screening showed high sensitivity but unstable specificity ( k = 10; 0.934/0.701 [0.460-0.865]; AUC 0.92). Triage of hrHPV-positive women was the smallest and weakest pool ( k = 4; sensitivity 0.805, 95% CI lower bound 0.624 - below the 90% safety threshold commonly cited for HPV-positive triage). External validation was reported in 10.9% of studies and 49.1% originated from China. Deeks' funnel asymmetry was borderline for screening ( P = 0.082) and significant for diagnostic assistance ( P = 0.007). SUMMARY:AI is closest to translation as diagnostic assistance during colposcopy. PosthrHPV triage - not primary screening - is the critical evidence gap. Future work should prioritize prospective multicentre multimodal (HPV + AI cytology + orthogonal biomarker) risk-calibrated triage models over further modality-pooled accuracy studies.
Purpose of review This review examines the current role of deep learning in the surgical management of gynecologic cancers. It aims to evaluate applications across surgical training, intraoperative guidance, and outcome prediction, while identifying limitations that hinder translation into routine clinical practice. Recent findings Deep learning-based systems show promising performance in enhancing surgical skills through objective assessment and simulation platforms. Intraoperatively, deep learning models can recognize anatomical structures, surgical phases, and tumor tissue, with high diagnostic accuracy in selected settings. Emerging techniques such as surgical optomics and hyperspectral imaging may further improve tumor detection. Additionally, predictive models integrating clinical, imaging, and intraoperative data demonstrate potential in estimating complications, resource utilization, and survival outcomes. However, most studies are retrospective, based on limited datasets, and lack external validation, with minimal evidence of real-world clinical impact. Summary Artificial intelligence, particularly deep learning algorithms, represents a rapidly evolving tool in gynecologic oncologic surgery, with potential to standardize and personalize care. Nevertheless, significant gaps remain between experimental performance and clinical implementation.
PURPOSE OF REVIEW:Cancer survivorship is increasingly characterized by long-term treatment sequelae, including cardiometabolic disease, fatigue, sleep disturbance, psychological distress, and risk of second malignancies. As survivorship populations expand, there is growing recognition that traditional symptom-focused follow-up does not adequately address modifiable drivers of long-term morbidity. This review evaluates lifestyle medicine as a structured framework integrating physical activity, nutrition, sleep health, psychological well being, and substance cessation to improve survivorship outcomes across solid tumors and hematologic malignancies. RECENT FINDINGS:Evidence from randomized trials, cohort studies, and consensus guidelines demonstrates that lifestyle interventions influence systemic inflammation, immune function, metabolic regulation, and functional capacity. Physical activity improves fatigue, cardiorespiratory fitness, and quality of life, while plant-forward dietary patterns are associated with improved survival outcomes. Sleep optimization and stress reduction interventions improve inflammatory signaling and psychological outcomes. Tobacco cessation and alcohol reduction reduce recurrence risk and mortality. Emerging literature highlights the relevance of cardiometabolic pathways and behavioral interventions as modifiable determinants of survivorship trajectories. SUMMARY:Lifestyle medicine provides a biologically plausible and clinically actionable framework to address shared mechanisms underlying cancer recurrence, treatment toxicity, and chronic disease risk. Integration of multidisciplinary interventions and digital health tools may enable scalable survivorship models focused on prevention, functional recovery, and long-term health optimization. Future research should prioritize mechanistic studies and pragmatic trials evaluating multimodal interventions across diverse cancer populations.
Pain affects 70-80% of patients with pancreatic adenocarcinoma and remains inadequately controlled in more than half of cases. Beyond its impact on quality of life, pain is now recognized as an independent prognostic factor, reflecting the unique neurobiological features of this malignancy. Perineural invasion drives a bidirectional dialogue between cancer cells and the peripheral nervous system, in which neurotrophic factors, neuropeptides, and immune mediators fuel both nociception and tumour progression. Current pain management relies on the WHO analgesic ladder supplemented by adjuvant agents (gabapentinoids, duloxetine, corticosteroids) and interventional procedures including celiac plexus neurolysis, intrathecal opioid delivery, and palliative radiotherapy. Recent advances, notably celiac plexus radiosurgery and evidence favouring early neurolysis, challenge the prevailing reactive approach. This review examines the pathophysiology of pancreatic cancer pain, critically appraises available treatments, identifies gaps in current evidence, and argues for a proactive, multimodal strategy initiated at diagnosis rather than reserved for refractory disease.
PURPOSE OF REVIEW:Systemic radionuclide therapy has become a cornerstone in the management of advanced gastro-entero-pancreatic neuroendocrine tumours (GEP-NETs). Following the establishment of β-emitting peptide receptor radionuclide therapy (PRRT) as an effective treatment for somatostatin receptor positive NETs, recent clinical and translational advances have substantially expanded its therapeutic scope. Several pivotal randomised trials published within the past 18 months justify a reassessment of radionuclide treatment strategies in GEP-NETs. RECENT FINDINGS:Recently published results of randomised phase III trials support a broader and more strategic use of PRRT, such as in selected high-grade well differentiated NETs. Direct comparisons of PRRT and targeted therapies redefine therapeutic sequencing. Radiosensitising combinations and next-generation theranostic platforms, including alpha-emitting radionuclides, are entering late-phase development. SUMMARY:Radionuclide therapy in GEP-NETs is transitioning from a late-line option toward a flexible, biology-driven treatment strategy with important implications for clinical practice.
PURPOSE OF REVIEW:Epithelioid sarcoma (ES) is one of the ultra-rare subtypes of soft tissue sarcomas, with an incidence <0.5 new cases/million/year. It is characterized by loss of SMARCB1 expression, a member of chromatin remodelling complexes, leading to transcriptional dysregulation and dependence on the PRC2 complex, with its histone methyltransferase EZH2. This review summarizes the current therapeutic landscape of ES and explores advances in its molecular characterization as well as potential new treatment options. RECENT FINDINGS:Loss of SMARCB1 in ES is mostly related to homozygous deletion of its locus in chromosome 22. Lack of SMARCB1 leads to global transcriptional changes and the identification of two distinct molecular subtypes that closely resemble the classical and proximal histological subtypes of ES. Transcriptional analyses revealed new potential therapeutic targets, including MYC, mTOR, and TEK. Dependence on EZH2 led to the approval of the EZH2 inhibitor tazemetostat for the treatment of advanced ES; however, multiple resistance mechanisms that decreased its activity have been characterized, and its use recently discontinued due to unexpected secondary hematological malignancies. SUMMARY:Despite progress in understanding ES biology, treatment options are limited, and prognosis remains poor. Further studies are needed, but the rarity of the disease limits opportunities for conducting dedicated clinical trials or broader molecular characterization.
PURPOSE OF REVIEW:Cancer-related cognitive impairment (CRCI) is a frequent and clinically meaningful consequence of cancer, yet current evidence is largely derived from older adult populations. Adolescents and young adults (AYAs) may be particularly vulnerable due to ongoing neurodevelopment, high cognitive demands, and cancer-related biological and psychosocial stressors. This review is timely given the growing interest in biological mechanisms and preventive models of CRCI, alongside the persistent lack of AYA-specific syntheses addressing cognitive trajectories, mechanisms, and optimal intervention timing. RECENT FINDINGS:Approximately 25-30% of AYAs experience CRCI, most commonly affecting attention, processing speed, executive functioning, and working memory. Cognitive alterations may be detectable prior to treatment initiation and can persist across the cancer trajectory. Emerging AYA-specific evidence implicates biological mechanisms such as systemic inflammation and altered neuroplasticity, including changes in brain-derived neurotrophic factor (BDNF). A consistent dissociation between subjective cognitive complaints and objective performance is observed, underscoring the functional impact of subtle inefficiencies in academic and early professional contexts. While non-pharmacological interventions show promise in the general CRCI literature, early and AYA-specific preventive interventions remain scarce. SUMMARY:CRCI in AYAs should be conceptualized as a dynamic, biologically grounded process embedded within ongoing neurodevelopment. Early, developmentally sensitive, and multimodal interventions may represent a key opportunity to preserve long-term cognitive, functional, and psychosocial outcomes in this vulnerable population.
PURPOSE OF REVIEW:Fluoropyrimidine regimens in gastrointestinal oncology have evolved empirically. Bolus 5-fluorouracil (5-FU)-containing combinations now coexist with continuous metronomic schedules and oral prodrugs, while immune checkpoint inhibitors (ICIs) seek chemotherapy partners for microsatellite-stable (MSS) gastrointestinal cancers. This review examines the intersection of bolus omission, metronomic scheduling, and biomarker-selected immunochemotherapy and proposes a shift from dose-based to exposure-based paradigms. RECENT FINDINGS:A real-world cohort of 11 765 patients showed that bolus omission from FOLFOX, FOLFIRI and FOLFIRINOX preserved survival and approximately halved grade 3-4 haematological toxicity. CAIRO3 validated low-dose continuous capecitabine maintenance, pharmacologically consistent with metronomic dosing. Preclinical murine studies suggest that fluoropyrimidine immune effects are dose-, schedule- and partner-dependent, with peak exposure activating NLRP3-driven pro-tumour pathways; relevance to human disease remains hypothetical. Two recent signals (POCHI and MEDITREME) share early-line treatment, immune or molecular enrichment, and an oxaliplatin-driven immunogenic cell death inducer; POCHI also avoids intravenous 5-FU bolus through its CAPOX backbone. SUMMARY:Recent failures of chemo-immunotherapy in MSS gastrointestinal cancers may partly reflect immunologically suboptimal chemotherapy backbones. Optimal outcomes likely require joint consideration of schedule, biomarker selection, and immunogenic partner. Prospective trials testing chemotherapy schedules are warranted.
Purpose of review Intimal sarcoma is an exceptionally rare and aggressive vascular malignancy that remains frequently misdiagnosed. This review synthesizes recent advances in epidemiology, diagnosis, molecular characterization and treatment, highlighting why updated guidance is urgently needed. Recent findings Current literature emphasizes persistent diagnostic delays due to nonspecific clinical and radiological features. Molecular studies consistently show recurrent amplification of MDM2, PDGFRA and CDK4 as key oncogenic drivers. Surgical resection remains the only potentially curative option, although complete removal is often challenging. Retrospective data suggest that multimodal therapy, particularly anthracycline-based chemotherapy, may improve outcomes in selected patients. Targeted therapies and immunotherapy have shown limited but emerging activity in moleculary defined subgroups. Summary Despite incremental progress, prognosis remains poor, underscoring the need for earlier recognition, molecularly guided treatment strategies and clinical trial participation. Management in specialized multidisciplinary centers is essential to optimized care and advance research in this ultra-rare sarcoma.
