Financial toxicity, defined as the material hardship and psychological distress associated with the costs of cancer care, has become a central concern in oncology as treatment complexity and patient cost-sharing increase. This review uses the Social-Ecological Model to conceptualize financial toxicity across multiple levels of influence, shifting focus from individual behaviors to the broader interpersonal, organizational, community, and societal systems that shape financial risk. Financial toxicity arises through interconnected drivers across the Social-Ecological Model. At the individual level, direct and indirect treatment costs contribute to material and psychological burden. Interpersonally, limited cost communication and negative insurance interactions exacerbate distress. Organizational factors, including billing practices, ancillary expenses, and inflexible workflows, shape time and financial demands. Community-level inequities such as transportation barriers and area deprivation further compound hardship. Promising interventions include essential-needs programs, patient navigation, food support, financial counseling, structured cost conversations, universal screening, reduced ancillary fees, consolidated appointments, and partnerships with community groups. Societal drivers - including insurance design, cost sharing, and rising out-of-pocket expenses - require policy reforms that expand coverage generosity, address drug pricing, improve utilization-management transparency, and strengthen protections against medical debt. Conceptualizing financial toxicity through a social-ecological lens underscores that meaningful progress requires multilevel interventions and coordinated efforts across patients, clinicians, institutions, communities, and policymakers.
This review highlights recent advances in immunotherapy for head and neck oncology, focusing on pivotal studies, both early-stage and late-stage, published or presented in 2025. Noteworthy results were reported with immune checkpoint inhibitors in mucosal squamous cell carcinoma of the head and neck (SCCHN) (KEYNOTE-689 and NIVOPOSTOP trials evaluating pembrolizumab and nivolumab, respectively, in the perioperative setting); in nasopharyngeal carcinoma (DIPPER and DIAMOND trials evaluating camrelizumab and toripalimab, respectively, in the curative setting with radiotherapy, and tagitanlimab in recurrent and/or metastatic disease); in cutaneous squamous cell carcinoma of the head and neck region (C-POST trial in the adjuvant setting and the combination of avelumab with cetuximab in the palliative setting); and in BRAF V600E-mutated anaplastic thyroid carcinoma (pembrolizumab with dabrafenib and trametinib). Passive immunotherapy targeting tumor-associated antigens also showed encouraging activity in R/M-SCCHN (petosemtamab, ficerafusp-alfa, amivantamab, enfortumab vedotin) and in heavily pretreated R/M nasopharyngeal carcinoma (antibody-drug conjugates becotatug vedotin and izalontamab brengitecan [iza-bren]). Recent advances highlight a rapid surge in positive immunotherapy trials across different head and neck cancer entities, with clinical benefit observed both when immune checkpoint inhibitors are moved earlier in the disease course and when they are combined with agents targeting resistance mechanisms or enabling more precise drug delivery to tumors.
The global rise in obesity, metabolic syndrome (MetS), insulin resistance (IR), and type 2 diabetes mellitus (T2DM) is reshaping the epidemiology of thyroid disorders, particularly thyroid nodular disease and differentiated thyroid cancer (DTC). This review summarizes emerging evidence linking metabolic dysfunction to thyroid nodule growth and tumorigenesis. Chronic hyperinsulinemia in IR states activates mitogenic pathways, including PI3K/AKT/mechanistic target of rapamycin (mTOR) and MAPK/ERK. These effects are amplified in thyrocytes overexpressing insulin receptor isoform A (INSR-A) and insulin-like growth factor 1 receptor (IGF1R). Dysfunctional adipose tissue further increases risk through enhanced leptin signaling, reduced adiponectin-mediated AMPK activation, and persistent systemic inflammation and oxidative stress. Environmental factors such as endocrine-disrupting chemicals and gut microbiota alterations add additional susceptibility. Clinical evidence supports these mechanistic links: patients with thyroid nodules consistently show higher HOMA-IR values, and large cohort studies identify MetS as an independent predictor of thyroid nodularity. Female-specific susceptibility appears to be mediated by estrogen receptor activity, adipokine profiles, and postmenopausal fat redistribution. Therapeutically, metformin shows promise via AMPK activation and mTOR inhibition, exerting both metabolic and antiproliferative effects, although randomized trials specific to thyroid cancer outcomes remain limited. Concerns about GLP-1 receptor agonists and thyroid safety are largely theoretical; current data suggest their established cardiometabolic benefits may outweigh potential risks. Converging epidemiological, molecular, and translational evidence underscores the complex interplay between metabolic dysfunction and thyroid diseases. Integrating metabolic health into prevention, risk stratification, and treatment strategies will be essential for advancing precision management of thyroid nodules and DTC.
PARP inhibitors (PARPi) have rapidly reshaped the treatment landscape for metastatic prostate cancer, moving from biomarker-selected monotherapy in metastatic castration-resistant prostate cancer (mCRPC) to first-line combination strategies with androgen receptor pathway inhibitors (ARPIs) and more recently, into metastatic hormone-sensitive disease (mHSPC). This review summarizes the evidence-based use of PARPi in metastatic prostate cancer, integrating the mechanistic rationale and guideline perspectives. We also highlight the resistance mechanisms that inform patient selection and underpin emerging strategies. The most consistent and clinically meaningful benefit from PARPi is observed among patients with deleterious BRCA1/2 alterations, whereas outcomes among patients with non- BRCA defective homologous recombination repair (HRR) gene subsets are heterogeneous and often modest. Pairing PARPi with ARPI in mCRPC patients bearing HRR mutations, especially BRCA1/2 mutations, not only improves clinical outcomes but also increases toxicity. Furthermore, uncertainty remains regarding the overall impact of the incremental benefit of PARPi/ARPI combinations over sequential therapy. Expansion into mHSPC further underscores the field's shift toward earlier, genomically guided treatment intensification strategies. Clinical practice is converging on early comprehensive genomic testing and prioritization of PARPi-based therapy for HRR-altered, especially BRCA1/2 -mutated, prostate cancer. Key research priorities include functional biomarkers beyond gene panels, rational combinations to prevent/overcome resistance, and optimized sequencing across disease states.
To review the current evidence and inform clinical guidance on the implications of incomplete ovarian function suppression (OFS), the utility of serum estradiol (E2) monitoring, and appropriate management strategies in premenopausal women with early breast cancer (eBC) receiving adjuvant luteinizing hormone-releasing hormone agonist (LHRHa)-based therapy for OFS. A universally accepted definition of incomplete OFS is currently lacking. Although biologically it is plausible that incomplete OFS may compromise the efficacy of endocrine therapy, its actual impact on clinical outcomes remains unclear. Currently, the reliability of E2 monitoring is limited by considerable variability in assay methods and reference ranges, raising concerns about its analytical validity. Notably, in a recent international survey of 205 oncologists managing patients with eBC, 43% reported routinely and 27% occasionally assessing E2 levels in premenopausal patients treated with LHRHa, suggesting inconsistent clinical practice. Standard immunoassays were the most frequently used (65%). However, interpretation of E2 values and subsequent management decisions varied widely, highlighting the absence of standardized clinical guidelines. Although not currently supported by high-level evidence, serum E2 monitoring is widely adopted in clinical practice. Prospective studies and evidence-based recommendations are urgently needed. Emerging strategies to overcome incomplete OFS include LHRH antagonists (e.g., degarelix) and oral SERDs.
High-quality research is essential to enhance the delivery and outcomes of supportive care for patients with cancer. In this review, we discuss key challenges and potential solutions for conducting supportive care clinical trials in oncology. Structural barriers to supportive care research include limited infrastructure and investigators, insufficient funding, a paucity of foundational research, and a lack of standardized terminologies. Process barriers involve challenges in patient recruitment and retention, intervention design, control selection, and outcome assessments. Recognition of these barriers enables the development of targeted strategies to overcome them. Encouragingly, there is growing awareness of the importance of supportive care among investigators, clinicians, patients, and healthcare administrators, leading to an increase in research activity, funding, and publications. Research centers and professional organizations dedicated to supportive care are actively building capacity and fostering collaboration. Additionally, innovative study designs, personalized outcome measures, and multicenter research networks offer promising strategies to enhance both the quantity and quality of clinical trials. Through interdisciplinary collaborations, we can continue to strengthen the infrastructure and refine the processes in supportive care trials. These efforts will help build a robust evidence base and ultimately improve outcomes for patients with cancer.
Acute myeloid leukemia (AML) characterized by NPM1 mutations or KMT2A rearrangements depends on abnormal epigenetic programs mediated by menin, a critical scaffold protein for sustaining the expression of oncogenic HOX/MEIS1 genes. Therefore, menin inhibitors have become a promising class of AML treatments. Early-phase trials have shown that agents such as revumenib, ziftomenib, bleximenib, and enzomenib are active, particularly in relapsed/refractory disease, with 23-48% of patients achieving composite complete remission. However, the durability of single-agent treatment remains limited, and resistance mechanisms, such as MEN1 mutations or transcriptional reprogramming, have been identified. Consequently, combination approaches involving venetoclax, hypomethylating agents, or chemotherapy are being investigated to improve response depth and duration. Recent SAVE, KOMET-007, and cAMeLot-2 trials have demonstrated high overall response rates (68%-100%) and encouraging MRD-negative complete remissions when combining menin inhibitors with venetoclax-based regimens. This has been observed even in patients who have previously received venetoclax. Combinations with intensive chemotherapy (e.g., 7 + 3) in the frontline setting have also yielded high CRc rates (up to 94% in NPM1-mutated AML) without exacerbating toxicity. These findings justify the integration of menin inhibitors into the AML therapeutic landscape, and support ongoing randomized trials to confirm their benefit in both frontline and relapse or refractory settings.
To summarize the development, validation, and current clinical use of the Skin and Ultraviolet Neoplasia Risk Assessment Calculator (SUNTRAC) tool. We also discuss key gaps, including the need for greater personalization, incorporation of additional risk factors, and clearer clinical protocols to support its integration into routine care. Skin cancer remains the most frequent malignancy in solid organ transplant recipients (SOTRs), driven by long-term immunosuppression and other patient-specific risk factors. The SUNTRAC tool was developed to stratify skin cancer risk in this population using five key variables: Caucasian ethnicity, prior history of skin cancer, older age at transplant, male sex, and thoracic organ transplantation. Based on these well established risk factors, patients are categorized into defined risk groups with tailored screening recommendations. Furthermore, large European studies have validated the SUNTRAC tool in diverse populations and extended its utility beyond squamous cell carcinoma to include basal cell carcinoma. Additional research has explored refinements to improve its accuracy and clinical applicability. The SUNTRAC tool is the most recent risk stratification model specifically designed to assess skin cancer risk in solid organ transplant recipients (SOTRs). Although international validation studies have demonstrated its utility across diverse populations, standardized guidelines for its clinical implementation remain lacking. Despite strong external validation and wide availability, SUNTRAC is still inconsistently implemented in transplant referral pathways and guideline-driven care, illustrating a persistent gap between evidence and routine practice.
Cancer survivorship is increasingly recognized as an important component of cancer care, yet access to high-quality care remains inconsistent globally. This review highlights priorities for advancing survivorship care worldwide, focusing on equity of access, outcomes for vulnerable populations, multidisciplinary models, technology-enabled interventions, and global collaboration. Survivorship needs differ across tumor streams and cancer sub-populations, especially older adults, adolescent, and people with advanced or metastatic cancers who face unique physical, psychosocial, and other practical challenges. Models that involve a variety of clinicians, such as oncologists and hematologists, primary care providers, nurses and allied health providers maintain quality of life, reduce healthcare costs, and support patient preferences, yet most countries still rely on oncologist-led follow-up. Digital health and artificial intelligence have the potential to enhance symptom monitoring, improve patient engagement, and deliver personalized care. Surveys led by the International Psycho-Oncology Society (IPOS) and Multinational Association of Supportive Care in Cancer (MASCC) reveal persistent disparities, particularly in low-income and middle-income countries and communities, highlighting evident gaps in supportive care access, infrastructure, and guideline implementation. Advancing high-quality survivorship care requires embedding equity into research and policy, expanding multidisciplinary and technology-enabled care models, and strengthening global collaboration. Longitudinal studies, region-specific guidelines, and capacity building in low-resource and middle-resource settings are essential. Implementing these strategies can optimize the outcomes and ensure sustainable care delivery for cancer survivors worldwide.
Smoldering myeloma (SMM) is an asymptomatic precursor condition of multiple myeloma (MM) with a prevalence of about 0.5% in those aged >40 years age. While the current standard of care is active surveillance, there is a growing interest to determine the effectiveness of early intervention in this condition. This review discusses the contemporary trials focussed on treating SMM and the case for additional data in this space. It is imperative to note that the risk stratification for SMM has constantly evolved over time. A proportion of patients with SLiM-CRAB [≥60% bone marrow plasma cells (BMPCs), free light chain ratio (sFLC-ratio) ≥100, and >1 MRI-defined ≥5 mm focal bony lesion, hypercalcemia, renal insufficiency, anaemia, lytic bone lesions], who were classified as high-risk-SMM in the past, have now been classified as MM, based on the IMWG-2014 diagnostic criteria. Current research on SMM risk stratification is focussed on developing models based on longitudinal trends, rather than single-point measures. Earlier trials were studying disease control strategy, working towards delaying disease progression. As the results were promising, currently, there are more trials utilizing intensive treatment approaches aiming at cure to eradicate disease clone (achieving sustained MRD negativity). Further ongoing trials, are attempting to refine disease control strategy and utilize immunotherapies. We need more high-quality evidence in post-SLiM-CRAB SMM cohort to better identify the subset of patients most likely to benefit from early intervention. Treatment approaches should be refined considering patient preferences and maintaining quality of life (QoL).
Supportive care is no longer a secondary aspect of oncology; it is the foundation that enables people with cancer not only to survive but to live with dignity, comfort, and relief throughout and beyond treatment. In 2025, as cancer survival improves globally, the need to integrate supportive care as a universal standard has become increasingly urgent. This review is timely and relevant as it examines the current global landscape of supportive care and the persisting inequities that threaten its implementation across health systems. Over the past three and a half decades, the Multinational Association of Supportive Care in Cancer (MASCC) has been central to the evolution of the field by advancing research, developing evidence-based guidelines, training health care professionals, and amplifying the voices of patients and caregivers. Despite this progress, major disparities remain. High-income countries increasingly embed supportive care within standard oncology practice, while many low- and middle-income countries face limited access to essential medicines, trained staff, and survivorship programs. This commentary reflects an international perspective on where supportive care stands and where it must go. It highlights MASCC's contributions and future vision through its Study Groups, Centers of Excellence, and the Supportive Care 2030 Movement, a global roadmap for equity, universal access, and improved patient-reported outcomes. Supportive care is not optional; it is a right and a prerequisite for quality cancer care and survivorship, requiring sustained innovation, inclusivity, and global commitment.
Reirradiation has emerged as a potentially valuable treatment strategy for recurrent glioblastoma, a disease characterized by inevitable local progression despite aggressive multimodal first-line therapy. Recent advances in radiotherapy techniques, improved patient selection, and evolving systemic treatment combinations have renewed clinical interest in this approach. This is reflected by recent publication of the first international consensus guidelines (ESTRO/EANO) and the initiation of an European phase III randomized trial on reirradiation of patients with recurrent glioblastoma. Retrospective and early-phase prospective studies have demonstrated that reirradiation is feasible and well tolerated in selected patients, with median overall survival ranging from 7 to 13 months. The ESTRO/EANO guidelines on reirradiation of glioma provide standardized recommendations for patient selection, dose constraints, and target volume delineation. Meta-analyses suggest improved outcomes when reirradiation is combined with systemic therapies, such as bevacizumab or lomustine. The phase III EORTC-2227-BTG (LEGATO) trial will provide definitive data on survival benefit. Reirradiation is gaining acceptance as a palliative yet potentially impactful treatment for recurrent glioblastoma. While current evidence supports its use in selected cases, results from ongoing phase III LEGATO trial will determine its future role in standard care and inform evidence-based clinical decision-making.
Antibody-drug conjugates (ADCs) have emerged as a significant therapeutic class in lung cancer, integrating the target specificity of monoclonal antibodies with the cytotoxic potency of chemotherapeutic agents. This review delineates ADC structure, mechanisms of action, and clinical advancements in nonsmall-cell lung cancer (NSCLC) and small-cell lung cancer (SCLC), with a focus on novel bispecific formats to address tumor heterogeneity and therapeutic approaches to overcome resistance mechanisms. Multiple ADCs have demonstrated significant clinical activity in biomarker-defined patient subsets. The human epidermal growth factor receptor 2 (HER2)-targeted ADC trastuzumab deruxtecan has demonstrated unprecedented efficacy in HER2 -mutant NSCLC, resulting in global regulatory approvals. Novel ADC targets such as TROP2, HER3, MET, CEACAM5, integrin β6, DLL3, B7-H3, and SEZ6 are undergoing clinical evaluation. Advancements in payload design, linker stability, and conjugation methodologies have enhanced therapeutic indices. Concurrently, bispecific ADCs are emerging to address challenges posed by intratumoral heterogeneity and antigen-loss-mediated resistance mechanisms. ADCs are transforming lung cancer therapy by delivering potent cytotoxics with manageable safety. Next-generation bispecific and biparatopic formats may broaden eligibility, improve tumor penetration, and delay resistance. Incorporating predictive biomarkers and real-time monitoring will be key to their use in earlier disease and to establishing ADCs as a cornerstone of precision oncology.
To summarize recent updates in the classification, clinical trial evidence, and evolving treatment strategies for nonclear cell renal cell carcinoma (nccRCC). The 2022 WHO classification eliminated the type 1/2 papillary paradigm, refined molecularly defined tumors such as fumarate hydratase (FH)-deficient and anaplastic lymphoma kinase-rearranged RCC, while acknowledging indolent tumors like clear cell papillary renal cell tumors. Prospective and retrospective data increasingly support the use of immune checkpoint inhibitor (ICI)-based regimens, particularly ICI/ tyrosine kinase inhibitor (TKI) combinations. KEYNOTE-B61 and ARON-1 demonstrated consistent activity of pembrolizumab + lenvatinib across nccRCC subtypes, while the randomized SUNNIFORECAST trial validated ipilimumab + nivolumab as a first-line option with overall survival (OS) benefit over standard therapy. Subtype-specific approaches are also emerging: bevacizumab + erlotinib and sintilimab + axitinib showed high response rates in FH-deficient RCC, and prognostic tools such as VENUSS remain valuable for papillary RCC risk stratification. Despite progress, many studies remain limited by histologic heterogeneity and small sample sizes. Multiple ongoing trials, including ICONIC, SAMETA, and PAPMET2, are expected to further clarify optimal management strategies in 2026. Therapeutic advances are reshaping the management of nccRCC, with IO/TKI regimens and histology-specific therapies showing promise. Continued integration of molecular classification, rare subtype-specific trials, and international collaboration will be essential to establish evidence-based treatment standards for this diverse and understudied population.
Remaining challenges in management of patients with germ cell tumors (GCTs) include selecting the optimal treatment modality in patients with early metastatic disease, biomarker development and developing newer treatments in patients with refractory disease. This review aims to highlight recent developments in these domains. For patients with testicular seminoma with low-volume retroperitoneal lymphadenopathy, retroperitoneal lymph node dissection is a viable treatment option. Novel biomarkers showing promise in patients with GCTs include circulating tumor DNA and microRNA 371; with further validation from larger prospective studies, these may be useful in clinical decision making in patients with GCTs. Claudin 6's ubiquitous expression in testicular GCTs has enabled the development of several ongoing clinical trials targeting it and these therapies may be promising in treating patients with refractory GCTs. Management of patients with GCT requires a multidisciplinary approach and patients with advanced disease being considered for surgery or those with refractory disease should be referred to a high-volume treatment center. Outcomes in refractory GCT remain poor, but several novel treatment options and approaches are being explored in clinical trials to improve cure rates in this patient population.
To examine the persistent global disparities in breast cancer outcomes, focusing on inequities in access to essential therapeutics, diagnostics, and emerging innovations, while highlighting current policy actions and international initiatives addressing these gaps. Although survival rates for breast cancer have improved in high-income countries, significant inequalities remain in low- and middle-income settings. Access to timely diagnosis, standard treatments, and novel therapeutics such as targeted agents and immunotherapies is uneven. Recent global initiatives, including the WHO Global Breast Cancer Initiative, aim to enhance early detection, standardize care pathways, and improve access to affordable, quality-assured treatments. Policy frameworks are increasingly addressing issues of availability, affordability, and infrastructure, yet implementation remains inconsistent. Bridging global breast cancer disparities demands coordinated action integrating health system strengthening, policy reform, and international collaboration. Equitable access to therapeutics and diagnostics must be prioritized to ensure that advancements in breast cancer care translate into improved outcomes worldwide.
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. 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. 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.
This review aims to summarize the current clinical evidence and future perspectives on the use of antiandrogen therapies in metastatic breast cancer, focusing on hormone receptor-positive and triple-negative subtypes, expressing androgen receptor (AR). We discuss recent clinical trials evaluating AR-targeted agents and explore mechanisms of resistance and novel therapeutic strategies. Clinical trials of androgen-targeting have shown modest activity in AR-positive metastatic breast cancer, with variable disease control rates and progression-free survival depending on AR expression levels, intrinsic AR-dependency and tumor subtype. Combination therapies targeting AR alongside pathways like CDK4/6 and PI3K/AKT/mTOR appear promising in overcoming therapeutic resistance. New-generation agents, including PROTACs, nonligand-binding domain AR inhibitors and epigenetic modulators offer innovative approaches to target AR signalling. Despite encouraging preclinical data, antiandrogen therapies have not demonstrated robust strong clinical efficacy in metastatic, AR-positive breast cancer, and their use in the clinical practice is still very limited. Improved patient selection using validated predictive biomarkers is crucial. Combination regimens and next-generation AR-targeting agents represent the future direction to overcome resistance and optimize therapeutic outcomes in AR-driven breast cancers.
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. 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. 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.
Psychological and existential distress are common across the cancer trajectory and can impair quality of life, treatment adherence, and family functioning. Although psychosocial and pharmacological interventions provide meaningful support, their overall effects are often modest. This review examines the emerging role of psychedelic-assisted therapy (PAT) as a potential approach to better address the multidimensional nature of cancer-related distress. PAT combines psychedelic compounds with structured psychotherapeutic support and typically includes preparatory sessions, a supervised dosing experience, and post-session integration. Psychedelics are thought to enhance neuroplasticity and emotional flexibility, creating conditions that may support sustained psychological change. Recent trials in advanced cancer populations report improvements in anxiety, depression, pain-related distress, and quality of life following one or two dosing sessions. Current evidence remains limited by small and demographically narrow samples, variable treatment protocols, and potential expectancy effects. Implementation also presents practical challenges, including training requirements, time demands, and resource intensity. Despite these limitations, growing international interest may facilitate further development, supporting the need for careful and rigorous evaluation of PAT as a novel intervention for cancer-related distress.