Immuno-Oncology in Cancer Therapy: Mechanistic Insights, Clinical Applications, and Future Perspectives

Abstract

Cancer remains a major global health challenge despite significant advances in conventional treatment modalities such as surgery, chemotherapy, and radiotherapy. These approaches are often limited by lack of specificity, systemic toxicity, tumor heterogeneity, and the development of therapeutic resistance. Immuno-oncology has emerged as a transformative paradigm in cancer therapy by harnessing the intrinsic ability of the immune system to recognize and eliminate malignant cells. This review provides a comprehensive overview of the fundamental principles underlying tumor–immune system interactions, including immune surveillance, cancer immunoediting, and mechanisms of tumor immune evasion. Major immunotherapeutic strategies such as immune checkpoint inhibitors, adoptive cell therapies, cancer vaccines, oncolytic viruses, and cytokine-based therapies are critically discussed with emphasis on their mechanisms of action and clinical relevance. The role of the tumor microenvironment, including immunosuppressive cell populations, stromal and vascular barriers, and the influence of the gut microbiome on immunotherapy response, is highlighted. Furthermore, the review examines predictive biomarkers such as PD-L1 expression, tumor mutational burden, microsatellite instability, Immunoscore, and emerging liquid biopsy approaches that aid in patient stratification and treatment optimization. Current clinical applications in solid tumors and hematologic malignancies, as well as combination immunotherapeutic strategies, are summarized. Finally, key challenges including immune-related adverse events, resistance mechanisms, and cost barriers are addressed, along with future directions focusing on personalized immunotherapy, artificial intelligence-driven approaches, next-generation cellular therapies, and multi-omics integration. Collectively, this review underscores the pivotal role of immuno-oncology in reshaping modern cancer treatment and its potential to deliver durable and personalized therapeutic outcomes.

Keywords

Introduction

Figure 1. Evolution of Cancer Therapy and the Emergence of Immuno-Oncology.

The figure 1. illustrates the limitations of conventional cancer treatment modalities, including surgery, chemotherapy, and radiation therapy, highlighting issues such as non-specific toxicity, treatment resistance, tumor heterogeneity, and persistence of minimal residual disease. It further depicts the historical progression and clinical milestones in immuno-oncology, from early immune stimulation approaches such as Coley’s toxins and interleukin-2 therapy to the development of immune checkpoint inhibitors targeting PD-1, PD-L1, and CTLA-4. The figure also emphasizes modern immunotherapeutic strategies, including CAR-T cell therapy and cancer vaccines, underscoring the paradigm shift toward harnessing the immune system for durable and targeted cancer treatment.

2.The Immune System and Cancer

2.1 Basics of the Innate and Adaptive Immune System

The immune system comprises two interlinked arms the innate and the adaptive which together play a pivotal role in recognizing and eliminating abnormal or transformed cells, including nascent cancer cells. The innate immune system serves as the first line of defense: cells such as natural killer (NK) cells, macrophages, and dendritic cells (DCs) patrol the body and can detect aberrations in stressed or transformed cells. NK cells, for instance, can recognize “stress-induced” ligands or altered expression of major histocompatibility complex (MHC) molecules on tumor cells, enabling rapid cytotoxic responses. Macrophages and dendritic cells contribute by engulfing transformed or dying cells, processing cellular debris, and generating antigenic peptides [9]. These antigenic peptides are then presented by antigen-presenting cells (APCs), such as dendritic cells or macrophages, to T lymphocytes thereby bridging innate and adaptive immunity. Through this antigen presentation, adaptive immune responses are primed: naïve T cells differentiate into effector subsets (e.g., cytotoxic CD8+ T cells, helper CD4+ T cells) tailored to recognize tumour-associated antigens displayed on MHC molecules. Once activated, cytotoxic T cells can directly kill transformed cells by releasing cytolytic effectors (e.g., perforin, granzymes) and by producing inflammatory cytokines such as interferon-gamma (IFN-γ) that further activate immune responses. Cytokines and chemokines small signalling proteins secreted by immune (and non-immune) cells play crucial roles in coordinating immune cell recruitment, activation, and effector functions. APCs and other immune cells secrete cytokines that shape the immune milieu; chemokines guide cellular trafficking to tissues (including sites of tumorigenesis), enabling immune surveillance and immune response orchestration. Thus, through coordinated actions of innate effectors, antigen presentation by APCs, and adaptive T-cell responses, the immune system maintains surveillance for aberrant (including potentially cancerous) cells, offering a potent defence against tumor development [10].

2.2 Cancer Immunoediting

The concept of “immune surveillance” that the immune system patrols and eradicates emerging cancer cells has evolved into a more nuanced paradigm known as cancer immunoediting. Immunoediting describes a dynamic, ongoing interplay between the host immune system and transformed cells, shaping whether a nascent tumor is eliminated, held in check, or allowed to progress. This process is typically resolved into three sequential but overlapping phases: Elimination, Equilibrium, and Escape.  In the Elimination phase, the innate and adaptive immune arms collaborate to identify and eradicate transformed or abnormal cells before they become clinically apparent. NK cells, macrophages, dendritic cells, along with cytotoxic T lymphocytes cooperate: dendritic cells present tumor-associated antigens to T cells, triggering antigen-specific immune responses; NK and cytotoxic T cells directly kill tumour cells; and cytokines such as IFN-γ and interleukins contribute to an inflammatory milieu conducive to tumour cell destruction. When elimination is complete, tissue homeostasis is restored and no tumour develops [11]. However, if elimination is incomplete for example because some transformed cells escape initial detection or resist killing those residual cells may enter the Equilibrium phase. In equilibrium, the immune system does not succeed in eradicating all malignant cells, but it suppresses their outgrowth. Under selective pressure from the immune system, tumour cells may accumulate mutations, lose immunogenic features, or undergo alterations that reduce their visibility to immune effectors. Over prolonged time, often years, immunological “editing” sculpts the tumour cell population, selecting for less immunogenic variants. This phase represents a balance a stalemate between anti-tumour immune pressure and tumour cell survival. Some malignant clones may remain dormant, or grow very slowly, held in check by immune surveillance, but not eliminated [12]. Eventually, in some cases, tumour cells may acquire additional changes (genetic, epigenetic, phenotypic) that enable them to overcome immune control. This marks the Escape phase: tumour cells proliferate, become clinically manifest, and often develop mechanisms to suppress or subvert local immune responses. At this stage, the tumour microenvironment is reshaped to favour immunosuppression, enabling tumour progression, invasion, and metastasis.  Thus, immunoediting describes not only how the immune system can suppress tumour formation, but also how it can inadvertently select for tumour variants better able to survive immune pressure a double-edged sword that is central to modern immuno-oncology thinking [13].

2.3 Mechanisms of Tumor Immune Evasion

To progress and manifest clinically, tumour cells frequently hijack or distort normal immune mechanisms, deploying multiple evasion strategies. One primary mechanism is upregulation of immune checkpoint molecules, such as programmed death-ligand 1 (PD-L1) or other inhibitory receptors/ligands. By expressing these “immune brakes,” tumour cells directly inhibit the activation or cytotoxic functions of T cells, preventing immune destruction even in the presence of antigen recognition.  Another critical mechanism is generation of an immunosuppressive tumour microenvironment (TME). Within the TME, tumour cells often recruit or reprogram non-malignant stromal and immune cells for example, suppressive myeloid cells, tumor-associated macrophages (TAMs), regulatory T cells (Tregs), and myeloid-derived suppressor cells (MDSCs) which collectively inhibit effective anti-tumour immune responses. These immunosuppressive cells secrete inhibitory cytokines (e.g., TGF-β, IL-10), metabolic mediators, and factors that impair effector T-cell function or survival, thereby fostering immune tolerance or exhaustion.  Defective antigen presentation represents another major evasion pathway. Tumour cells may downregulate expression of MHC class I molecules or other components essential for antigen processing and presentation. They may also impair the maturation or function of antigen-presenting cells (e.g., dendritic cells), preventing effective priming of T cells. Without appropriate antigen presentation, cytotoxic T cells cannot recognize or respond to tumour antigens, allowing tumour cells to persist undetected. Finally, expansion of regulatory T cells (Tregs) within the TME contributes to immune suppression. Tregs inhibit effector T-cell activity and cytokine production, dampening anti-tumour immunity and providing a permissive environment for tumour growth and progression.  These mechanisms often operate in concert tumour cells may downregulate antigen presentation while upregulating checkpoint molecules and inducing immunosuppressive stromal elements thereby constructing a multi-layered barrier against immune-mediated elimination. This complexity underlies the difficulty many cancers exhibit in responding to immunotherapy, and also explains why immune-based therapies must be carefully designed to overcome several evasion strategies simultaneously [14].

3. Immuno-Oncology Therapeutic Strategies

3.1 Immune Checkpoint Inhibitors (ICIs)

Immune checkpoint inhibitors have revolutionized modern cancer therapy by restoring T-cell–mediated antitumor immunity. Among the most widely used ICIs are inhibitors targeting the PD-1/PD-L1 pathway. The programmed cell death protein-1 (PD-1), expressed on activated T cells, interacts with its ligands PD-L1 and PD-L2 on tumor cells and antigen-presenting cells, leading to T-cell exhaustion and immune tolerance. Monoclonal antibodies such as nivolumab and pembrolizumab block this interaction and reactivate cytotoxic T-cell responses, resulting in significant improvements in survival across malignancies including melanoma, non-small cell lung cancer (NSCLC), renal cell carcinoma, and head and neck cancers [15]. Another major checkpoint pathway involves cytotoxic T-lymphocyte–associated protein-4 (CTLA-4), which acts during early T-cell priming. Ipilimumab, the first FDA-approved CTLA-4 inhibitor, demonstrated survival benefit in advanced melanoma, marking a pivotal breakthrough in immuno-oncology. The mechanisms of action of ICIs rely on the removal of inhibitory signals that normally constrain T-cell activation, thereby enabling robust and durable antitumor immunity. Numerous clinical trials have established their efficacy, resulting in broad regulatory approvals worldwide. However, ICIs can trigger immune-related adverse events affecting multiple organs, which remain a key clinical challenge. Despite this, ICIs continue to represent a cornerstone of modern oncology, offering durable responses in a subset of patients and reshaping therapeutic standards across cancer types [16].

3.2 Adoptive Cell Therapies (ACT)

Adoptive cell therapy is an advanced immunotherapeutic approach that involves the ex vivo modification or expansion of immune cells followed by reinfusion into the patient to achieve targeted tumor destruction. One of the most transformative modalities within ACT is chimeric antigen receptor T-cell (CAR-T) therapy, in which patient-derived T cells are genetically engineered to express synthetic receptors that redirect them toward tumor-associated antigens [17]. CAR-T therapies such as tisagenlecleucel and axicabtagene ciloleucel have achieved remarkable success in hematologic malignancies, particularly B-cell lymphomas and acute lymphoblastic leukemia, where high complete remission rates have been reported. In addition to CAR-T cells, TCR-engineered T-cell therapies enhance natural T-cell receptor specificity toward intracellular tumor antigens presented via MHC complexes. These therapies offer promise in treating solid tumors, although issues such as antigen heterogeneity and MHC restriction present ongoing challenges. Another important ACT strategy involves tumor-infiltrating lymphocytes (TILs). These lymphocytes are isolated directly from tumor tissue and expanded to large numbers before reinfusion, allowing for polyclonal recognition of multiple tumor antigens. TIL therapy has demonstrated notable success in metastatic melanoma, with durable responses observed in heavily pretreated patients. Despite their advantages, ACT approaches are associated with limitations including high manufacturing complexity, cytokine release syndrome, neurotoxicity, and limited efficacy against solid tumors due to hostile tumor microenvironments. Nevertheless, ongoing innovations in synthetic biology and cell engineering continue to enhance the safety and effectiveness of ACT in clinical practice [18].

3.3 Cancer Vaccines

Cancer vaccines aim to stimulate the immune system to recognize and eliminate malignant cells by presenting tumor-associated or tumor-specific antigens. These vaccines can be categorized as preventive or therapeutic. Preventive vaccines, such as the HPV and HBV vaccines, work by protecting against virus-associated malignancies and represent one of the earliest successes of immuno-oncology [19]. Therapeutic cancer vaccines, designed to trigger immune responses against established tumors, employ a variety of platforms including peptide-based, dendritic cell-based, and nucleic acid vaccines such as DNA and mRNA constructs. Sipuleucel-T, a dendritic cell vaccine approved for metastatic castration-resistant prostate cancer, demonstrated improved overall survival and paved the way for further development of personalized vaccine strategies. Recent advances in genome sequencing have enabled the development of neoantigen-based vaccines that target tumor-specific mutations unique to individual patients. These personalized vaccines have shown encouraging immunogenicity and favorable safety profiles in early-phase clinical trials. Despite their promise, cancer vaccines face challenges including antigen variability, suboptimal immunogenicity, and the immunosuppressive nature of the tumor microenvironment. Continued efforts in combination strategies and vaccine adjuvant development are expected to significantly enhance their therapeutic potential [20].

3.4 Oncolytic Virus Therapy

Oncolytic virus therapy utilizes genetically engineered or naturally occurring viruses that selectively infect and lyse tumor cells while simultaneously activating systemic antitumor immunity. The therapeutic mechanism involves direct tumor-cell destruction via viral replication, followed by the release of tumor antigens and inflammatory signals that promote immune activation. This dual mechanism offers a unique advantage over conventional therapies [21]. Talimogene laherparepvec (T-VEC), a modified herpes simplex virus type-1 expressing GM-CSF, became the first FDA-approved oncolytic virus for melanoma after demonstrating improved durable response rates in clinical trials [8]. Emerging viral platforms, including adenoviruses, vaccinia viruses, and reoviruses, are currently undergoing clinical evaluation for a variety of solid tumors. Oncolytic viruses also show promise as part of combination therapies, particularly with immune checkpoint inhibitors, due to their ability to modulate the tumor microenvironment and enhance antigen presentation. While safety profiles are generally favorable, challenges such as antiviral immunity, delivery limitations, and variable tumor susceptibility remain barriers to widespread clinical integration. Nevertheless, ongoing advancements in viral engineering continue to expand the therapeutic potential of this modality [22].

3.5 Cytokine-Based Therapies

Cytokine-based immunotherapies aim to amplify antitumor immune responses by administering immune-modulating proteins such as interleukin-2 (IL-2) and interferon-alpha (IFN-α). High-dose IL-2 has demonstrated durable responses in subsets of patients with metastatic melanoma and renal cell carcinoma, marking one of the earliest successes in immuno-oncology. IFN-α has also been used in hematologic malignancies and melanoma, where it provides immune stimulation and exhibits antiproliferative effects. Despite their therapeutic potential, first-generation cytokines are limited by severe systemic toxicities, narrow therapeutic windows, and modest response rates. To address these limitations, next-generation engineered cytokines have been developed to enhance specificity, reduce toxicity, and prolong half-life. Pegylated cytokines and receptor-biased cytokine variants represent promising strategies that aim to maximize antitumor efficacy while minimizing systemic adverse effects. Although challenges remain, cytokine therapies continue to hold significant potential, particularly in combination regimens with ICIs, ACT, or cancer vaccines, where synergistic effects have been observed [23].

4 Tumor Microenvironment (TME) And Immunotherapy

4.1 Immunosuppressive Cell Types

Within solid tumours the immune landscape is often dominated by specialized cell populations that actively suppress anti-tumour immunity and blunt the efficacy of immunotherapies. Regulatory T cells (Tregs), characterized by expression of the transcription factor FoxP3, accumulate in many malignancies where they inhibit effector T cell proliferation and cytokine production through contact-dependent mechanisms and secretion of immunosuppressive cytokines such as IL-10 and TGF-β. Their abundance in the tumour bed correlates with poorer clinical outcomes in a number of cancers and Treg depletion or functional modulation has emerged as a potential strategy to enhance checkpoint blockade and adoptive cell therapies [24]. Myeloid-derived suppressor cells (MDSCs) comprise a heterogeneous group of immature myeloid cells that expand during malignancy and systemic inflammation and suppress T cell responses by multiple mechanisms including arginine depletion, inducible nitric oxide synthase activity, reactive oxygen species production, and by driving regulatory cell networks. MDSCs also support tumour progression non-immunologically by promoting angiogenesis and facilitating metastatic dissemination; consequently, therapeutically targeting MDSC recruitment, differentiation or suppressive functions is actively pursued to relieve an important axis of resistance to immunotherapy [25]. Tumour-associated macrophages (TAMs) are highly plastic and are often skewed toward an alternatively activated, tumour-promoting phenotype within the TME. TAMs foster tumour growth by stimulating angiogenesis, remodeling extracellular matrix, promoting invasion and metastasis, and by expressing checkpoint ligands and immunosuppressive mediators that inhibit cytotoxic T cells. Because of their multifaceted pro-tumour roles, strategies aimed at repolarizing TAMs to a pro-inflammatory phenotype, blocking their recruitment, or inhibiting their trophic functions are being combined with checkpoint inhibitors in preclinical and clinical studies [26].

4.2 Stromal and Vascular Barriers

The non-cellular tumour stroma and the abnormal tumour vasculature together create physical and biochemical barriers that restrict immune cell infiltration and function. Extracellular matrix (ECM) remodeling is a dynamic process in tumours: malignant and stromal cells alter the composition, crosslinking and stiffness of ECM components, which both supports malignant cell survival and mechanically impedes T cell trafficking into tumour islets. Proteolytic remodeling releases matrix-bound growth factors and generates bioactive fragments that further sculpt immune behaviour and can create niches favourable for immune suppression rather than immune clearance [27]. Tumour vasculature is typically irregular, leaky and poorly perfused, producing regions of hypoxia and acidosis that directly impair effector T cell metabolism and favour recruitment or activation of suppressive populations such as MDSCs and Tregs. Hypoxia-driven signalling upregulates multiple immunosuppressive pathways, including VEGF and adenosine axes, and contributes to resistance against checkpoint blockade and other immune-based therapies. Approaches that normalize tumour blood vessels or reduce hypoxia can therefore improve immune cell access and function and synergize with immunotherapy, a concept now supported by both preclinical models and early clinical data [28]. Because stromal and vascular alterations are not merely passive barriers but active modulators of immune phenotype, combination strategies that target ECM remodeling enzymes, stromal signaling or vascular normalization are being tested to convert “immune-cold” tumours into “immune-hot” ones more amenable to checkpoint blockade [29].

4.3 Role of Microbiome in Immunotherapy Response

Accumulating evidence demonstrates that the composition and diversity of the gut microbiome influence systemic anti-tumour immunity and the clinical activity of immune checkpoint inhibitors (ICIs). Studies in melanoma and other cancers have shown that particular microbial communities and species are associated with improved responses to anti-PD-1 therapy, whereas antibiotic exposure or dysbiosis often correlates with poorer outcomes. Mechanistically, gut microbes can modulate systemic T cell priming, antigen cross-presentation, and the balance of pro- versus anti-inflammatory metabolites that ultimately shape tumour immune surveillance [30]. These findings have prompted interventional strategies including fecal microbiota transplantation, defined probiotic consortia, dietary modification, and cautious use of antibiotics aimed at manipulating the microbiome to enhance ICI efficacy. While promising, the field is nascent: inter-patient variability, the context-dependent effects of specific taxa, and safety concerns require carefully controlled clinical trials to determine which microbiome interventions are reproducibly beneficial and how they should be integrated with existing immunotherapies [31].

5. Predictive Biomarkers in Immuno-Oncology

Predictive biomarkers play a crucial role in identifying patients who are most likely to benefit from immuno-oncology therapies. Programmed death ligand-1 expression has been extensively studied as a biomarker for response to immune checkpoint inhibitors. Tumors with higher PD-L1 expression on cancer cells or immune infiltrates have shown improved responses to anti-PD-1 and anti-PD-L1 therapies, particularly in non-small cell lung cancer and melanoma. However, variability in assay platforms, scoring systems, and tumor heterogeneity has limited its universal applicability [32]. Tumor mutational burden represents another important predictive marker, reflecting the total number of somatic mutations within a tumor genome. A high tumor mutational burden increases the likelihood of neoantigen formation, thereby enhancing tumor immunogenicity and responsiveness to immune checkpoint blockade. Clinical studies have demonstrated improved outcomes with immunotherapy in tumors exhibiting elevated tumor mutational burden, including melanoma and lung cancer, although standardized cut-off values remain under debate [33]. Microsatellite instability results from defects in the DNA mismatch repair system and leads to genomic instability. Tumors with high microsatellite instability display increased immune cell infiltration and robust responses to immune checkpoint inhibitors, prompting tissue-agnostic regulatory approvals for PD-1 inhibitors in microsatellite instability-high cancers [34]. The Immunoscore, based on quantifying immune cell populations within the tumor microenvironment, has emerged as a powerful prognostic and predictive tool, particularly in colorectal cancer. Gene expression signatures reflecting immune activation and interferon signaling pathways further complement biomarker-based patient selection [6]. Emerging biomarkers such as circulating tumor DNA and tumor-derived exosomes offer non-invasive approaches to monitor treatment response and resistance in real time, representing a promising frontier in immuno-oncology biomarker research [35].

6. Clinical Applications and Current Evidence

6.1 Immunotherapy in Solid Tumors

Immunotherapy has transformed the treatment landscape of several solid tumors. In melanoma, immune checkpoint inhibitors targeting PD-1 and CTLA-4 have demonstrated durable responses and significant survival benefits, even in advanced disease stages. Combination checkpoint blockade has further improved efficacy, albeit with increased toxicity. In lung cancer, immunotherapy has become a cornerstone of treatment, both as monotherapy and in combination with chemotherapy, significantly improving overall survival in patients with advanced non-small cell lung cancer [36]. Renal cell carcinoma has also shown remarkable responsiveness to immunotherapy, with checkpoint inhibitors replacing cytokine-based therapies as first-line treatment options. Similarly, in colorectal cancer, immunotherapy has shown profound efficacy in microsatellite instability-high tumors, establishing a biomarker-driven approach to treatment selection [37].

6.2 Immunotherapy in Hematologic Malignancies

In hematologic cancers, immunotherapy has achieved unprecedented success. Lymphomas have benefited from immune checkpoint inhibitors, particularly in Hodgkin lymphoma, where genetic alterations lead to PD-L1 overexpression [38]. In leukemias, chimeric antigen receptor T-cell therapy has demonstrated high remission rates in refractory acute lymphoblastic leukemia. Multiple myeloma has also shown encouraging results with CAR-T therapies targeting B-cell maturation antigen, resulting in deep and durable responses in heavily pretreated patients [39].

6.3 Combination Therapies

Combination strategies have been developed to overcome resistance and enhance therapeutic efficacy. The integration of immunotherapy with chemotherapy can increase antigen release and immune activation, leading to synergistic effects. Combining immunotherapy with targeted therapies has shown promise in modulating the tumor microenvironment and improving immune infiltration. Dual immune checkpoint blockade, particularly PD-1 and CTLA-4 inhibition, has demonstrated superior efficacy in certain malignancies, although careful patient selection is essential to manage toxicity [40].

CHALLENGES AND LIMITATIONS

Despite remarkable clinical success, immuno-oncology faces several challenges. Immune-related adverse events result from immune system hyperactivation and can affect multiple organ systems, ranging from mild dermatitis to severe endocrinopathies and colitis [41]. The heterogeneity of tumor response remains a significant obstacle, as not all patients derive benefit from immunotherapy. Resistance mechanisms, including primary and acquired resistance to immune checkpoint inhibitors and CAR-T therapies, are increasingly recognized and involve complex interactions within the tumor microenvironment. Additionally, the high cost of immunotherapies and limited accessibility pose major concerns, particularly in low- and middle-income countries, restricting widespread adoption [42].

8. Future Directions in Immuno-Oncology

The future of immuno-oncology lies in personalized and precision medicine approaches that integrate patient-specific tumor and immune characteristics. Advances in artificial intelligence and computational biology are enabling accurate neoantigen prediction and optimized treatment selection [43]. Next-generation CAR-T technologies, including armored and allogeneic CAR-T cells, aim to improve persistence, safety, and accessibility. Multi-omics integration combining genomics, transcriptomics, proteomics, and metabolomics is expected to refine patient stratification and therapeutic outcomes [44]. Additionally, the identification of novel immune targets and development of emerging therapeutic platforms such as bispecific antibodies and cancer vaccines continue to expand the immuno-oncology landscape [45].

CONCLUSION

Immuno-oncology has fundamentally reshaped the landscape of cancer therapy by shifting treatment paradigms from direct tumor targeting to immune system modulation. Advances in immune checkpoint inhibitors, adoptive cell therapies, cancer vaccines, and oncolytic viruses have demonstrated durable clinical responses across a wide range of malignancies. A deeper understanding of tumor–immune interactions, the tumor microenvironment, and predictive biomarkers has enabled more rational patient selection and therapeutic optimization. Despite these successes, challenges such as immune-related toxicities, resistance mechanisms, tumor heterogeneity, and economic barriers continue to limit the universal effectiveness of immunotherapy. Ongoing research focused on personalized and precision immuno-oncology, supported by artificial intelligence, next-generation cellular platforms, and multi-omics integration, holds promise for overcoming current limitations. Continued translational and clinical efforts are essential to fully realize the potential of immuno-oncology and to ensure its broader accessibility and long-term impact on cancer management.

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