Highlighting New Advances in
Immuno-Oncology Management
A Summary Report from the 2025 ESMO
Immuno-Oncology Congress (December 10-12)
Simron Singh, MD, MPH, FRCPC; Neil Chua, MD, FRCPC; Ashley Marton, MDCM;
Martin Smoragiewicz, MDCM, PhD, FRCPC; and Elizabeth Faour, MD, FRCPC
ABSTRACT
Since the introduction of immune checkpoint inhibitors in the 2010s, immunotherapy has become an integral component of the treatment armamentarium for many patients with cancer. At the same time, novel immunological pathways and mechanisms of action continue to emerge for more effective, durable, and safer treatment of patients across the spectrum of cancer types. At the 2025 European Society for Medical Oncology Immuno-Oncology Congress, held in London, United Kingdom, international researchers and clinicians presented data on innovative management approaches in immuno-oncology in both experimental and real-world settings. This white paper provides summaries of presentations of interest selected by the authors.
INTRODUCTION
Despite the early work of Busch,¹ Fehleisen,² and Coley³⁻⁴ to recognize the immune response of malignant tumors and the potential to treat patients with cancer using heat-inactivated bacteria, immunotherapy in oncology remains a relatively novel and emerging therapeutic strategy. Cytokine agents were the first active immunotherapy for cancer treatment; interferon-α2 (IFN-α2) was approved by the United States Food and Drug Administration (FDA) in 1986 for patients with hairy cell leukemia and interleukin-2 (IL-2) was approved in 1992 for renal cell carcinoma (RCC);⁵ however, their use was limited by severe toxicity. Immune checkpoint inhibitors (ICIs), introduced in the 2010s, represented a paradigm shift in cancer therapy. The benefits of ICI use stimulated further research that led to the development of other immuno-oncology modalities, including chimeric antigen receptor T-cell therapy, tumor-infiltrating lymphocyte (TIL) therapy, monoclonal antibodies (mAbs) bispecific agents, antibody-drug conjugates (ADCs), and neoantigen vaccines.⁵
IMMUNO-ONCOLOGY THERAPIES
According to Alexander Eggermont, MD, PhD (Utrecht, Netherlands), the failure of first-generation IL-2 agonists in Phase 3 trials was principally associated with a lack of full understanding of the mechanism of action, premature transition from Phase 2 to Phase 3 trials, disease and tumor microenvironment heterogeneity, incorrect or lacking biomarkers, and lack of single-agent activity.⁶ He highlighted that the advent of ICIs also renewed interest in the use of cytokines, particularly next-generation agents in combination therapy. Dr. Eggermont underlined positive early outcomes with NKTR-214 (bempegaldesleukin) in combination with nivolumab in advanced solid tumors;⁷ however, no improvement in overall response rate was observed with this combination vs nivolumab monotherapy in an open-label Phase 3 trial with patients who had previously untreated, unresectable, or metastatic melanoma.⁸ He also presented data from 2 promising bispecific antibodies. Ivonescimab (AK112), a first-in-class anti-programmed cell death (PD)-1 / anti-vascular endothelial growth factor agent, was associated with significantly longer progression-free survival (PFS) compared with pembrolizumab in treatment-naïve patients with advanced PD-L1-positive non-small cell lung cancer (NSCLC),⁹ and the improvement in PFS with first-line ivonescimab + chemotherapy compared with tislelizumab + chemotherapy among patients with advanced squamous NSCLC was significant irrespective of PD-L1 expression.¹⁰ Cadonilimab, a first-in-class anti-PD-1 / anti-cytotoxic T lymphocyte antigen-4 (CTLA-4) agent, was found to have good antitumor activity and a manageable safety profile when combined with paclitaxel and cisplatin as first-line therapy in patients with unresectable locally advanced or metastatic esophageal squamous cell carcinoma.¹¹ Dr. Eggermont presented positive data supporting the benefit of intratumoral injection of daromun (combination of fibronectin-targeting immunocytokines L19IL2 and L19TNF) vs surgery in metastatic melanoma¹² and numerically superior outcomes with deep/visceral vs superficial injection of vusolimogene oderparepvec (RP1) patients with anti-PD-1-failed cutaneous melanoma.¹³
AUTHOR COMMENTS:
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Canadian doctors are already re-exploring the role of new-generation cytokines through clinical trials.
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Results of Chinese trials should be interpreted with caution when implementing in a Canadian population in regard to applicability.
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In the new era of ICI, there is a steep learning curve in toxicity management for patients and providers. Appropriate resources will be required.
ADCs are a particularly potent combination of targeted therapy and chemotherapy comprising 3 core components: the mAb seeks out the target antigen on the cancer cell and delivers the toxic payload, the linker binds the molecular structure, and the chemotherapy payload enters and induces cell death (Figure 1). In her review of ADCs, Elizabeth Nally, MBBS (London, United Kingdom), emphasized that the chemotherapy agents delivered as the payload – typically microtubule inhibitors and deoxyribonucleic acid (DNA) alkylating agents – are more potent and toxic than the agents to which they are accustomed using.¹⁴ She explained that beyond targeted chemotherapy delivery, ADCs may also be effective through other pathways, including diffusion through target cell membranes and attacking nearby cancer cells that are not expressing the target antigen to the same degree (bystander effect), blocking survival mechanisms that have developed in cancer cells, and creation of an immunomodulatory effect.
FIGURE 1. CORE COMPONENTS OF AN ADC
Reproduced with permission from Elizabeth Nally, MBBS.
DNA, deoxyribonucleic acid; HER2, human epidermal growth factor receptor 2; TROP2, trophoblast cell-surface antigen 2
Dr. Nally presented results of studies with promising new ADCs in breast cancer, urothelial cancer, and NSCLC. She highlighted advances in the treatment of patients with human epidermal growth factor receptor 2 (HER2)-positive breast cancer and pretreated triple negative / HER2-low breast cancer with trastuzumab deruxtecan.¹⁵⁺¹⁶ Results were also positive in studies involving patients with pretreated triple negative / HER2-low breast cancer with agents such as sacituzumab govitecan,¹⁷ datopotamab deruxtecan,¹⁸ and sacituzumab tirumotecan.¹⁹ In patients with urothelial cancer, physicians have been limited for many years to platinum-based chemotherapy, as the addition of ICIs did not confer a survival benefit in clinical trials.²⁰⁻²² Enfortumab vedotin, which targets nectin-4, was combined with pembrolizumab in the Phase 3 EV-302 trial and resulted in statistically significant and clinically meaningful improvement in overall survival (OS) and PFS vs chemotherapy in patients with untreated advanced urothelial cancer.²³ Enfortumab vedotin + pembrolizumab was approved for patients with locally advanced or metastatic urothelial cancer who are ineligible for cisplatin-containing chemotherapy by the FDA and in patients who have unresectable or metastatic urothelial cancer who are eligible for platinum-containing chemotherapy by the European Medicines Agency.²⁴⁻²⁵ In NSCLC, single-agent ADCs have had limited success in clinical trials in terms of survival benefit. Dr. Nally explained that NSCLC tumors are more heterogeneous than those of breast cancer, with more antigen expression on the cell surface; thus, a clearer biological picture is likely required to identify which patients are likely to respond to ADCs. She highlighted that several studies are investigating biomarkers in NSCLC. In the Phase 3 OptiTROP-Lung04 trial involving patients with epidermal growth factor receptor (EGFR)-mutated locally advanced or metastatic nonsquamous NSCLC, the group that received sacituzumab tirumotecan experienced significantly longer median OS and PFS than the group that received pemetrexed + platinum-based chemotherapy.²⁶
Additional research is underway to explore combination ADCs, bispecific ADCs, ADCs and targeted therapy, and ADCs with a dual payload. As described by Laurence Buisseret, MD, PhD (Brussels, Belgium), combination ADC + ICI has the biologic rationale to enhance antigen release, convert cold tumors to hot, amplify T-cell activation, and overcome resistance to either of the individual modalities.²⁷ She presented several studies showing increased duration of response with combination ADC + anti-PD-1 ICI in patients with ovarian or cervical cancer.²⁸⁻³¹ The Phase 3 ASCENT-04/KEYNOTE-D19 trial determined that sacituzumab govitecan + pembrolizumab demonstrated statistically significant and clinically meaningful improvement in PFS vs chemotherapy + pembrolizumab in patients with previously untreated PD-L1–positive advanced triple-negative breast cancer.³² In patients with advanced NSCLC, first-line datopotamab deruxtecan + pembrolizumab demonstrated durable antitumor activity.³³ Several studies are exploring the safety and efficacy of other ADC + ICI combinations in advanced NSCLC.
Toxicity associated with ADCs is predictable and typically specific to the components. The mAb can cross-react with antigens expressed on healthy cells, such as HER2 (cardiotoxicity), Trop2 (rash, mucositis), nectin-4 (rash, dysgeusia), and tissue factor (bleeding).³⁴ While the standard linker is noncleavable, some agents employ cleavable linkers, which allow the payload to be released early into the bloodstream. Topoisomerase 1 inhibitors, a common component of ADC payloads, are associated with diarrhea and neutropenia. In combination ADC + ICI therapy, overlapping toxicities are a particular concern, notably pneumonitis and rash.
AUTHOR COMMENTS:
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ADCs provide targeted chemotherapy to cancer cells but may also have other mechanisms of providing benefit, including the bystander effect and immunomodulatory effects.
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ADCs have been shown to provide significant survival benefit in breast cancer and urothelial cancers.
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Single-agent ADCs have yet to show significant benefit in NSCLC, which is believed to be related to the heterogeneous nature of the disease, compared to breast cancer.
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The data for enfortumab vedotin + pembrolizumab are transformational in bladder cancer. If similarly impactful in breast cancer, this class of drugs will have a major footprint in cancer and generate much additional research interest.
TIL therapy is a promising and potent new cancer treatment in which endogenous immune cells (cluster of differentiation [CD]8+, CD4+, regulatory T cells, B cells, and natural killer [NK] cells) are harvested, enhanced and multiplied in a laboratory, and then infused back into the individual patient.³⁵⁻³⁶ The accelerated FDA approval of lifileucel for the treatment of patients with unresectable or advanced melanoma represents the first approvals of a TIL and of a cellular therapy for a solid tumor. TIL therapy is associated with several benefits, including highly personalized treatment, durability, the ability of the multiple T-cell clones to recognize a variety of tumor antigens, and an alternative treatment strategy for patients with cancers that are resistant to conventional therapy.³⁶⁻³⁷ TIL therapy is a complex multistep process, however, and simplified scalable strategies such as point-of-care manufacturing are required to optimize availability of this treatment, as noted by Alena Gros, PhD (Barcelona, Spain).³⁸ Dr. Gros’s group investigated potential options to move from passive tumor-reactive T-cell expansion to a more generalizable approach, including discovery of biomarkers expressed on tumor-reactive TILs. She said that such a technology could be leveraged to select the population of interest and potentially expand or generate more personalized TIL therapies.
To reduce the barriers of standard tumor biopsy for procurement of immune cells, Dr. Gros’s group explored the use of circulating tumor (ct) DNA in peripheral blood for selection of marker-specific T cells, based on the findings of Garcia Garijo et al.³⁹ They considered the risk that peripheral sampling may fail to recognize the heterogeneity of neoantigens in patients with advanced cancer. Tumor biopsy and peripheral blood sampling were performed in a patient with metastatic colorectal cancer. The group found a high tumor mutation burden (2873 mutations) and concordance in the tumor from the biopsy and the ctDNA (1697 were shared), and shared mutations were present in a higher clonal fraction compared to unique mutations. To determine if any mutations were recognized by T cells from peripheral blood, the researchers labeled peripheral blood lymphocytes with anti-PD-1 and anti-CD39 antibodies; a very small population of T cells was found to express PD-1 and CD39. CD8+ and CD4+ lymphocytes expressing PD-1 and/or CD39 harbored T cells targeting neoantigens. It was determined that cell-free / ctDNA not only recognized 27 of 33 neoantigens in common with the tumor biopsy but recognized 3 neoantigens not captured by biopsy. The group concluded that peripheral blood is a viable source of TILs that better captures tumor heterogeneity and systemic antitumor T-cell response than biopsy-acquired lymphocytes.
AUTHOR COMMENTS:
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Peripheral blood is an easily accessible sample source, requiring fewer resources and easy to translate into clinical practice.
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Usage will be variable depending on accessibility to ctDNA, which is unavailable across Canada on a large scale at present.
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There are several unanswered questions with respect to ctDNA TILs, including selection of target neoantigens, effectiveness in patients with lower mutational burden compared to melanoma, large-scale manufacturing and delivery, and utility across different tumor sites.
TREATMENT -REFRACTORY CANCERS
As reported by Amanda Psyrri, MD, PhD (Haidari, Greece), 60% of patients with recurrent/metastatic head and neck squamous cell carcinoma (HNSCC) do not respond to initial anti-PD-1 ICI and only 20%–30% of patients achieve durable disease control with ICIs.⁴⁰ She outlined the 3 potential therapeutic approaches to overcoming anti-PD-1 resistance: enhancing T-cell function and infiltration, increasing tumor immunogenicity, and targeting of the immune suppressive tumor microenvironment. Unlike in other cancers, combination immunotherapy agents have not demonstrated improvements in OS in clinical trials including patients with recurrent/metastatic HNSCC. Dr. Psyrri said that the impact of unfavourable genomics and epigenomics can affect interferon signalling. She explained that mutations in nuclear receptor-binding SET domain protein 1, which controls gene expression, lead to immune exclusion and suppressed interferon signalling. Dazostinag, a novel stimulator of interferon genes agonist, has been shown to induce type 1 interferon and enhance antitumor immunity. In the Phase 1/2 iintune-1 study, dazostinag + pembrolizumab demonstrated antitumor activity in patients with advanced/metastatic HN tumors that had progressed on ICI monotherapy.⁴¹ A Phase 2 trial is underway.
Enhancement of tumor immunogenicity has also been demonstrated by select ADCs. First-line becotatug vedotin + pucotenlimab (targeting EGFRs) in patients with recurrent/metastatic HNSCC was associated with positive and durable antitumor activity and a manageable safety profile in a Phase 1/2 trial.⁴² A Phase 2 trial of ozuriftamab vedotin, which binds the cell-surface transmembrane receptor protein ROR2, demonstrated a high rate of disease control with acceptable tolerability in patients with heavily pretreated HNSCC.⁴³ Efficacy was particularly notable in patients whose cancer was refractory to anti-PD-1.
Regarding improvement of the tumor microenvironment, Dr. Psyrri reported on bispecific antibodies that have demonstrated promising efficacy in terms of overall response rate (ORR) and tumor shrinkage in early-phase trials of ficerafusp α (targeting EGFR and transforming growth factor-β) + pembrolizumab,⁴⁴ amivantamab (targeting EGFR and mesenchymal-epithelial transition),⁴⁵ and petosemtamab (targeting EGFR and leucine-rich repeat-containing G-protein coupled receptor 5).⁴⁶
AUTHOR COMMENTS:
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Current therapeutic approaches include enhancing tumor immunogenicity with use of ADCs such as becotatug vedotin and ozuriftamab vedotin and priming with human papillomavirus vaccine.
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Another approach is to improve the tumor microenvironment using a bispecific antibody (ficerafusp α, amivantamab, or petosemtamab).
Éric Vivier, DVM, PhD (Marseille, France) discussed the potential roles of NK cells to overcome ICI resistance.⁴⁷ NK cells are involved in the natural recognition and elimination of cancer cells, including metastatic tumor cells.⁴⁸ They are classified into 3 prominent NK subsets: NK1, NK2, and NK3, which vary in their protein expression.⁴⁹ NK1 exhibits high expression of the activating receptor CD16, which mediates antibody-dependent cellular cytotoxicity. NK2 expresses high levels of CD56bright, which have cytokine- and chemokine-producing and immunomodulatory roles. NK3 was described by Dr. Vivier as being “memory-like” cells to previous infection, as well as expressing CD16. NK cell subset distribution varies by tumor type.
Dr. Vivier presented data on the anti-NKG2A ICI monalizumab, which promotes anti-tumor immunity by promoting both NK and CD8+ T-cell effector function.⁵⁰ In the Phase 2 COAST study, durvalumab + monalizumab was associated with increased ORR and longer PFS vs durvalumab alone,⁵¹ and the ongoing Phase 3 Pacific 9 trial is further assessing this combination.⁵² He also discussed antibody-based NK cell engagers developed by his group that target activating receptors NKp46 and CD16 on NK cells and a tumor antigen on cancer cells.⁵³ Their trispecific anti-CD123 NKp46×CD16 NK cell engager received fast-track designation by the FDA for the treatment of hematological malignancies.⁵⁴ A Phase 1 trial of allogeneic NK cells with a bispecific innate cell engager in 42 patients with refractory relapsed lymphoma determined a 66.7% complete response rate.⁵⁵
AUTHOR COMMENTS:
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NK cells play an important role in recognition and elimination of cancer cells; however, there are no currently available therapies harnessing NK cells.
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ANKET is an interesting new therapeutic approach to harness innate immunity in cancer therapy and would be an area to follow by clinicians.
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Further improvements include looking at arming the engager with IFN-α2 and IL-18.
Drew Pardoll, MD, PhD (Baltimore, MD, US) presented surprising results that his team found while examining the impact of common comorbidities associated with aging and senescence in patients with cancer.⁵⁶ They determined that response to anti-PD-1 ICI was significantly higher among patients with osteoarthritis than those without. On separate analysis in a mouse anterior cruciate ligament transection (ACLT) model, it was found that joint injury-induced osteoarthritis is associated with delayed distal tumor growth and increased ICI response in cold tumors, even when the ACLT is on the contralateral side to the tumors. This phenomenon may be driven by the observed increase in T-cell migration in the presence of arthritis, including tumor-specific T cells. Dr. Pardoll’s team related this effect (at least in part) to serum factors associated with ACLT, especially to proteins associated with vascular development and senescent cells. Serum analysis identified that pericytes (regulators of blood vessel formation, stability, and function) were interpolated with vascular endothelial cells in mice with ACLT and cancer but were dissociated from endothelial cells in mice without ACLT. As well, P-selectin, a key component of vascular endothelial activation leading to T-cell migration into tumors, was found to be present in higher concentration in mice with ACLT. Senescent cells have the important contribution of disrupting the vasculature; deletion of senescent cells is associated with loss of ICI effect. These findings have been observed in early analysis of human models with renal, thyroid, and endometrial cancers, and Dr. Pardoll’s team has initiated a study involving serum transfer from mice with osteoarthritis receiving an ICI to those without osteoarthritis to ascertain whether the above benefits can be induced.
AUTHOR COMMENTS:
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Preclinical research demonstrates that an osteoarthritis environment can be induced in mice; i.e. turning a cold tumor hot.
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Further research is needed to determine the clinical relevance of these findings.
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Unanswered questions include patient selectionand how to mitigate the risk of toxicity.
In his talk on therapeutic approaches to oligoprogression, Lambros Tselikas, MD, PhD (Villejuif, France) emphasized the important role of targeted local treatment in patients who were largely maintained by systemic therapy.⁵⁷ A proper management plan must differentiate oligoresistance (primary resistance; ‘oligo’ meaning ‘few’), for which the treatment intent is curative, from oligoprogression (secondary resistance), for which the treatment intent is palliative.⁵⁸ Dr. Tselikas presented the case of a 59-year-old woman with metastatic recurrence of intrahepatic cholangiocarcinoma (p53 mutation), for which she was initially treated with chemotherapy (gemcitabine and cisplatin) and durvalumab and subsequently maintained on durvalumab. A mass was subsequently identified on her third lumbar vertebra with epidural involvement.
Electrochemotherapy was given, in which an electrical field was applied around the target tumor for localization of chemotherapy.⁵⁹ After 3 months, a near complete response was observed in the bone metastasis as well as an abscopal effect in the liver tumors.
Dr. Tselikas stressed the benefit of maintaining systemic therapy when there is evidence of benefit and adding targeted local therapy for oligoresistant or oligoprogressive tumors, for which no major safety concerns have been identified.58 He reported a high rate of oligoprogression (~50%) in patients receiving tyrosine kinase inhibitors for NSCLC vs 13% among patients receiving chemotherapy + ICI.⁶⁰ In the iAblation study, Dr. Tselikas’ group demonstrated that thermal ablation + ICI over 10 years in patients with various primary cancers (lung, skin, kidney, other) was associated with significantly better survival outcomes for oligoresistant tumors than oligoprogressive or symptomatic cancer.⁶¹
AUTHOR COMMENTS:
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It is important to start labelling clinical scenarios specifically in order to begin understanding their natural history and response to various treatments, and therefore incorporating terms like oligoprogression vs polyprogression vs oligoresistance into practice.
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The underlying biology of these distinctions is poorly understood and needs further investigation to determine whether one modality would be better than another (surgery vs radiation vs other technique).
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Metastasis-directed therapy is well established in some cancers (e.g., RCC), but the full scope of potential benefit (or harms) is an area of active research and not necessarily standard of care in most cancers.
IMMUNE-RELATED TOXICITY
According to Jarushka Naidoo, MB, BCH, MHS (Dublin, Ireland), the prevalence of specific toxicities associated with ICI use across nearly all organ systems has spawned a new field in immune-oncology called immune-related adverse event (irAE) medicine.⁶²⁻⁶³ She predicted that research over the next decade will be focused on understanding the natural history of acute and chronic irAE, identifying why patients experience different irAE risk, improving treatment based on biology and data, and advancing monitoring strategies. Dr. Naidoo underlined that the priority of patient monitoring should be based on irAE severity, patient immune status, and natural history (Table 1).⁶⁴
TABLE 1. PRIORITIZING PATIENT MONITORING FOR IRAES
ᵃ listed by decreasing severity.
irAE, immune-related adverse event
Dr. Naidoo reviewed the current guidelines for monitoring, describing the European Society for Medical Oncology guidelines as having a more dynamic view that includes more recommendations than the American Society of Clinical Oncology / National Comprehensive Cancer Network® guidelines for pretreatment testing and monitoring.⁶⁵⁻⁶⁶ About half of irAEs occur early (median 3.4 months) and 30% are late onset (median 16.6 months).⁶⁷ Endocrine toxicities were among the earliest toxicities with which physicians became familiar. Thyroid dysfunction (hypo-, hyper-, and thyroiditis) occurs in up to 20% of patients receiving anti-PD-L1 agents, and hypophysitis is the most commonly occurring irAE in patients receiving a CTLA-4 inhibitor.⁶⁸ Monitoring recommendations include measurement of thyroid-stimulating hormone and free thyroxine levels every 3-6 weeks;⁶⁵ however, several additional organ-specific recommendations have been published, so Dr. Naidoo recommended early consultation with an organ specialist to coordinate management and monitoring. Pneumonitis is an uncommon but potentially fatal irAE defined as a focal or diffuse inflammation of the lung parenchyma, and it is more common in patients with lung cancer.⁶⁹ Natural history and clinical outcomes of pneumonitis remain poorly understood. Recurrent pneumonitis was found to occur in 8.5% of patients, most commonly in men and in patients with RCC and hepatocellular carcinoma.⁷⁰ The incidence of chronic pneumonitis was 34.6%, of which nearly all cases comprise a single chronic event.
Of the cardiovascular irAEs, myocarditis is the most common (0.27%–1.14% incidence)⁷¹ and it is associated with the highest fatality rate (40%).⁷² Dr. Naidoo highlighted effective cardiac monitoring strategies for cardiomyopathy, including serial troponin-I monitoring and prospective treatment,⁷³⁻⁷⁴ and emerging monitoring algorithms.⁷⁵ Dr. Naidoo also summarized findings in MMM syndrome – myocarditis, myasthenia gravis, and myositis – which is associated with frequent high-grade toxicity and particularly poor outcomes.⁷⁶ She advocated for multidisciplinary care in patients with MMM syndrome.⁷⁷
The rates of irAEs are especially high in patients with autoimmune conditions,⁷⁸ requiring more diligent monitoring while they are on ICIs. Dr. Naidoo reviewed strategies for the delicate balance of effective cancer therapy with preservation of solid organ transplants involving tailored immunosuppression.⁷⁹⁻⁸¹
AUTHOR COMMENTS:
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A new era of irAE management is coming,
with more tailored monitoring and management guidelines. -
Recommendations for a multidisciplinary approach are ideal but logistically challenging.
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Depending on the centre, organ specialists have varying degrees of familiarity with and/or interest in irAE management.
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Resource limitations can also be challenging. This particular example was a protocol monitoring troponin and triggering cardiac magnetic resonance imaging, which may be very challenging to implement at scale in our current environment.
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It is beneficial to have the natural histories defined of various irAEs, such as pneumonitis and myocarditis.
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Research is underway to define strategies and outcomes for immunotherapy treatment in patients with a solid organ transplant.
Dr. Singh is a Medical Oncologist and Affiliate Scientist, Odette Cancer Research Program, Sunnybrook Research Institute, and an Associate Professor, University of Toronto, Toronto, Ontario.
Dr. Chua is a Clinical Oncologist, Cross Cancer Institute, Edmonton, Alberta.
Dr. Marton is a Hemato-oncologist, Hôpital Cité de la Santé, Laval, Québec.
Dr. Smoragiewicz is a Medical Oncologist, Kingston Health Sciences Centre, and an Assistant Professor, Queen’s University, Kingston, Ontario.
Dr. Faour is a Medical Oncologist, Cancer Care Program, Memorial University of Newfoundland, St. John’s, Newfoundland.