Перезаправка Кюре в Множественной Миэломе: Достигаем ли мы движущейся цели?

Introduction

Multiple myeloma (MM), a plasma cell malignancy, exemplifies therapeutic progress and persistent challenges. Advances in proteasome inhibitors (PIs), immunomodulatory drugs (IMiDs), and immunotherapies have improved 5‐year survival beyond 60% in developed nations [ 1 ]. Yet, relapse within 2–5 years remains common, even with therapies achieving high response rates [ 2 , 3 , 4 ]. This paradox raises a provocative question: are we chasing a moving target in our pursuit of a cure for MM?

The traditional definition of cure, complete and permanent eradication of disease, is increasingly at odds with the biological complexity of MM. Intratumoral heterogeneity, driven by subclonal evolution, and the protective bone marrow microenvironment (BMM) confound therapeutic efforts [ 5 ]. This perspective challenges the binary cure paradigm, proposing a redefinition that encompasses sustained MRD negativity, functional cure (long‐term disease control without symptoms), and preservation of QoL. By integrating insights from pathophysiology, emerging therapies, and patient‐centric outcomes, the author aims to reframe MM management and chart future directions for achieving durable remissions.

Pathophysiology: A Barrier to Cure

MM arises from the clonal expansion of terminally differentiated plasma cells, driven by genetic aberrations such as translocations (e.g., t(11;14), t(4;14)) and hyperdiploidy, detected in 90% of cases at diagnosis [ 6 ]. These initiating events trigger dysregulated signaling pathways, including Myelocytomatosis Oncogene (MYC), Rat Sarcoma Oncogene (RAS), and Nuclear Factor kappa‐light‐chain‐enhancer of Activated B Cells (NF‐κB), promoting uncontrolled proliferation and resistance to apoptosis [ 7 ]. The BMM, comprising stromal cells, immune cells, and extracellular matrix, plays a pivotal role in MM pathogenesis. Stromal cells secrete interleukin‐6 (IL‐6) and vascular endothelial growth factor (VEGF), fostering MM cell survival and angiogenesis, while regulatory T‐cells and myeloid‐derived suppressor cells create an immunosuppressive niche [ 8 ].

This dynamic interplay sustains MM clones and facilitates immune evasion. A critical barrier to cure lies in intratumoral heterogeneity. Single‐cell RNA sequencing studies reveal that MM tumors harbor multiple subclones with distinct mutational profiles, even at diagnosis [ 9 ]. Subclonal evolution, driven by selective pressure from therapies, leads to the emergence of resistant clones. For instance, BCMA‐targeted therapies, while initially effective, often fail due to antigen loss or downregulation in 20%–30% of patients [ 10 ]. Additionally, dormant MM cells, residing in hypoxic BMM niches, exhibit stem‐like properties and resist conventional therapies, serving as a reservoir for relapse [ 11 ]. The persistence of these minimal residual clones, detectable via next‐generation sequencing (NGS) at sensitivities of 10 −6 , underscores the challenge of achieving a true cure [ 12 ]. This complex pathophysiology challenges the notion that MM can be eradicated with current approaches.

The interplay of genetic diversity, BMM‐mediated protection, and immune dysregulation suggests that a cure may require targeting both active and dormant clones while reprogramming the tumor microenvironment.

Challenging the Cure Paradigm

The conventional cure model, focused on complete disease eradication, is ill‐suited to MM's complexity. Patients achieving stringent CR and MRD negativity (10 − 6 sensitivity) often relapse within 12–24 months post‐chimeric antigen receptor T‐cell (CAR‐T) due to subclonal resurgence [ 3 ]. MRD, while prognostic, may miss extramedullary clones, oversimplifying MM's heterogeneity [ 13 ].

Emerging evidence suggests that a subset of MM patients, particularly those with low‐risk cytogenetics, may achieve long‐term remission akin to a functional cure. For instance, Attal et al. reported sustained MRD negativity (> 10 − 6 ) in 20% of patients post‐autologous stem cell transplantation, with 10‐year PFS exceeding 40% in low‐risk groups [ 14 ]. Similarly, Engelhardt et al. describe functional cure in patients treated with novel immunotherapies, where sustained MRD negativity correlates with symptom‐free survival [ 15 ]. However, relapse remains prevalent, that even deep responders face subclonal resurgence due to MM's heterogeneity [ 16 ]. This supports our proposed model of cure as a spectrum, integrating sustained MRD negativity and long‐term disease control.

Aggressive MM treatments, such as prolonged lenalidomide maintenance or front‐line quadruplets (e.g., daratumumab‐bortezomib‐lenalidomide‐dexamethasone), often yield suboptimal outcomes in frail patients, who comprise ~60% of MM cases. Toxicities like peripheral neuropathy (30% incidence) and infections (20% risk) reduce adherence in frail populations [ 17 ]. Aggressive regimens may not extend overall survival in frail patients compared to less intensive doublets, emphasizing the need for frailty‐adapted approaches [ 18 ]. Tools like the International Myeloma Working Group (IMWG) Frailty Index can guide tailored regimens, balancing efficacy with tolerability to improve outcomes in this vulnerable group.

The reliance on MRD negativity as a sole endpoint is limited by its inability to detect extramedullary or low‐density clones. PET‐CT negativity, increasingly used in clinical trials (e.g., CASSIOPEIA) and practice, complements MRD assessment by identifying residual lesions. PET‐CT negativity alongside MRD negativity predicts superior PFS (hazard ratio 0.4) in newly diagnosed MM. Integrating both endpoints provides a more comprehensive measure of response depth, supporting our redefined cure model that accounts for MM's spatial heterogeneity.

Moreover, the cure paradigm often prioritizes survival over QoL. Aggressive regimens, including high‐dose chemotherapy and Autologous Stem Cell Transplantation (ASCT), impose significant toxicities, with 40% of patients reporting neuropathy or fatigue persisting beyond 12 months. For elderly or frail patients, comprising 60% of MM cases, such approaches may compromise QoL without proportional survival benefits [ 17 ]. This raises an ethical question: Is the pursuit of cure justified if it undermines patients' well‐being?

Patient‐centered outcomes are critical to redefining cure. Many multiple myeloma patients define “cure” less as complete disease eradication and more as the ability to resume normal life roles [ 19 ]. Symptom‐free survival and maintaining quality of life are prioritized, with some patients even declining life‐prolonging treatments that would severely impact their daily functioning [ 19 ]. Standardized tools like the European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire—Myeloma Module 20 (QLQ‐MY20) capture PROs, revealing that fatigue and neuropathy significantly impact patient well‐being [ 20 ]. Incorporating these perspectives ensures that therapeutic goals align with patient priorities, reinforcing the need for a holistic cure model.

The author proposes a redefined cure model that integrates three pillars:

Sustained MRD Negativity: Achieving and maintaining MRD negativity at high sensitivity (> 10 6 ) as a marker of deep remission.

Functional Cure: Long‐term disease control without symptoms, allowing patients to resume normal activities.

QoL optimization: Balancing efficacy with tolerability, incorporating patient‐reported outcomes (PROs) to guide therapy.

This model acknowledges MM's chronicity while aligning clinical goals with patient priorities. It challenges the field to move beyond survival metrics and embrace a holistic definition of success. Table 1 summarizes the redefined cure model, outlining its pillars, metrics, and implications for MM management [ 19 , 20 , 21 ].

New Insights and Therapeutic Innovations

Recent advances in MM therapy offer hope for redefining cure. CAR‐T therapies like idecabtagene vicleucel targeting B‐cell maturation antigen (BCMA) have achieved overall response rates (ORR) of 80%–90%, with 50%–60% of patients achieving CR [ 2 ]. Bispecific antibodies, such as teclistamab, demonstrate ORR of 60%–70% in relapsed/refractory MM (RRMM), with manageable toxicities [ 3 ]. However, these therapies face limitations, including cytokine release syndrome (CRS) in 70% of CAR‐T patients and relapse due to antigen escape [ 10 ].

Beyond BCMA‐targeted therapies, non‐BCMA immunotherapies expand treatment options. CD38‐targeted monoclonal antibodies like daratumumab achieve an ORR of 80% in RRMM, with a reported 12‐month PFS benefit in combination regimens [ 22 ]. CD138‐targeted antibody‐drug conjugates, such as indatuximab ravtansine, demonstrate significant clinical activity in early trials, achieving objective response rates of up to 71.7% in heavily pretreated patients with relapsed or refractory multiple myeloma [ 23 ]. These approaches complement BCMA therapies, addressing antigen heterogeneity and enhancing response durability.

Emerging immunotherapies like elranatamab (65% ORR in RRMM) and cevostamab (50%–55% ORR in high‐risk RRMM) expand treatment options with manageable toxicities [ 24 , 25 ]. Patient‐centric trials using PROs (e.g., EORTC QLQ‐MY20) balance efficacy with QoL [ 26 ]. Building on MM's complexity, novel therapies address heterogeneity and resistance.

Personalized medicine leverages cytogenetic and immune signatures to tailor MM therapy. High‐risk cytogenetic abnormalities, such as t(4;14), t(14;16), del(17p), or +1q, are associated with poorer outcomes in multiple myeloma [ 27 ]. The MASTER trial ( NCT03224507 ) used FISH‐based cytogenetic profiling to stratify patients and applied MRD response‐adapted therapy with Dara‐KRd and autologous hematopoietic cell transplantation (AHCT), achieving a 2‐year PFS of 97% in patients with one high‐risk cytogenic abnormalities (HRCA) and 58% in those with two or more HRCAs, with Kaplan–Meier estimates suggesting approximately 70%–75% 18‐month PFS for patients with two or more HRCAs [ 27 ]. Immune signatures, such as pretreatment natural killer cell abundance and high T‐cell receptor diversity, predict immunotherapy response [ 28 ]. Integrating these with PROs, ensures treatments align with both biological and patient priorities [ 26 ].

Emerging strategies aim to overcome these barriers. Multi‐antigen targeting, combining BCMA with G Protein‐Coupled Receptor Class C Group 5 Member D (GPRC5D) or Cluster of Differentiation 38 (CD38), reduces antigen loss and enhances durability, with early trials reporting PFS exceeding 24 months [ 29 ]. Bispecific T‐cell engagers (BiTEs) and antibody‐drug conjugates (ADCs) offer off‐the‐shelf alternatives to CAR‐T, improving accessibility [ 30 ]. Additionally, precision medicine approaches, leveraging single‐cell genomics, enable identification of patient‐specific driver mutations, guiding targeted therapies like venetoclax for t(11;14) MM [ 31 ]. AI‐driven risk stratification represents a frontier in MM management. Machine learning models integrating genomic, proteomic, and clinical data predict relapse risk with 85% accuracy, enabling tailored maintenance therapies [ 32 ]. Furthermore, targeting the BMM—via IL‐6 inhibitors or anti‐VEGF agents—disrupts MM's protective niche, enhancing immunotherapy efficacy [ 8 ]. These innovations suggest that cure may be achievable through synergistic, personalized approaches that address MM's complexity.

Future Directions

To redefine cure, the MM field must address several priorities:

Optimizing combination therapies: Clinical trials should evaluate multi‐antigen immunotherapies combined with BMM modulators to target both active and dormant clones. For example, combining BCMA/GPRC5D CAR‐T with siltuximab (anti‐IL‐6) could enhance durability [ 33 ].

Targeting dormant clones: Novel agents, such as BH3 mimetics or epigenetic modifiers, should be explored to eliminate stem‐like MM cells in hypoxic niches [ 11 ].

Integrating PROs: Standardized PRO measures, like the EORTC QLQ‐MY20, should guide therapy selection, ensuring QoL is prioritized alongside efficacy [ 20 ].

Leveraging AI and genomics: AI‐driven platforms should be scaled to predict treatment response and relapse, integrating real‐world data to refine risk models [ 32 ].

Global access: Efforts to reduce costs of CAR‐T and bispecifics, such as allogeneic CAR‐T or biosimilars, are critical to ensure equitable access [ 30 ].

Global disparities in access to novel MM therapies, such as CAR‐T and bispecific antibodies, remain a critical challenge, particularly in low‐ and middle‐income countries (LMICs) such as Tanzania. High costs per CAR‐T infusion and limited infrastructure restrict access in LMICs [ 34 ]. Solutions like biosimilars, allogeneic CAR‐T, and regional manufacturing hubs could democratize access, ensuring equitable benefits from therapeutic advances.

The proposed cure model has far‐reaching implications for clinical trial design, regulatory decisions, and health policy. Adaptive platform trials such as the Multiple Myeloma Research Consortium (MMRC) Horizon One platform, offer a master protocol design that allows investigational arms to enter or exit dynamically based on interim efficacy, enabling efficient testing of combination therapies and accelerating drug development [ 35 ]. Regulatory agencies should prioritize composite endpoints like MRD and PET‐CT negativity, alongside PROs, to reflect patient‐centric outcomes. Health policies must fund precision medicine initiatives, such as AI‐driven risk stratification, to ensure sustainable access to personalized therapies.

These directions require collaborative efforts among researchers, clinicians, and policymakers. Regulatory agencies should prioritize adaptive trial designs to accelerate approval of combination therapies, while funding agencies should support translational research into BMM‐targeted agents.

Conclusion

The pursuit of a cure in MM is a moving target, shaped by the disease's biological complexity and therapeutic advances. By challenging the traditional cure paradigm, I propose a redefined model that integrates sustained MRD negativity, functional cure, and QoL. Insights from pathophysiology, coupled with innovations in immunotherapy, precision medicine, and AI, offer a path toward durable remissions. However, achieving this vision demands a paradigm shift embracing MM's chronicity, prioritizing patient‐centric outcomes, and addressing global disparities. As we navigate this evolving landscape, the question is not whether we can cure MM, but how we define and achieve success in a disease that defies simple solutions.

Author Contributions

Jacob Henry Kitundu conceptualized the perspective, conducted the literature review, drafted the manuscript, and critically revised it for intellectual content.

Ethics Statement

The author has nothing to report.

Conflicts of Interest

The author declares no conflicts of interest.

Transparency Statement

The lead author, Jacob Henry Kitundu, affirms that this manuscript is an honest, accurate, and transparent account of the study being reported; that no important aspects of the study have been omitted; and that any discrepancies from the study as planned (and, if relevant, registered) have been explained.

Acknowledgments

Jacob Henry Kitundu approved the final version of the manuscript for submission. The author has read and approved the final version of the manuscript. All data cited are publicly available in the referenced sources. The author takes full responsibility for the integrity of the data and the accuracy of the data analysis.

Kitundu J. H., “Redefining Cure in Multiple Myeloma: Are We Chasing a Moving Target?,” Health Science Reports 8 (2025): 1‐5, 10.1002/hsr2.71581.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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Associated Data

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.