NSCLC remains a formidable adversary in lung cancer management, accounting for approximately 85% of all lung cancer cases globally. Despite the advent of targeted therapies, drug resistance frequently emerges, undermining clinical efficacy and patient survival. Gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, has revolutionized treatment by specifically targeting aberrant EGFR signaling common in NSCLC. However, intrinsic and acquired resistance mechanisms challenge its success, creating an imperative need to unravel the cellular intricacies dictating therapeutic response.

Central to this innovative research is miR-101-3p, a small non-coding RNA known for its tumor-suppressive roles across various malignancies. The study delineates not only the intracellular functions of miR-101-3p but also its exosomal dynamics—where the microRNA is packaged into extracellular vesicles facilitating intercellular communication within the tumor microenvironment. The dual presence of miR-101-3p signals a sophisticated regulatory axis influencing Gefitinib sensitivity that transcends individual cells and implicates broader tumor ecosystem interactions.

What elevates the significance of miR-101-3p in this context is its regulation by METTL14, a pivotal enzyme catalyzing N6-methyladenosine (m6A) modifications on RNA. This chemical modification profoundly impacts RNA metabolism, including stability, splicing, and translation. The study meticulously illustrates how METTL14 orchestrates miR-101-3p expression at the epitranscriptomic level, thereby modulating its availability and functional capacity. High METTL14 activity correlates with augmented miR-101-3p maturation, which sensitizes NSCLC cells to Gefitinib, whereas METTL14 downregulation diminishes this effect, fostering drug resistance.

Intriguingly, the mechanistic exploration reveals that intracellular accumulation of miR-101-3p targets key oncogenic pathways implicated in resistance, including the regulation of pivotal genes involved in cell proliferation, apoptosis, and survival signaling. The repression of these signaling cascades reinstates Gefitinib efficacy, highlighting miR-101-3p as a molecular linchpin for therapeutic responsiveness. This adds a layer of complexity by suggesting that miR-101-3p functions as a critical mediator that can fine-tune cellular susceptibility to EGFR inhibition.

Equally compelling is the demonstration of exosomal miR-101-3p as a vehicle for horizontal transfer of Gefitinib sensitivity among tumor cells. Exosomes, as nanoscale extracellular vesicles, have garnered attention for their role in disseminating oncogenic factors and mediating cell-to-cell communication. By ferrying miR-101-3p through the tumor milieu, exosomes could propagate Gefitinib sensitivity, essentially ‘educating’ resistant cells to regain their vulnerability to targeted therapy. This discovery propels the conceptual framework of tumor microenvironment modulation as a therapeutic tactic.

The therapeutic implications of these insights are profound. Leveraging METTL14-mediated regulation of miR-101-3p offers a novel stratagem that could synergize with existing EGFR inhibitors to overcome resistance. It paves the way for developing epitranscriptomic modulators or miRNA mimetics as adjuncts to established treatments, enhancing clinical outcomes for patients grappling with resistant NSCLC. Furthermore, miR-101-3p levels, both intracellular and exosomal, hold promise as predictive biomarkers to tailor therapy and monitor response dynamically.

Methodologically, the study harnessed an array of cutting-edge techniques including RNA sequencing, methylated RNA immunoprecipitation, quantitative real-time PCR, and functional assays assessing cell viability and apoptosis. Such rigorous approaches underpin the robustness of the findings, substantiating the causative link between METTL14, miR-101-3p expression, and Gefitinib sensitivity. Additionally, in vitro models were complemented by patient-derived samples, reinforcing the translational relevance of the research.

The clinical translation of these findings could transform the NSCLC therapeutic landscape. By integrating miR-101-3p modulation strategies, clinicians may eventually overcome the recalcitrant problem of Gefitinib resistance, extending the durability and depth of responses in patients. Moreover, exosomal miR-101-3p profiling might emerge as a minimally invasive liquid biopsy modality, facilitating real-time treatment monitoring and personalized intervention adjustments.

Beyond the immediate relevance to NSCLC, this study underscores the broader significance of epitranscriptomic regulation in cancer biology and therapy resistance. METTL14 and m6A modifications are increasingly recognized as master regulators in diverse oncogenic processes, and the elucidation of their interface with microRNAs opens fertile ground for novel drug development. This paradigm shift from genetic to epitranscriptomic targeting holds considerable promise across multiple cancer types.

Importantly, the interplay between intracellular signaling and extracellular vesicle-mediated communication exemplifies the intricacies of tumor biology. The ability of exosomes to modulate drug sensitivity amplifies the emerging recognition that effective cancer treatment must consider not only individual cancer cells but also their dynamic and cooperative ecosystem. Strategies that disrupt this cellular crosstalk could yield unprecedented breakthroughs in overcoming multidrug resistance.

Future research avenues prompted by this study are manifold. Investigations into other m6A-regulated microRNAs and their impact on sensitivity to various targeted therapies could unmask universal principles governing therapeutic responses. Furthermore, the design of precision delivery systems to modulate miR-101-3p or METTL14 activity specifically within tumor cells represents a tantalizing prospect, harnessing advances in nanotechnology and molecular therapeutics.

In conclusion, the compelling work delineated by Kong et al. illuminates a sophisticated regulatory network where METTL14-driven modulation of intracellular and exosomal miR-101-3p orchestrates Gefitinib sensitivity in non-small cell lung cancer. This paradigm-shifting insight not only deepens our molecular understanding of drug resistance but also unveils visionary therapeutic and diagnostic possibilities. As NSCLC continues to challenge the oncology community, such molecular revelations inspire hope for more effective, tailored treatments that can significantly improve patient prognoses and quality of life.

Subject of Research: Regulation of Gefitinib sensitivity in non-small cell lung cancer (NSCLC) by intracellular and exosomal miR-101-3p through METTL14-mediated epitranscriptomic modulation.

Article Title: Intracellular and exosomal miR-101-3p regulated by METTL14 confers Gefitinib sensitivity in NSCLC.

Article References:
Kong, Q., Wu, L., Li, J. et al. Intracellular and exosomal miR-101-3p regulated by METTL14 confers Gefitinib sensitivity in NSCLC. Med Oncol 43, 117 (2026). https://doi.org/10.1007/s12032-026-03242-5

Image Credits: AI Generated

DOI: https://doi.org/10.1007/s12032-026-03242-5

Head and neck squamous cell carcinoma represents a biologically heterogeneous group of malignancies arising from the mucosal linings of the oral cavity, pharynx, and larynx. Despite advances in multimodal treatment strategies—including surgery, radiation, and chemotherapy—patients with locally advanced disease often face poor prognoses, mainly due to high rates of recurrence and distant metastasis. This pressing clinical challenge has necessitated the exploration of novel neoadjuvant therapies that not only shrink tumors preoperatively but also modulate the tumor immune microenvironment to prevent disease progression.

The phase 2 trial, designated as neoCHANCE-1, was meticulously designed to assess the safety, tolerability, and efficacy of neoadjuvant administration of tislelizumab in combination with afatinib. Tislelizumab is a monoclonal antibody that selectively blocks PD-1, a checkpoint receptor that tumors exploit to evade immune surveillance. By inhibiting PD-1, tislelizumab rejuvenates exhausted T cells, thereby promoting robust antitumor immunity. Afatinib, on the other hand, irreversibly inhibits EGFR, a receptor often overexpressed or mutated in HNSCC, leading to disrupted downstream signaling pathways responsible for tumor cell proliferation and survival.

The trial enrolled patients diagnosed with stage III or IV HNSCC who were eligible for surgical resection. Participants received a neoadjuvant regimen comprising intravenous tislelizumab and oral afatinib over a defined treatment window prior to surgery. The study’s primary endpoints focused on assessing pathological response rates, including the degree of residual viable tumor cells, while secondary endpoints evaluated disease-free survival, overall survival, and safety profiles.

Preliminary results from neoCHANCE-1 have illustrated a compelling improvement in pathological complete response (pCR) rates compared to historical controls treated with standard therapies. Notably, the combinatorial regimen demonstrated pronounced tumor downsizing, facilitating less extensive surgeries and potentially sparing critical anatomical structures. Such outcomes hold profound implications for functional preservation and quality of life, which are pivotal concerns in head and neck oncology.

Mechanistically, afatinib’s inhibition of EGFR not only hampers tumor proliferation programs but also induces immunogenic cell death, releasing tumor antigens that prime immune responses. When used concurrently with PD-1 blockade via tislelizumab, this antigenic surge catalyzes amplified cytotoxic T cell infiltration into the tumor microenvironment. This interplay underscores a critical synergy wherein targeted molecular therapies enhance the efficacy of immunotherapy through modulation of tumor-host immune dynamics.

Further immune profiling of patient tumor biopsies revealed elevated expression of interferon-gamma related genes post-treatment alongside an increase in CD8+ T cell populations, hallmark indicators of an activated antitumor immune milieu. These findings corroborate the hypothesis that neoadjuvant combination therapies can recalibrate immunosuppressive networks, potentially overcoming resistance mechanisms borne out by checkpoint monotherapies.

Safety evaluations indicated that the combined therapeutic regimen was generally well tolerated. Adverse events observed were consistent with known toxicities associated with EGFR inhibition, such as manageable skin rash and diarrhea, and immune-related adverse events typical for checkpoint blockade, including transient fatigue and mild inflammatory reactions. Crucially, no unexpected grade 4 or 5 toxicities were reported, affirming the regimen’s suitability for preoperative administration.

The translational potential of neoCHANCE-1’s findings is extensive. This trial pioneers a clinically actionable paradigm that leverages precision immunomodulation to convert an immunogenically ‘cold’ tumor microenvironment into a ‘hot’ one, thus enhancing surgical candidacy and long-term tumor control. These outcomes not only inspire integration of combined immunotherapy and targeted agents in HNSCC but also suggest avenues for similar strategies in other solid tumor malignancies characterized by EGFR dysregulation and immune evasion.

As immuno-oncology continues to evolve at an unprecedented pace, the integration of multifaceted biological insights into rational drug combinations becomes imperative. NeoCHANCE-1 exemplifies such translational synergy, combining molecular targeting and immune reactivation in a temporally optimized neoadjuvant setting. Future investigations are warranted to validate these findings in larger, multicenter randomized trials and to explore biomarkers predictive of response and resistance.

The trial’s success also beckons exploration of sequential or maintenance therapies post-surgery to consolidate immune-mediated tumor surveillance. Moreover, optimizing dosing schedules, managing immune-related adverse events proactively, and understanding long-term effects on immune memory remain pivotal research priorities.

Given the aggressive nature of locally advanced HNSCC and the historical stagnation in therapeutic innovation, the neoCHANCE-1 trial heralds a new dawn. By reimagining neoadjuvant treatment through the lens of immune and molecular synergy, this approach promises to rewrite the clinical narrative for patients facing a daunting diagnosis.

In summary, the convergence of PD-1 immune checkpoint blockade with EGFR inhibition via tislelizumab and afatinib respectively, administered prior to surgery, manifests a potent antitumor strategy in locally advanced head and neck squamous cell carcinoma. The phase 2 neoCHANCE-1 trial’s encouraging efficacy and manageable safety profile underscore the transformative potential of this therapeutic alliance, setting the stage for enhanced survival and preservation of function in a highly vulnerable patient subset.

As the oncology community eagerly awaits further data, this study undoubtedly propels neoadjuvant immunotherapy combined with targeted inhibition into the spotlight, marking a significant milestone in precision cancer medicine. The implications for patient care transcend HNSCC, potentially informing treatment frameworks across diverse malignancies where immune escape and aberrant receptor signaling coalesce to fuel tumor growth.

Subject of Research: Neoadjuvant combination immunotherapy and targeted therapy for locally advanced head and neck squamous cell carcinoma.

Article Title: Neoadjuvant tislelizumab with afatinib for locally advanced head and neck squamous cell carcinoma (neoCHANCE-1): a phase 2 clinical trial.

Article References:
Wei, Zg., Chen, Hj., Wang, Dj. et al. Neoadjuvant tislelizumab with afatinib for locally advanced head and neck squamous cell carcinoma (neoCHANCE-1): a phase 2 clinical trial. Nat Commun 16, 8918 (2025). https://doi.org/10.1038/s41467-025-63978-y

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Conducted by researchers Tan and Song, this investigation harnesses data from the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS), spanning more than nine years from early 2015 through March 2024. By deploying advanced disproportionality analysis methods—which include reporting odds ratio (ROR), proportional reporting ratio (PRR), and information component (IC)—the study quantitatively probes the association between osimertinib and muscle-related adverse events. These rigorous statistical tools are fundamental in pharmacovigilance, as they enable the detection of drug-event signals that may be rare yet clinically consequential, thus providing essential post-marketing surveillance insights beyond clinical trial data.

The analysis identified 121 reported cases involving osimertinib-related myotoxicity, unmasking a safety signal that had not been fully appreciated in prior clinical evaluations. Strikingly, the data reveal a pronounced demographic pattern: the majority of these adverse events occurred in females, comprising approximately 61% of cases, and nearly half of the affected patients were over 65 years old. This demographic distribution underscores the importance of age and sex as potential modifying factors in drug tolerance and side effect manifestation, warranting heightened clinical vigilance when prescribing osimertinib to these populations.

The temporal profile of onset for these muscle-related toxicities is particularly noteworthy. The median time to adverse event onset was calculated at 40 days, with a broad interquartile range spanning from roughly two weeks to over five months. This variation suggests that myotoxicity can manifest relatively early during treatment or emerge insidiously with longer drug exposure, emphasizing the need for ongoing monitoring rather than short-term observation alone. Clinicians should maintain an index of suspicion for muscle symptoms throughout the course of osimertinib therapy.

Among the specific myotoxic manifestations, elevated blood creatine phosphokinase (CPK) levels emerged as the most significant signal, with a lower bound 95% confidence interval of the ROR at 5.00, clearly indicating a strong correlation with osimertinib use. Elevated CPK is a recognized biomarker of muscle injury and demands prompt clinical assessment to prevent progression to more severe muscle damage. Additionally, both myositis—inflammatory muscle disease—and myopathy—disorders of muscle function—were also identified with significant risk signals, albeit at comparatively lower magnitudes. These findings collectively highlight a spectrum of potential muscle injury phenotypes associated with the drug.

The molecular underpinnings of osimertinib-induced myotoxicity remain to be fully elucidated, but hypotheses include off-target effects on muscle tissue, immune-mediated damage, or mitochondrial dysfunction precipitated by tyrosine kinase inhibition. Given that EGFR signaling pathways intersect with various cellular processes beyond tumor cell proliferation, unintended interference with muscle cell homeostasis is plausible. This recognition could catalyze further mechanistic studies aimed at pinpointing vulnerability factors and protective strategies.

Importantly, the study’s real-world dataset provides actionable intelligence for oncologists and multidisciplinary care teams. Awareness of these adverse event patterns should prompt preemptive strategies such as baseline muscle function assessments, routine monitoring of CPK levels, and patient education regarding symptom recognition. Early detection and management can mitigate severity, potentially involving dose adjustments, temporary treatment interruptions, or adjunctive therapies to address muscle inflammation and prevent irreversible damage.

Moreover, this research serves as a compelling example of how pharmacovigilance databases like FAERS can fill critical knowledge gaps left by randomized controlled trials, which often exclude or underrepresent older adults or those with comorbidities. By capturing heterogeneous patient experiences in broader clinical settings, such analyses bring to light safety considerations that can influence regulatory policies, clinical guidelines, and personalized medicine approaches.

While osimertinib continues to represent a breakthrough agent, the findings by Tan and Song advocate for a balanced perspective that weighs therapeutic benefit against emerging risks. Their study calls for integration of myotoxicity surveillance into routine practice and encourages collaborative research efforts to refine mitigation strategies. Ultimately, enhancing the drug’s safety profile will sustain its transformative role in NSCLC management and improve patients’ quality of life.

These insights also catalyze a broader discussion about the cardiac and muscular safety of tyrosine kinase inhibitors more generally, as similar agents have reported cardiomyopathy, arrhythmias, and skeletal muscle effects. The study thus contributes a vital piece to the evolving puzzle of kinase inhibitor toxicities, inspiring clinicians and researchers alike to deepen their understanding and optimize treatment paradigms.

In conclusion, the identification of osimertinib-related myotoxicity through disproportionality analysis represents a significant advance in the pharmacovigilance of a widely used targeted therapy. It underscores the necessity of continuous vigilance in the post-marketing phase and exemplifies the power of real-world data to detect adverse events that impact patient outcomes. As oncologic treatments evolve, so too must the frameworks for monitoring and managing their safety profiles, ensuring that innovation does not outpace patient protection.

Clinicians are encouraged to incorporate vigilance for muscle-related symptoms into their clinical routines and to report suspected adverse events accordingly, thereby enriching the collective understanding and ensuring ongoing refinement of osimertinib’s safety profile. The journey toward optimizing cancer care must harmonize efficacy with safety, and studies such as this one pave the way toward that equilibrium.

The findings also advocate for patient-centered communication strategies wherein individuals prescribed osimertinib are informed about possible muscle-related side effects and empowered to seek timely medical attention. Collaborative care models involving oncologists, pharmacists, and primary care providers will be fundamental in translating these research outcomes into improved clinical practice.

As the oncology community continues to embrace targeted agents, this study’s revelation about osimertinib-induced myotoxicity highlights a paradigm where precision medicine must be paired with precision safety monitoring. Future research is anticipated to delineate predictive biomarkers for susceptibility and to design preventive interventions that could attenuate this adverse effect without compromising anti-cancer efficacy.

Ultimately, the ongoing dialogue informed by pharmacovigilance and clinical research will enhance therapeutic decision-making and patient safety, fortifying osimertinib’s role as a leading agent in lung cancer treatment while safeguarding the well-being of those receiving it.

Subject of Research: Osimertinib-induced myotoxicity and its safety profile analyzed through real-world pharmacovigilance data.

Article Title: Osimertinib-related myotoxicity: a disproportionality analysis of the FDA adverse event reporting system.

Article References:
Tan, Y., Song, Q. Osimertinib-related myotoxicity: a disproportionality analysis of the FDA adverse event reporting system. BMC Cancer 25, 1360 (2025). https://doi.org/10.1186/s12885-025-14743-3

Image Credits: Scienmag.com

DOI: https://doi.org/10.1186/s12885-025-14743-3

This comprehensive meta-analysis encompassed six pivotal clinical studies, aggregating data from a cohort of 562 patients afflicted with NSCLC who developed acquired MET-driven resistance after prior EGFR-TKI therapy. By meticulously analyzing response rates, survival metrics, and adverse events, the investigators endeavored to delineate the therapeutic landscape of MET-TKI and EGFR-TKI combination regimens in this complex clinical niche. The findings herald a significant stride forward in pinpointing efficacious intervention strategies tailored to molecular resistance profiles.

At the forefront of the results, the pooled objective response rate (ORR) to the combination of MET-TKIs and EGFR-TKIs approached an encouraging 49.2%, coupled with a disease control rate (DCR) of 78.6%. These figures suggest that nearly half of the patients manifested measurable tumor shrinkage, while over three-quarters achieved disease stabilization or better. Importantly, the median duration of response (mDOR) spanned approximately 6.85 months, indicating a substantive period during which tumor regression was sustained. Complementing these outcomes, the median progression-free survival (mPFS) reached 5.62 months, underscoring the regimen’s capacity to delay disease advancement.

Dissecting the data further, the investigators parsed out differences contingent on the generation of EGFR-TKIs employed alongside MET-TKIs. Notably, combining MET-TKIs with third-generation EGFR-TKIs yielded numerically superior outcomes compared to first-generation EGFR-TKI combinations in patients who were T790M-negative but exhibited MET-dependent resistance. While statistical significance narrowly eluded some efficacy endpoints—such as ORR (56.8% vs. 47.8%) and DCR (81.6% vs. 75%)—the median duration of response and median progression-free survival favored the third-generation combinations, with mPFS notably extending to 7.45 months versus 4.55 months in the first-generation groups (p=0.05). These observations underscore the clinical advantage offered by newer-generation EGFR inhibitors in overcoming complex resistance mechanisms.

Beyond the generational distinction of EGFR-TKIs, the meta-analysis juxtaposed the efficacy profiles of three prominent MET inhibitors: capmatinib, savolitinib, and tepotinib. Remarkably, the objective response rates across these agents converged around 48-51%, signaling broadly comparable anti-tumor activity. Disease control rates, while showing some variability—savolitinib achieving the highest at 84.9% and tepotinib the lowest at 63.3%—did not consistently translate to statistically significant differences (p=0.02 in some cases). Median durations of response and progression-free survival similarly demonstrated no marked distinctions, suggesting interchangeability of MET-TKIs in efficacy when paired with EGFR-TKIs.

Safety profiles, however, unveiled subtle yet clinically meaningful distinctions pivoting around hepatotoxicity. Capmatinib-based combinations were associated with numerically lower incidences of elevated liver enzymes—specifically, increased AST and ALT levels—when compared to savolitinib and tepotinib counterparts. For instance, elevated AST occurred in 12.8% of capmatinib-treated patients versus nearly 19% with savolitinib and 17.4% with tepotinib. Furthermore, the rate of severe treatment-related adverse events (grade ≥3 TRAEs) trended lower in the capmatinib subgroup (30%) relative to savolitinib (46.7%) and tepotinib (41.2%), bordering on statistical significance (p=0.07). These findings advocate for a nuanced assessment of safety and tolerability alongside efficacy in clinical decision-making.

Taken together, these data coalesce into a compelling argument for integrating MET-TKI plus EGFR-TKI combination therapy into the treatment paradigm for NSCLC patients exhibiting acquired MET alterations after EGFR-TKI resistance. The synergy harnessed by targeting both molecular drivers simultaneously appears instrumental in circumventing resistance, enhancing tumor response, and prolonging progression-free intervals.

Mechanistically, resistance to EGFR-TKIs in NSCLC frequently arises via MET amplification or mutation, which reactivate downstream signaling pathways such as PI3K/AKT and MAPK, circumventing EGFR inhibition. By introducing MET-TKIs, clinicians can abrogate these bypass tracks, reinstating susceptibility to EGFR inhibition. This rationale finds tangible validation in the analyzed clinical outcomes and underscores the value of comprehensive molecular profiling in tailoring targeted therapies.

Third-generation EGFR-TKIs, exemplified by osimertinib, offer refined selectivity and efficacy, particularly against resistant T790M mutations. Their preferential pairing with MET-TKIs may optimize blockade of divergent resistance pathways. This meta-analysis hints that such combinations might amplify survival benefit compared to earlier-generation EGFR-TKIs, though further confirmatory trials are warranted.

In addition to addressing resistance, safety remains paramount given the potential toxicities intrinsic to kinase inhibitors. Hepatotoxicity, manifesting as elevated aminotransferase levels, constitutes a notable adverse effect with MET-TKIs. The observed relative hepatoprotective profile of capmatinib could influence therapeutic choices, especially in patients with pre-existing hepatic concerns or when long-term treatment is anticipated.

Despite this promising therapeutic horizon, several limitations temper the current landscape. The pooled studies exhibit heterogeneity in patient selection, MET alteration definitions, and treatment regimens, necessitating cautious interpretation. The lack of randomized head-to-head comparisons between different MET-TKIs or optimized EGFR-TKI combinations leaves gaps for future research.

Nevertheless, these insights mark a pivotal advance in NSCLC management, offering a beacon of hope to patients confronting resistance to frontline EGFR-targeted therapies. Continued exploration through large-scale prospective trials, paired with real-world evidence, will be crucial to refine these regimens and solidify their role in personalized lung cancer care.

In the era of precision oncology, the marriage of MET and EGFR inhibitors epitomizes a rational, mechanism-driven approach to overcoming drug resistance. This meta-analysis not only illuminates the therapeutic promise but also charts a course for future investigation aimed at maximizing patient outcomes amidst the molecular complexity of NSCLC.

As lung cancer remains a leading cause of cancer-related mortality worldwide, innovations that extend survival and preserve quality of life have profound clinical and societal impact. The emergence of MET-TKI plus EGFR-TKI combinations represents a tangible stride toward transforming resistance from an insurmountable barrier into a manageable challenge, rekindling hope for patients and clinicians alike.

Ongoing studies are poised to delve deeper into biomarkers predicting response, optimal sequencing strategies, and combination regimens potentially incorporating immunotherapy. This integrative approach may unlock synergistic effects, further propelling survival gains and redefining standards of care in NSCLC.

Ultimately, the convergence of translational research, molecular diagnostics, and targeted therapeutics embodied by these findings underscores the dynamic evolution of cancer treatment from empirical to exquisitely tailored intervention. The future of NSCLC therapeutics promises continued breakthroughs fueled by such rigorous scientific inquiry.

Subject of Research: Combination therapy using MET tyrosine kinase inhibitors and EGFR tyrosine kinase inhibitors in NSCLC patients with EGFR mutations and acquired MET alterations.

Article Title: MET tyrosine kinase inhibitors in combination with EGFR tyrosine kinase inhibitors in NSCLC patients with EGFR mutations and acquired MET alterations: a systematic review and meta-analysis.

Article References:
Hu, D., Hu, Y., Lei, S. et al. MET tyrosine kinase inhibitors in combination with EGFR tyrosine kinase inhibitors in NSCLC patients with EGFR mutations and acquired MET alterations: a systematic review and meta-analysis. BMC Cancer 25, 732 (2025). https://doi.org/10.1186/s12885-025-14145-5

Image Credits: Scienmag.com

DOI: https://doi.org/10.1186/s12885-025-14145-5