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Relevant Articles About Research and Clinical Trials in Lung Cancer

RELATED :SCLC (Small Cell Lung Cancer):NSCLC (Non-Small Cell Lung Cancer)

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OncWeekly Featured Trials

NSCLC (Non-Small Cell Lung Cancer)Datopotamab deruxtecanPembrolizumabRilvegostomigRecruitingAustraliaAustriaBelgiumBrazilCanadaGermanyHungaryIndiaItalyJapanKorea, Republic ofPolandSpainTaiwanTurkeyUnited KingdomUnited States 9NCT06357533Phase 3TROPION-Lung10
Phase III, Open-label, Study of First-line Dato-DXd in Combination With Rilvegostomig for Advanced Non-squamous NSCLC With High PD-L1 Expression (TC ≥ 50%) and Without Actionable Genomic Alterations

Phase III, Open-label, Study of First-line Dato-DXd in Combination With Rilvegostomig for Advanced Non-squamous NSCLC With High PD-L1 Expression (TC ≥ 50%) and Without Actionable Genomic Alterations

NSCLC (Non-Small Cell Lung Cancer)Datopotamab deruxtecanOsimertinibRecruitingAustraliaCanadaChinaGermanyItalyKorea, Republic ofSpainTaiwanThailand 9NCT06350097Phase 3TROPION-Lung14
Phase III, Open-label Study of First-line Osimertinib With or Without Datopotamab Deruxtecan for EGFRm Locally Advanced or Metastatic Non-small Cell Lung Cancer

Phase III, Open-label Study of First-line Osimertinib With or Without Datopotamab Deruxtecan for EGFRm Locally Advanced or Metastatic Non-small Cell Lung Cancer

MelanomaNSCLC (Non-Small Cell Lung Cancer)Other CancersSCC (Squamous Cell Carcinoma)Biological: T3011Combination Product: T3011 + pembrolizumabRecruitingAustraliaUnited States 0NCT04370587Phase 1Phase 2
A Clinical Study of Intratumoral MVR-T3011 (T3011) Given as a Single Agent and in Combination With Intravenous Pembrolizumab in Participants With Advanced or Metastatic Solid Tumors

A Clinical Study of Intratumoral MVR-T3011 (T3011) Given as a Single Agent and in Combination With Intravenous Pembrolizumab in Participants With Advanced or Metastatic Solid Tumors

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The Important Role of a Pharmacist in Treating Patients With NSCLC

Oncology Weekly (OW) spoke with Yvette C. Terrie, BS Pharm, RPh, consultant pharmacist, to gain insight into why pharmacists are a crucial part of the care team for patients with non-small-cell lung cancer (NSCLC).

OW: How has the role of clinical pharmacists in the multidisciplinary oncology team evolved in treating NSCLC-targeted cancer therapies?

Terrie: Pharmacists’ multifaceted roles have continued to evolve from simply preparing and dispensing medications to becoming integral members of the multidisciplinary healthcare team in caring for patients with NSCLC. Pharmacists collaborate with prescribers and other healthcare providers to devise patient-centered treatment plans tailored to patient needs, goals, and preferences. This collaborative approach to care aims to optimize therapeutic responses and minimize adverse effects.

How do pharmacists collaborate to provide comprehensive care for NSCLC patients in the community setting?

Due to their drug expertise, pharmacists can provide prescribers, other clinicians, and patients with valuable information regarding the efficacy, safety, and clinical advantages of targeted therapies for the treatment of NSCLC, including higher rates of response, and longer progression-free survival, fewer ADRS, and personalized treatment tailored to patient need. Pharmacists can also monitor and ensure that prescribed therapies are appropriate based on the patient’s medical and medication history and genetic profile. They can also provide information about ongoing clinical trials and research and direct patients and caregivers to resources that provide education about living with NSCLC and patient cost-saving programs.

What responsibilities do pharmacists have in managing NSCLC-targeted therapy treatment options?

Pharmacists are integral in ensuring the proper preparation, administration, handling, and storage of NSCLC-targeted therapies. Pharmacists are also instrumental in identifying key drug/drug interactions and contraindications, ensuring that prescribers and patients know potential warnings and precautions, and identifying and managing potential ADRs associated with these therapies.  Through medication therapy management, pharmacists can also ensure that medications are dosed appropriately and make recommendations when changes are warranted. Other key responsibilities include patient education and providing patients and caregivers with information about treatment expectations, the clinical benefits associated with targeted therapies, the goals of therapy, therapy administration, frequency, and potential ADRs.

How do pharmacists provide emotional and practical support to patients and their families throughout the NSCLC treatment journey?

Receiving a cancer diagnosis is associated with enormous physical, psychological, emotional, and financial burdens, and in addition to medication, emotional support is an integral component of care. Due to their frequent encounters with patients, pharmacists are well-poised to direct patients to the various support resources available, including information about NSCLC, potential drug therapies, and cost savings programs. Pharmacists can also encourage patients to take an active role in their care, maintain routine care from their oncologist, and adhere to the recommended treatment plan. By showing empathy to patients battling NSCLC, pharmacists can engage patients in conversation to assess their goals for treatment, assess their response to therapy, address any concerns, and help patients during the challenging journey as they receive treatment.

How do pharmacists advocate for patients in treatment decisions in the community setting?

Due to frequent encounters with patients, pharmacists often act as patient educators and advocates and may also identify patients at risk for and/or exhibiting signs of NSCLC and encourage these patients to seek further medical evaluation from their primary healthcare provider. Pharmacists are also well poised to identify patients who may be ideal candidates for certain therapies and/or enrollment in clinical trials. Patient counseling is an integral component of health care, and through patient education, patients can make informed decisions about their health. Pharmacists can also direct patients to resources that are often sponsored by manufacturing companies that may expand patient access and affordability to medications. During counseling, pharmacists can encourage patients to discuss concerns with the primary healthcare provider and take an active role in their care.

How can the advocacy efforts of pharmacists be further supported and integrated into the broader healthcare system?

Enhancing support for patients with NSCLC involves recognizing the essential roles of pharmacists in patient care. This recognition can be furthered by promoting additional training in oncology care and supporting pharmacists’ roles as drug experts in the multidisciplinary care of patients. Additionally, developing patient education programs that include pharmacists can ensure that patients and caregivers are well-informed about NSCLC and possible treatment options, therefore empowering patients to make informed decisions about their health.

YAP1-EIF4A3 Regulates Circ_0007386 in NSCLC Progression

KEY TAKEAWAYS

  • The study aimed to explore how hypoxia-regulated circ_0007386 affects NSCLC progression through YAP1-EIF4A3 and the miR-383-5p/CIRBP axis.
  • Researchers noticed that circ_0007386, driven by hypoxia and YAP1-EIF4A3, promotes NSCLC progression.

The progression of non-small cell lung cancer (NSCLC) is significantly influenced by circular RNAs (circRNAs), especially in the tumor hypoxia microenvironment. However, the precise functions and underlying mechanisms of dysregulated circRNAs in NSCLC remain largely unexplored.

Lixia Li and the team aimed to assess the oncogenic potential of circ_0007386 and its impact on NSCLC progression through these molecular interactions and pathways.

They performed an inclusive analysis of differentially expressed circRNAs in NSCLC tissues using high-throughput RNA sequencing. The characteristics of circ_0007386 were rigorously confirmed through Sanger sequencing, RNase R treatment, and actinomycin D treatment.

The effects of circ_0007386 on cell proliferation and apoptosis were investigated in vitro using CCK8, colony formation assays, TUNEL staining, and flow cytometry assays. In vivo, xenograft tumor models were employed to assess its impact on tumor growth.

Mechanistically, the regulatory relationships between circ_0007386, miR-383-5p, and CIRBP were examined through dual luciferase reporter assays and rescue experiments. Additionally, the binding of EIF4A3 to CRIM1 pre-mRNA was detected by RNA immunoprecipitation, and the interaction between YAP1 and EIF4A3 under hypoxic conditions was analyzed by co-immunoprecipitation.

About the investigation, a novel circRNA, designated as circ_0007386, was identified as upregulated in NSCLC tissues and cell lines. Circ_0007386 was found to modulate proliferation and apoptosis in NSCLC both in vitro and in vivo. Functionally, circ_0007386 acted as a sponge for miR-383-5p, targeting CIRBP, which influenced NSCLC cell proliferation and apoptosis through the PI3K/AKT signaling pathway.

Under hypoxic conditions, the interaction between YAP1 and EIF4A3 was enhanced, leading to the displacement of EIF4A4 from binding to CRIM1 pre-mRNA. This process facilitated the back-splicing of CRIM1 pre-mRNA, increasing the formation of circ_0007386. The circ_0007386/miR-383-5p/CIRBP axis was significantly associated with the clinical features and prognosis of patients with NSCLC.

The study concluded that circ_0007386, regulated by the YAP1-EIF4A3 interaction under hypoxic conditions, plays an oncogenic role in NSCLC progression through the miR-383-5p/CIRBP axis.

This study was funded by the Affiliated Hospital of Guangdong Medical University “Clinical Medicine+” CnTech Co-operation Project, “Start-up of scientific research funding for high-level talents” (202217); the Project of Zhanjiang City (2021A05052), the Basic and Applied Basic Research Programs of Science and Technology Commission Foundation of Guangdong Province (2021A1515011062, 2022A1515011731), Clinical Research Project of Affiliated Hospital of Guangdong Medical University (LCYJ2023B003).

Source: https://pubmed.ncbi.nlm.nih.gov/39030638/

Li L, Liu D, Chen T, et al. (2024). “Hypoxia-enhanced YAP1-EIF4A3 interaction drives circ_0007386 circularization by competing with CRIM1 pre-mRNA linear splicing and promotes non-small cell lung cancer progression.” J Exp Clin Cancer Res. 2024 Jul 20;43(1):200. doi: 10.1186/s13046-024-03116-6. PMID: 39030638.

Evaluating Pembrolizumab MONO vs. COMB in High PD-L1 NSCLC

KEY TAKEAWAYS

  • The study aimed to compare long-term outcomes of pembrolizumab monotherapy versus combination therapy in patients with high PD-L1 NSCLC.
  • Researchers noticed that combination therapy may offer benefits as a 1L treatment for selected patients with NSCLC.

Selecting pembrolizumab monotherapy (MONO) or pembrolizumab plus platinum-based chemotherapy (COMB) for patients with non-small cell lung cancer (NSCLC) and high programmed death-ligand 1 (PD-L1) expression is an important issue in clinical practice.

Yasuyuki Ikezawa and the team aimed to conduct a retrospective multicenter observational study of patients with NSCLC and high PD-L1 expression who received MONO or COMB as a first-line (1L) treatment and evaluated the long-term outcomes.

They performed an inclusive analysis of 298 patients with NSCLC and high PD-L1 expression who received MONO or COMB as a 1L treatment between December 2018 and January 2020. Medical records were reviewed to assess clinical efficacy and toxicity, utilizing a prolonged data cutoff for comprehensive evaluation.

About 164 patients (median age: 74 years) and 134 patients (median age: 68 years) received MONO and COMB, respectively; patients who received COMB were younger and had better performance statuses (0-1). At the prolonged data cutoff, the median follow-up was 20.2 (range: 0.1-41.4) months. The median progression-free survivals (PFS) were 7.5 and 13.1 months, and overall survivals (OSs) were 17.2 and 33.7 months for MONO and COMB, respectively.

Treatment discontinuation rates were 21.9% and 20.1% for MONO and COMB, respectively. With prolonged follow-up, although COMB demonstrated an OS benefit and higher objective response rate than MONO, in the propensity score matching analysis COMB didn’t demonstrate a significant benefit compared to MONO.

The study concluded that while COMB may offer a survival benefit and higher objective response rate compared to MONO, it did not show a significant advantage over MONO in the propensity score matching analysis. This suggests that COMB could be effective as a 1L treatment for NSCLC with high PD-L1 expression in a selected subset of patients.

The study did not receive any funds.

Source: https://pubmed.ncbi.nlm.nih.gov/39030894/

Ikezawa Y, Morita R, Mizugaki H, et al. (2024). “Real-world first-line treatment with pembrolizumab for non-small cell lung carcinoma with high PD-L1 expression: Updated analysis.” Cancer Med. 2024 Jul;13(14):e70036. doi: 10.1002/cam4.70036. PMID: 39030894; PMCID: PMC11258199.

SH3PXD2A-AS1 Promotes DDP Resistance in NSCLC via FOXM1/SIRT7

SH3PXD2A-AS1 Promotes DDP Resistance in NSCLC via FOXM1/SIRT7

KEY TAKEAWAYS

  • The study aimed to examine SH3PXD2A-AS1’s impact on DDP resistance in patients with NSCLC.
  • SH3PXD2A-AS1 enhances DDP resistance in NSCLC cells via FOXM1/SIRT7, suggesting a promising therapeutic approach.

Long noncoding RNAs (lncRNAs) have crucial regulatory roles in non-small cell lung cancer (NSCLC). Cisplatin (DDP) resistance has significantly reduced the effectiveness of DDP-based chemotherapy in patients with NSCLC.

Yunfeng Chen and the team aimed to investigate how SH3PXD2A antisense RNA 1 (SH3PXD2A-AS1) affects DDP resistance in patients with NSCLC.

The study detected proliferation and apoptosis of DDP-resistant NSCLC cells using cell counting kit-8 and flow cytometry assays. The interaction between SH3PXD2A-AS1 and sirtuin 7 (SIRT7) was assessed through co-immunoprecipitation (Co-IP), RNA pull-down, RNA immunoprecipitation (RIP), RNA fluorescence in situ hybridization, and immunofluorescence assays.

Succinylation (SUCC) of Forkhead Box M1 (FOXM1) was analyzed by IP and Western blot assays. The role of SH3PXD2A-AS1 in patients was explored using a xenografted tumor model.

The results showed elevated expression of SH3PXD2A-AS1 in DDP-resistant NSCLC cells, with its knockdown leading to suppressed cell viability and increased apoptosis. Silencing SH3PXD2A-AS1 also reduced FOXM1 protein levels while increasing FOXM1-SUCC levels.

SIRT7 interacted with FOXM1, inhibiting FOXM1 SUCC at the K259 site in HEK-293T cells. Overexpressing SIRT7 reversed the increased FOXM1-SUCC protein levels and apoptosis, and the decreased cell viability caused by SH3PXD2A-AS1 silencing.

In tumor-bearing mice, inhibiting SH3PXD2A-AS1 suppressed tumor growth and reduced Ki67, SIRT7, and FOXM1 protein levels.

The study concluded that SH3PXD2A-AS1 promotes DDP resistance in NSCLC cells by regulating FOXM1 SUCC through SIRT7, suggesting a promising therapeutic approach for NSCLC.

This work was supported by Xuzhou Science and Technology Bureau Focuses on Research and Development Plan, Open Subject of Key Laboratory of Universities in Jiangsu Province,Scientific Research Project of Jiangsu Provincial Health Commission and Development Fund of The Affiliated Hospital of Xuzhou Medical University.

Source: https://pubmed.ncbi.nlm.nih.gov/39020302/

Chen Y, Wu S, Han Y, et al. (2024). “LncRNA SH3PXD2A-AS1 facilitates cisplatin resistance in non-small cell lung cancer by regulating FOXM1 succinylation.” BMC Cancer. 2024;24(1):848. Published 2024 Jul 17. doi:10.1186/s12885-024-12624-9

EGFR-Mutated NSCLC: TGF-β Blockade Enhances Anti-PD-1

KEY TAKEAWAYS

  • The study aimed to determine the effects of TGF-β on the TME and to assess the efficacy of anti-PD-1 immunotherapy in treating EGFR-mutated pts with NSCLC.
  • Researchers made it evident that blocking of TGF-β enhanced anti-PD-1 efficacy in EGFR-mutated NSCLC.

EGFR mutation-carrying patients (pts) with non-small cell lung cancer (NSCLC) exhibit a detrimental response to immune checkpoint inhibitor (ICI) monotherapy, with a usually immunosuppressed tumor microenvironment (TME).

TGF-β plays an important role in immunosuppression; however, the impacts of TGF-β on the TME and the efficacy of anti-PD-1 immunotherapy against EGFR-mutated tumors remained unclear.

Huayan Huang and the team aimed to investigate the effects of TGF-β on the TME and to assess the efficacy of anti-PD-1 immunotherapy in treating EGFR-mutated NSCLC.

Researchers conducted in vitro studies employing the TCGA database, clinical specimens, and self-constructed SJT1601 cell lines with EGFR mutations. They utilized C57BL/6N and humanized M-NSG subjects bearing EGFR-mutated NSCLC to investigate the impacts of TGF-β on the TME and the combined efficacy of TGF-β blockade + anti-PD-1 therapy.

Flow cytometry was utilized for continuous monitoring of immune cell alterations. Clinical samples affirmed the correlation between TGF-β and immunotherapy outcomes of EGFR-mutated NSCLC.

They noticed that TGF-β was upregulated in EGFR-mutated NSCLC by EGFR activation and subsequent ERK1/2-p90RSK phosphorylation. TGF-β directly inhibited CD8+ T cell infiltration, proliferation, and cytotoxicity both in vitro and in vivo, but blocking TGF-β did not suppress the growth of EGFR-mutated tumors in vivo.

Anti-TGF-β antibody combined with anti-PD-1 antibody significantly inhibited the proliferation of recombinant EGFR-mutated tumors in C57BL/6N, which was superior to their monotherapy. Mechanistically, the combination of anti-TGF-β + anti-PD-1 antibodies significantly increased the infiltration of CD8+ T cells and enhanced the anti-tumor function of CD8+ T cells.

Moreover, the expression of TGF-β1 in EGFR-TKI-resistant cell lines was significantly enhanced relative to parental cell lines. The combination of anti-TGF-β + nivolumab significantly inhibited the proliferation of EGFR-TKI-resistant tumors in humanized M-NSG subjects and prolonged their survival.

The study concluded that TGF-β expression is upregulated in pts with EGFR-mutated NSCLC through the EGFR-ERK1/2-p90RSK signaling pathway. High TGF-β expression inhibited the CD8+ T cells infiltration and anti-tumor function, which contributied to the “cold” TME of EGFR-mutated tumors.

Blocking TGF-β can potentially reincarnate the TME, and may enhance the therapeutic efficacy of anti-PD-1 in EGFR-mutated NSCLC tumors, which will provide a potent immunotherapy technique for advanced EGFR-mutated pts with NSCLC.

The study was funded by National Natural Science Foundation of China.

Source: https://pubmed.ncbi.nlm.nih.gov/39004699/

Huang H, Zhu X, Yu Y, et al. (2024). “EGFR mutations induce the suppression of CD8+ T cell and anti-PD-1 resistance via ERK1/2-p90RSK-TGF-β axis in non-small cell lung cancer.” J Transl Med. 2024 Jul 14;22(1):653. doi: 10.1186/s12967-024-05456-5. PMID: 39004699.

Targeting SUMOylation and MEK in KRAS-Mutant MYC Cancers

KEY TAKEAWAYS

  • The study aimed to investigate the effectiveness of SUMOylation inhibition in KRAS-mutant cancer cells.
  • Researchers noticed that dual inhibition of SUMOylation and MEK effectively downregulates MYC and enhances DNA damage in KRAS-mutant cancer cells.

KRAS mutations frequently occur in cancers, particularly pancreatic ductal adenocarcinoma, colorectal cancer, and non-small cell lung cancer. Although KRASG12C inhibitors have recently been approved, effective precision therapies have not yet been established for all KRAS-mutant cancers.

Many treatments for KRAS-mutant cancers, including epigenome-targeted drugs, are currently under investigation. Small ubiquitin-like modifier (SUMO) proteins are a family of small proteins covalently attached to and detached from other proteins in cells via the processes called SUMOylation and de-SUMOylation.

Hiroshi Kotani and the team aimed to assess the impact of SUMOylation inhibition on MYC expression in KRAS-mutant cancer cells.

They performed an inclusive analysis to assess the efficacy of the 1-in-class SUMO-activating enzyme E inhibitor TAK-981 (subasumstat) in multiple human and mouse KRAS-mutated cancer cell lines. A gene expression assay using a TaqMan array was utilized to identify biomarkers of TAK-981 efficacy. Additionally, the biological roles of SUMOylation inhibition and subsequent regulatory mechanisms were investigated using immunoblot analysis, immunofluorescence assays, and mouse models.

They discovered that TAK-981 downregulated the expression of the currently undruggable MYC and effectively suppressed the growth of MYC-expressing KRAS-mutant cancers across different tissue types. Moreover, TAK-981-resistant cells were sensitized to SUMOylation inhibition via MYC overexpression. TAK-981 induced proteasomal degradation of MYC by altering the balance between SUMOylation and ubiquitination and promoting the binding of MYC and Fbxw7, a key factor in the ubiquitin-proteasome system.

The efficacy of TAK-981 monotherapy in immunocompetent and immunodeficient mouse models using a mouse-derived CMT167 cell line was significant but modest. Since MAPK inhibition of the KRAS downstream pathway is crucial in KRAS-mutant cancer, it was expected that co-inhibition of SUMOylation and MEK might be a good option.

The combination treatment with TAK-981 and trametinib dramatically induced apoptosis in multiple cell lines and gene-engineered mouse-derived organoids.

Moreover, combination therapy resulted in long-term tumor regression in mouse models using cell lines of different tissue types. Researchers revealed that combination therapy complementarily inhibited Rad51 and BRCA1 and accumulated DNA damage.

The study concluded that MYC downregulation occurred via SUMOylation inhibition in KRAS-mutant cancer cells. The findings indicate that dual inhibition of SUMOylation and MEK may be a promising treatment for MYC-expressing KRAS-mutant cancers by enhancing DNA damage accumulation.

This study was funded by P-CREATE from AMED under grant number 21cm0106513h0006 (to SY), Kanazawa University Hospital SAKIGAKE project 2022–2023 (to HK and SY), and JSPS KAKENHI grant number JP23744746 (to HK).

Source: https://pubmed.ncbi.nlm.nih.gov/38992694/

Kotani H, Oshima H, Boucher JC, et al. (2024). “Dual inhibition of SUMOylation and MEK conquers MYC-expressing KRAS-mutant cancers by accumulating DNA damage.” J Biomed Sci. 2024 Jul 11;31(1):68. doi: 10.1186/s12929-024-01060-3. PMID: 38992694.

Mapping Hot SPOTS in EGFR-TKI Targeted Therapeutics for NSCLC

KEY TAKEAWAYS

  • The study aimed to conduct a bibliometric analysis to summarize the trends in research on resistance to EGFR TKIs in patients with EGFR-mutant NSCLC.
  • The study identified hot spots in EGFR-TKI resistance in NSCLC therapeutics.

Activating mutations in epidermal growth factor receptor (EGFR) have been identified to be majorly predictive in personalized treatment with EGFR tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer (NSCLC), aiding in improving patient response rates and survival.

However, resistance challenges the efficacy of these treatments, with a limited understanding of post-resistance therapeutics. A deeper understanding of the biology and resistance mechanisms of EGFR-mutant NSCLC is urgently needed for the development of novel treatment strategies.

Jun Shao and the team aimed to conduct a bibliometric analysis to summarize the trends in research on resistance to EGFR TKIs in EGFR-mutant NSCLC to understand the biology of resistance mechanisms and to identify potential novel treatment approaches post-resistance.

Researchers retrieved research papers based on EGFR inhibitor-resistant NSCLC from the Web of Science Core Collection (WoSCC). Bibliometric tools like CiteSpace, VOSviewer, and other platforms were employed for comprehensive analysis and visualization of the outcomes.

Data analysis revealed that the WoSCC database contained a total 5866 documents on resistance to EGFR TKIs treatment, comprising 4727 articles (93.48%) and 1139 reviews (6.52%). These documents originate from 81 countries and regions and involve 4792 institutions, with contributions from 23,594 authors.

Since 2016, there has been a notable increase in publications in this field, indicating growing research interest and activity globally. China leads in publication output, reflecting significant contributions to the literature on EGFR-TKI resistance, while the United States has garnered the highest citation count for papers, underscoring the impact of research originating from this region.

Among the top contributors to research in this area, Harvard University stands out with the highest number of publications. The top 10 journals publishing on EGFR-TKI resistance include Clinical Cancer Research, which boasts the highest impact factor at 11.5. Notably, 90% of these journals are classified in Q1 or Q2 categories, indicating their high academic standing.

Key subjects of research focused on genetic testing, understanding resistance mechanisms, and developing strategies for managing resistance once it occurs. Influential authors such as Rafael Rosell being the most influential authors in the area had significantly shaped this field, ranking high in both publication volume and citation count, pinpointing their impact on advancing knowledge in EGFR-TKI resistance.

The study provided a firm basis for identifying hot spots in EGFR-TKI resistance research in NSCLC, offering reliable guidance in finding authoritative references, understanding research trends, and exploring potential directions.

The study was supported by the National Natural Science Foundation of China (No.82272669, No.82203010).

Source: https://pubmed.ncbi.nlm.nih.gov/38947223/

Shao J., Gu Y., Guo R., et al. (2024). “A Visual Analysis of the Research Dynamics in Resistance to EGFR Inhibitors for NSCLC.” Drug Des Devel Ther. 2024 Jun 26;18:2571-2591. doi: 10.2147/DDDT.S465238. PMID: 38947223; PMCID: PMC11214774.

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