scholarly journals SERS Platform Based on Bimetallic Au-Ag Nanowires-Decorated Filter Paper for Rapid Detection of miR-196ain Lung Cancer Patients Serum

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Ji Xia ◽  
Yifan Liu ◽  
Menglin Ran ◽  
Dan Lu ◽  
Xiaowei Cao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Filter Paper ◽  
Rapid Detection ◽  
Lung Cancers ◽  
Lung Cancer Patients ◽  
Single Base Mismatch ◽  
Liver Cancers ◽  
Surface Enhanced Raman ◽  
Potential Applications

Detecting microRNA (miRNA) biomarkers expression is of great significance for the diagnosis and treatment of lung cancer. Surface-enhanced Raman scattering (SERS) has achieved microRNA sensing for the diagnosis of primary liver cancers. In this work, we developed a SERS technology for the rapid detection of lung cancers-related miRNA (miR-196a) using bimetallic Au-Ag nanowire (AgNW@AuNPs) substrates coupled with the target hairpin DNA. The finite-difference time-domain simulation proved that a large number of “hot spots” were generated between the AgNW and AuNPs, which resulted in a huge enhancement of the signal of Raman reporters. Filter paper treated by hexadecenyl succinic anhydride hydrophobic and modified with AgNWs@AuNPs was used as capturing substrate. The detection limits of miR-196a in PBS and serum were as low as 96.58 aM and 130 aM, respectively. Studies on nonspecific sequence and single-base mismatch of miRNA demonstrated that SERS-based platform was highly selective, excellent uniform, and reproducible. Finally, the platform was used to show that the miR-196a expression in the serum of lung cancer patients was much higher than that in healthy people. The detection results indicated that the SERS platform had potential applications in cancer diagnosis and might be a viable alternative to the conventional miRNA detection method, the real-time polymerase chain reaction (RT-PCR) technology.

scholarly journals Soluble c-Met Is a Reliable and Sensitive Marker to Detect c-Met Expression Level in Lung Cancer

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Huilai Lv ◽  
Baoen Shan ◽  
Ziqiang Tian ◽  
Yong Li ◽  
Yuefeng Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Tissue Sample ◽  
Sample Collection ◽  
Lung Cancers ◽  
Lung Cancer Patients ◽  
Lung Cancer Therapy ◽  
Reliable Marker ◽  
Soluble C ◽  
Sensitive Marker

c-Met has been demonstrated as an attractive target in lung cancer therapy. Current studies showed that detection of c-Met status in tumor is critical in Met-targeted therapy. However not all patients are suitable for tissue sample collection. It is important to discover novel surrogate markers to detect c-Met status. In the study, soluble c-Met (s-Met) in plasma from 146 Chinese lung cancer patients and 40 disease-free volunteers was measured by enzyme-linked immunosorbent. In parallel, expression of c-Met in those tumors was also assessed by immunohistochemistry. Results showed that, in 146 lung cancer patients, 93 were c-Met expression positive and 74 of 93 were overexpressed. In c-Met-overexpressed patients, plasma s-Met was significantly increased. And further studies showed that plasma s-Met linearly correlated with c-Met expression in tumor. After tumor was removed in Met-overexpressed patients via resection, plasma s-Met significantly decreased to basal level. In addition, plasma s-Met showed to be poorly correlated with tumor size in Met-overexpressed patients. These results demonstrated that plasma s-Met is a sensitive and reliable marker to detect c-Met overexpression in lung cancers, and it is independent of tumor volume.

Comprehensive cancer genomics-based screening of new therapeutic targets and biomarkers for lung cancer.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e21031-e21031
Author(s):  
Yataro Daigo ◽  
Atsushi Takano ◽  
Yusuke Nakamura
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Therapeutic Target ◽  
Cancer Genomics ◽  
Cancer Biomarkers ◽  
Lung Cancer Cells ◽  
Lung Cancers ◽  
Lung Cancer Patients ◽  
Target Molecules

e21031 Background: Since the clinical outcome of advanced lung cancer patients is still poor after standard therapies, development of new anti-cancer drugs with minimum risk of adverse effects and cancer biomarkers for precision medicine is urgently required. Methods: We have been screening new therapeutic target molecules and molecular biomarkers for lung cancers as follows; i) To identify overexpressed genes in lung cancers by the gene expression profile analysis, ii) To verify the target genes for their scarce expression in normal tissues, iii) To validate the clinicopathologic importance of their protein expression by tissue microarray covering 263 lung cancers, and iv) To confirm their function for the growth and/or invasive ability of the lung cancer cells by siRNAs and gene transfection assays. Results: We identified dozens of candidate target molecules and selected a gene encoding protein with a GAP domain, LAPG1 (lung cancer-associated protein with Gap domain 1). Immunohistochemical analysis showed that LAPG1 expression was observed in 69.9% of lung cancers. Moreover positivity of LAPG1 expression was associated with poor prognosis of lung cancer patients. Knockdown of LAPG1 expression by siRNAs suppressed growth of lung cancer cells. Introduction of LAPG1 increased the invasive activity of mammalian cells, indicating that LAPG1 could be a prognostic biomarker and therapeutic target for lung cancers. Conclusions: Comprehensive cancer genomics-based screening could be useful for selection of new cancer biomarkers and molecular targets for developing small molecules, antibodies, nucleic acid drugs, and immunotherapies.

Systematic approach for development of new immunotherapeutics for lung cancers through cancer genomics analysis.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 3092-3092
Author(s):  
Yataro Daigo ◽  
Atsushi Takano ◽  
Yusuke Nakamura
Keyword(s):  
Lung Cancer ◽  
Phase I ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Clinical Studies ◽  
Critical Role ◽  
Phase I Clinical Trials ◽  
Lung Cancers ◽  
Lung Cancer Patients ◽  
High Immunogenicity

3092 Background: Oncoantigens are defined to be proteins that are very specifically expressed in cancer cells and that have the oncogenic activity and high immunogenicity, and are considered to be promising targets for immunotherapy such as therapeutic cancer vaccines. Methods: We have established a strategy as follows to identify new oncoantigens; i) screening of highly transactivated genes in the majority of 120 lung cancers using cDNA microarray representing 27,648 genes coupled with enrichment of tumor cells by laser microdissection, ii) verification of no expression of each candidate gene in normal tissues by northern-blot analysis, iii) validation of the clinicopathological significance of its high level of expression with tissue microarray containing 300 lung cancers, iv) verification of a critical role of each gene in the growth or invasiveness of cancer cells by RNAi and cell growth/invasion assays, v) screening of the epitope peptides recognized by HLA-A*0201- or A*2402-restricted cytotoxic T lymphocyte (CTL). We conducted phase I clinical trials of these therapeutic peptide vaccines for lung cancer patients. Results: We identified 35 oncoantigens and screened dozens of 10-amino-acid peptides, each of which corresponded to a part of TTK, LY6K, IMP-3, CDCA1, KIF20A, CDC45L, and FOXM1, and was a candidate to be presented on the surface of HLA-A*0201 or HLA-A*2402 that induced in vitro CTL response. Phase I clinical studies indicated that five epitope peptides could strongly induce the CTL activity in cancer patients. For example, we conducted a phase I study for HLA-A*2402-positive, advanced non-small cell lung cancer patients who failed to standard therapy, using the combination of 1, 2 or 3 mg/body of each peptides from LY6K, CDCA1, and KIF20A mixed with adjuvant once a week. This cancer vaccine therapy demonstrated tolerability and had very high immunogenicity of even 1 mg/body dose to induce antigen-specific CTLs in cancer patients. Conclusions: Through systematic genomics-based approach and clinical study, we have identified five epitope peptides, which could induce CTLs very effectively in cancer patients, and therefore it warrants further clinical studies. Clinical trial information: NCT01069575.

Therapeutic and prognostic impacts of specific gene alterations for squamous cell lung cancer: A result of nationwide genome screening in Japan (LC-SCRUM-Japan).

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. 9060-9060
Author(s):  
Terufumi Kato ◽  
Shingo Matsumoto ◽  
Shigeki Umemura ◽  
Kiyotaka Yoh ◽  
Kazumi Nishino ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Large Scale ◽  
Small Cell ◽  
Specific Gene ◽  
Small Cell Lung ◽  
Lung Cancers ◽  
Lung Cancer Patients ◽  
Genome Screening ◽  
Gene Alterations

9060 Background: Various gene alterations occur during the development of squamous cell lung cancer (SqLC), but specific gene alterations for SqLC and their clinical significance remain unknown. Methods: In a nationwide genome screening project (LC-SCRUM-Japan), we have prospectively analyzed lung cancer patients for genetic alterations using a next-generation sequencing (NGS) system, Oncomine Comprehensive Assay, and have established a large-scale clinico-genomic database. Results: Since February 2013 to December 2018, a total of 6692 lung cancer patients (686 SqLCs, 5360 non-squamous non-small cell lung cancers [Non-sq] and 646 small cell lung cancers [SCLCs]) had been enrolled in the LC-SCRUM-Japan. The success rate of the NGS assay was 91%. Of 639 SqLCs analyzed, 274 (48%) had potentially targetable gene alterations, including 77 NFE2L2 (encoding NRF2) mut, 50 PIK3CA mut, 46 FGFR1 amp, 40 EGFRmut/amp, 36 PTEN mut, 23 KRAS mut, 6 AKT1 mut, 6 MET ex14skip, 5 ALK fusions, 2 FGFR3 fusions. Among the alterations detected, NFE2L2 mut and FGFR1 amp were significantly frequent in SqLC than Non-sq or SCLC (NFE2L2, 12.1% vs. 1.0% vs. 1.3%; p < 0.001, and FGFR1, 7.2% vs. 1.1% vs. 3.4%; p < 0.001). In advanced SqLC patients who received platinum-containing chemotherapies, the median progression-free survival (mPFS) was significantly shorter in NFE2L2-mutated patients (NRF2-type) than NFE2L2/FGFR1-negative patients (nonNF-type) (3.8 [95%CI, 2.9-5.1] vs. 4.5 [95%CI, 3.8-5.4] months, p = 0.03), and similarly, the mPFS of FGFR1-amplified patients (FGFR1-type) (3.5 months [95%CI, 1.5-4.9]) tended to be shorter than that of nonNF-type (p = 0.07), although the response rates were equivalent among the three types. NRF2-type also showed shorter overall survival (OS) than nonNF-type (median OS, 10.4 [95%CI, 6.9-22.3] vs. 16.6 [95%CI, 13.6-21.7] months, p = 0.10). Therapeutic efficacy of nivolumab or pembrolizumab was not different among these types in the current follow-up data. Conclusions: Our large scale genome screening identified specific gene alterations for SqLC and the alterations were associated with a less efficacy of chemotherapy and worse prognosis, suggesting the need for the development of genotype-directed therapeutic strategy for SqLC patients.

scholarly journals Molecular characteristics and clinical outcomes of complex ALK rearrangements identified by next-generation sequencing in non-small cell lung cancers

2021 ◽  
Author(s):  
Peiyi Xia ◽  
Lan Zhang ◽  
Pan Li ◽  
Enjie Liu ◽  
Wencai Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Next Generation Sequencing ◽  
Cancer Patients ◽  
Small Cell ◽  
Molecular Characteristics ◽  
Fusion Partner ◽  
Small Cell Lung ◽  
Lung Cancers ◽  
Lung Cancer Patients ◽  
Generation Sequencing

Abstract Background Complex kinase rearrangement, a mutational process involving one or two chromosomes with clustered rearrangement breakpoints, interferes with the accurate detection of kinase fusions by DNA-based next-generation sequencing (NGS). We investigated the characteristics of complex ALK rearrangements in non-small cell lung cancers using multiple molecular tests. Methods Samples of non-small cell lung cancer patients were analyzed by targeted-capture DNA-based NGS with probes tilling the selected intronic regions of fusion partner genes, RNA-based NGS, RT-PCR, immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH). Results In a large cohort of 6576 non-small cell lung cancer patients, 343 (5.2%) cases harboring ALK rearrangements were identified. Fourteen cases with complex ALK rearrangements were identified by DNA-based NGS and classified into three types by integrating various genomic features, including intergenic (n = 3), intragenic (n = 5) and “bridge joint” rearrangements (n = 6). All thirteen cases with sufficient samples actually expressed canonical EML4-ALK fusion transcripts confirmed by RNA-based NGS. Besides, positive ALK IHC was detected in 13 of 13 cases, and 9 of 11 cases were positive in FISH testing. Patients with complex ALK rearrangements who received ALK inhibitors treatment (n = 6), showed no difference in progression-free survival (PFS) compared with patients with canonical ALK fusions(n = 36, P = 0.9291). Conclusions This study firstly reveals the molecular characteristics and clinical outcomes of complex ALK rearrangements in NSCLC, sensitive to ALK inhibitors treatment, and highlights the importance of utilizing probes tilling the selected intronic regions of fusion partner genes in DNA-based NGS for accurate fusion detection. RNA and protein level assay may be critical in validating the function of complex ALK rearrangements in clinical practice for optimal treatment decision.

Second primary cancer of the larynx in patients with lung cancer

1998 ◽  
Vol 112 (3) ◽  
pp. 252-257 ◽  
Author(s):  
Yoav P. Talmi ◽  
Lev Bedrin ◽  
Alexander Waller ◽  
Zeev Horowitz ◽  
Yair Skurnik ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Laryngeal Cancer ◽  
Second Primary ◽  
Second Primary Cancer ◽  
Lung Cancers ◽  
Lung Cancer Patients ◽  
Large Databases ◽  
Second Primary Malignancies ◽  
Cancer Of The Lung

AbstractSynchronous or metachronous second primary malignancies of the lung are sometimes encountered in patients with laryngeal cancer while the occurrence of a laryngeal second primary following cancer of the lung is rare.A two-armed study was conducted. A prospective arm in which the larynges of 56 terminal lung cancer patients were examined, and a retrospective arm incorporating both a chart study of 126 terminal head and neck cancer patients (HNCP) and a computerized search of all hospital records of patients with laryngeal and lung cancers. No laryngeal malignancy was found in the lung cancer patients' group and no antedating pulmonary malignancy was recorded in the terminal HNCP. The computerized search of 1778 lung cancer patients and 213 laryngeal cancer patients also failed to demonstrate cases where the former preceded the latter.In conclusion. No second primary of the larynx was found in lung cancer patients. These results compare with reports of large databases where cancer of the larynx was found in a negligible percentage of lung cancer survivors and theories explaining this are discussed.

869 Anti-LunX targeting therapy for lung cancer

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A921-A921
Author(s):  
Xiaohu Zheng ◽  
Weihua Xiao ◽  
Zhigang Tian
Keyword(s):  
Lung Cancer ◽  
Lymph Nodes ◽  
Cancer Patients ◽  
Therapeutic Target ◽  
Xenograft Model ◽  
Therapeutic Antibody ◽  
Antibody Treatment ◽  
Lung Cancers ◽  
Lung Cancer Patients ◽  
Novel Therapeutic

BackgroundThe identification of novel therapeutic targets in lung cancer for the generation of targeted drugs is an urgent challenge. Lung-specific X (LunX) is a member of the palate, lung, and nasal epithelium clone (PLUNC) protein family. Some reports have suggested that the human PLUNC gene (also named LUNX) might be a potential marker for NSCLC, and PLUNC mRNA has been identified in peripheral blood and mediastinal lymph nodes from NSCLC patients.It is unclear whether LunX expression is associated with the pathological type and pathological severity in lung cancer patients. The utility of LunX as a potential therapeutic target in NSCLC is uncertain.MethodsClinically, 80% of lung cancers are non-small-cell lung cancers (NSCLCs). Here, we analyzed 158 NSCLC samples and detected LunX expression.ResultsIt showed that the expression of LunX were elevated in 90% (108/150) lung cancers by IHC staining, which accompanied with significantly lower rate of postsurgery survival. Further evaluation of LunX expression in invasive tumor cells in subclavicular lymph nodes, draining lymph nodes, hydrothorax of lung cancer patients, turned out that LunX is highly expressed in invasive lung cancer cells. These data indicated that LunX overexpresses in lung cancer and associates with tumorigenesis and tumor progression.Mechanistically, we discovered that LunX bound to 14-3-3 protein and facilitated their activation by maintaining these proteins in a dephosphorylated state, thereby contributing to the activation of pathways downstream of 14-3-3 protein, such as the Erk1/2 and JNK pathways. Thus, LunX promoted tumor growth and metastasis.Furthermore, we generated a therapeutic antibody specific for lung cancer, which not only inhibited lung cancer growth and reduced Ki67 staining and angiogenesis in xenograft model of subcutaneously transplanted tumor, but also blocked tumor metastasis and invasion, improved the survival of these mice. We also detected that antibody treatment induces LunX antigen-antibody complex endocytosis and the degradation of LunX protein.ConclusionsOur study suggests that LunX is a novel therapeutic target in lung cancer and that the LunX-targeted therapeutic antibody may have considerable clinical benefit.

scholarly journals Molecular characteristics and clinical outcomes of complex ALK rearrangements identified by next-generation sequencing in non-small cell lung cancers

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Peiyi Xia ◽  
Lan Zhang ◽  
Pan Li ◽  
Enjie Liu ◽  
Wencai Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Next Generation Sequencing ◽  
Cancer Patients ◽  
Small Cell ◽  
Molecular Characteristics ◽  
Fusion Partner ◽  
Small Cell Lung ◽  
Lung Cancers ◽  
Lung Cancer Patients ◽  
Generation Sequencing

Abstract Background Complex kinase rearrangement, a mutational process involving one or two chromosomes with clustered rearrangement breakpoints, interferes with the accurate detection of kinase fusions by DNA-based next-generation sequencing (NGS). We investigated the characteristics of complex ALK rearrangements in non-small cell lung cancers using multiple molecular tests. Methods Samples of non-small cell lung cancer patients were analyzed by targeted-capture DNA-based NGS with probes tilling the selected intronic regions of fusion partner genes, RNA-based NGS, RT-PCR, immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH). Results In a large cohort of 6576 non-small cell lung cancer patients, 343 (5.2%) cases harboring ALK rearrangements were identified. Fourteen cases with complex ALK rearrangements were identified by DNA-based NGS and classified into three types by integrating various genomic features, including intergenic (n = 3), intragenic (n = 5) and “bridge joint” rearrangements (n = 6). All thirteen cases with sufficient samples actually expressed canonical EML4-ALK fusion transcripts confirmed by RNA-based NGS. Besides, positive ALK IHC was detected in 13 of 13 cases, and 9 of 11 cases were positive in FISH testing. Patients with complex ALK rearrangements who received ALK inhibitors treatment (n = 6), showed no difference in progression-free survival (PFS) compared with patients with canonical ALK fusions n = 36, P = 0.9291). Conclusions This study firstly reveals the molecular characteristics and clinical outcomes of complex ALK rearrangements in NSCLC, sensitive to ALK inhibitors treatment, and highlights the importance of utilizing probes tilling the selected intronic regions of fusion partner genes in DNA-based NGS for accurate fusion detection. RNA and protein level assay may be critical in validating the function of complex ALK rearrangements in clinical practice for optimal treatment decision.

scholarly journals Untangling the KRAS mutated lung cancer subsets and its therapeutic implications

2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Kulshrestha Ritu ◽  
Pawan Kumar ◽  
Amit Singh ◽  
K. Nupur ◽  
Sonam Spalgias ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Targeted Therapies ◽  
Kinase Inhibitors ◽  
Prognostic Impact ◽  
Kras Mutations ◽  
Lung Cancers ◽  
Therapeutic Implications ◽  
Lung Cancer Patients ◽  
Response To Chemotherapy

AbstractThe Kirsten rat sarcoma virus transforming protein (KRAS) mutations (predominate in codons 12, 13, and 61) and genomically drive nearly one-third of lung carcinomas. These mutations have complex functions in tumorigenesis, and influence the tumor response to chemotherapy and tyrosine kinase inhibitors resulting in a poorer patient prognosis. Recent attempts using targeted therapies against KRAS alone have met with little success. The existence of specific subsets of lung cancer based on KRAS mutations and coexisting mutations are suggested. Their interactions need further elaboration before newer promising targeted therapies for KRAS mutant lung cancers can be used as earlier lines of therapy. We summarize the existing knowledge of KRAS mutations and their coexisting mutations that is relevant to lung cancer treatment, in this review. We elaborate on the prognostic impact of clinical and pathologic characteristics of lung cancer patients associated with KRAS mutations. We briefly review the currently available techniques for KRAS mutation detection on biopsy and cytology samples. Finally, we discuss the new therapeutic strategies for targeting KRAS-mutant non-small cell lung cancer (NSCLC). These may herald a new era in the treatment of KRASG12Cmutated NSCLC as well as be helpful to develop demographic subsets to predict targeted therapies and prognosis of lung cancer patients.

Correlation of microsatellite-instable (MSI) status and genomic characteristics in 12,000 Chinese lung cancer patients.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e21019-e21019
Author(s):  
Liufu Su ◽  
Xinyi Liu ◽  
Xiaochun Huang ◽  
Mengli Huang
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Large Scale ◽  
Objective Response ◽  
The Other ◽  
Egfr Mutations ◽  
Molecular Characteristics ◽  
Genetic Profile ◽  
Lung Cancers ◽  
Lung Cancer Patients

e21019 Background: Microsatellite-instable-high (MSI-H) is a strong biomarker for favorable response to immune checkpoint blockade (ICI) therapies. The objective response rate was 30%̃40% in advanced MSI-H solid tumors receiving ICI treatment, while MSI status is rarely considered in lung cancer in setting of ICI treatment. MSI-H occurred in 0.8%̃2% lung cancer patients tested by PCR method. Immune microenvironment of MSI-H lung cancer had not been studied on a large scale. We explored the association of MSI status, genetic profile and PD-L1 expression in a large Chinese lung cancer cohort to elucidate the molecular characteristics of MSI-H lung cancer. Methods: MSI status was determined by PCR test in tumor tissue and by an in-house algorithm in blood specimen. The tumor samples were sequenced by next-generation sequencing to call single nucleotide variants (SNVs) and copy number variants (CNVs). PD-L1 expression was evaluated by TPS. Results: 67 pts were determined as MSI-H in total of 12,485 pts, namely the frequency of MSI-H was 0.5% in Chinses lung cancer. 26 MSI-H pts were harboring EGFR mutations, including Ex19del in 10 pts, L858R in 6 pts, T790M in 5 pts, EGFR gain in 4 pts, and other uncommon mutations such as C797, L861Q. Interestingly, no EGFR Ex20ins was detected. In the other 41 non-EGFR-mutant pts, RET fusion were detected in 2 pts, FGFR2/3 SNV were detected in 5 pts, KRAS activating SNVs were detected in 5 pts, and PIK3CA SNV/amplification were detected in 8 pts. No ICI response negative alterations (CDKN2A/B loss, MDM2/4 gain) were detected in MSI-H patients. 125 genes, including MSH6, MLH1, BRCA2, NOTCH1, TGFBR2, ACVR2A and etc, had higher frequency in MSI-H lung cancers than MSS lung cancers in our cohort. Moreover, only MAP3K1 gene SNV occurred more frequently in MSS lung cancers (4.5% vs 7.7%, p < 0.001). MSI-H lung cancer had a trend for enrichment of PD-L1 positivity (TPS > 1%) but no significance (58% vs 43%, p = 0.205). Conclusions: About 50% MSI-H lung cancers harbored actionable mutations for targeted agents (EGFR TKIs or other TKIs), while EGFR Ex20ins might exist mutually exclusively with MSI-H. MSI-H lung cancer had much more mutational genes than MSS lung cancer, which was consistent with previous studies. On the other hand, MAP3K1 was the only gene with lower mutational frequency in MSI-H lung cancer. Our results revealed the genetic mutational characteristics of MSI-H lung cancer and provided suggestions for treatment decisions of this patient population.

Sign in / Sign up

Export Citation Format

Share Document