Investigating the genomic alteration improved the clinical outcome of aged patients with lung carcinoma

Abstract Background Lung carcinoma is a common geriatric disease. The development of genotype-targeted therapies greatly improved the management of lung carcinoma. However, the treatment for old patients can be more complex than that for young individuals. Results To investigate the benefits of gene...

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Main Authors: Sixian Chen, Aizhen Fu, Yuan Lu, Wei Lu, Yongfeng Chen, Shuiqiang Hong, Suli Zhou, Tianmin Xiang, Zhenzhen Zhang, Yongguang Cai
Format: Article
Language:English
Published: BMC 2022-01-01
Series:BMC Genomics
Subjects:
Online Access:https://doi.org/10.1186/s12864-021-08289-4
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author Sixian Chen
Aizhen Fu
Yuan Lu
Wei Lu
Yongfeng Chen
Shuiqiang Hong
Suli Zhou
Tianmin Xiang
Zhenzhen Zhang
Yongguang Cai
author_facet Sixian Chen
Aizhen Fu
Yuan Lu
Wei Lu
Yongfeng Chen
Shuiqiang Hong
Suli Zhou
Tianmin Xiang
Zhenzhen Zhang
Yongguang Cai
author_sort Sixian Chen
collection DOAJ
description Abstract Background Lung carcinoma is a common geriatric disease. The development of genotype-targeted therapies greatly improved the management of lung carcinoma. However, the treatment for old patients can be more complex than that for young individuals. Results To investigate the benefits of genetic detection for older patients with lung carcinoma, we explored the genomic profiling of 258 patients with more than 55 years using a targeted next generation sequencing, and some of these patients were treated with targeted therapies based on the results of genomic detection. KRAS codon 61 mutations were found in 15.2% KRAS-mutated patients, which tend to be co-existing with other classical activating mutations other than codons 12/13. Acquired EGFR C797S mutations were identified in 2 cases and ERBB2 amplification was identified in 1 case. All these 3 cases developed resistance to EGFR tyrosine kinase inhibitors and showed expected results of their followed therapies. The median progression-free survival and median overall survival of patients treated with molecular targeted therapies were better than those of patients treated with chemoradiotherapy alone. Conclusions Our findings revealed the specific genomic profiles of patients older than 55 years with lung carcinoma and suggested that these old patients have been benefit from the genetic detection, which helped identify druggable mutations and distinguish resistance mechanisms.
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spelling doaj.art-b99836e918df4a19b3b696660b2bb0222022-12-22T04:09:14ZengBMCBMC Genomics1471-21642022-01-0123111210.1186/s12864-021-08289-4Investigating the genomic alteration improved the clinical outcome of aged patients with lung carcinomaSixian Chen0Aizhen Fu1Yuan Lu2Wei Lu3Yongfeng Chen4Shuiqiang Hong5Suli Zhou6Tianmin Xiang7Zhenzhen Zhang8Yongguang Cai9Medical Oncology Department V, Guangdong Nongken Central HospitalGynecology Department, Affiliated Hospital of Guangdong Medical UniversityMedical Oncology Department V, Guangdong Nongken Central HospitalMedical Oncology Department V, Guangdong Nongken Central HospitalMedical Oncology Department V, Guangdong Nongken Central HospitalMedical Oncology Department V, Guangdong Nongken Central HospitalMedical Oncology Department V, Guangdong Nongken Central HospitalSinglera Genomics Inc.Singlera Genomics Inc.Medical Oncology Department V, Guangdong Nongken Central HospitalAbstract Background Lung carcinoma is a common geriatric disease. The development of genotype-targeted therapies greatly improved the management of lung carcinoma. However, the treatment for old patients can be more complex than that for young individuals. Results To investigate the benefits of genetic detection for older patients with lung carcinoma, we explored the genomic profiling of 258 patients with more than 55 years using a targeted next generation sequencing, and some of these patients were treated with targeted therapies based on the results of genomic detection. KRAS codon 61 mutations were found in 15.2% KRAS-mutated patients, which tend to be co-existing with other classical activating mutations other than codons 12/13. Acquired EGFR C797S mutations were identified in 2 cases and ERBB2 amplification was identified in 1 case. All these 3 cases developed resistance to EGFR tyrosine kinase inhibitors and showed expected results of their followed therapies. The median progression-free survival and median overall survival of patients treated with molecular targeted therapies were better than those of patients treated with chemoradiotherapy alone. Conclusions Our findings revealed the specific genomic profiles of patients older than 55 years with lung carcinoma and suggested that these old patients have been benefit from the genetic detection, which helped identify druggable mutations and distinguish resistance mechanisms.https://doi.org/10.1186/s12864-021-08289-4Lung cancerGenomic alterationsKRAS codon 61Targeted treatmentMechanism of resistance
spellingShingle Sixian Chen
Aizhen Fu
Yuan Lu
Wei Lu
Yongfeng Chen
Shuiqiang Hong
Suli Zhou
Tianmin Xiang
Zhenzhen Zhang
Yongguang Cai
Investigating the genomic alteration improved the clinical outcome of aged patients with lung carcinoma
BMC Genomics
Lung cancer
Genomic alterations
KRAS codon 61
Targeted treatment
Mechanism of resistance
title Investigating the genomic alteration improved the clinical outcome of aged patients with lung carcinoma
title_full Investigating the genomic alteration improved the clinical outcome of aged patients with lung carcinoma
title_fullStr Investigating the genomic alteration improved the clinical outcome of aged patients with lung carcinoma
title_full_unstemmed Investigating the genomic alteration improved the clinical outcome of aged patients with lung carcinoma
title_short Investigating the genomic alteration improved the clinical outcome of aged patients with lung carcinoma
title_sort investigating the genomic alteration improved the clinical outcome of aged patients with lung carcinoma
topic Lung cancer
Genomic alterations
KRAS codon 61
Targeted treatment
Mechanism of resistance
url https://doi.org/10.1186/s12864-021-08289-4
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