# Assessing mutation-clinical correlations and treatment outcomes in Vietnamese non-small cell lung cancer patients

**Authors:** Hoang-Bac Nguyen, Bang-Suong Nguyen-Thi, Huu-Huy Nguyen, Minh-Khoi Le, Quoc-Trung Lam, Tuan-Anh Nguyen

PMC · DOI: 10.1016/j.plabm.2025.e00477 · Practical Laboratory Medicine · 2025-05-23

## TL;DR

This study analyzes genetic mutations and treatment outcomes in Vietnamese non-small cell lung cancer patients to guide personalized therapies.

## Contribution

The study identifies mutation patterns and their clinical correlations in a Vietnamese NSCLC cohort, emphasizing EGFR and KRAS mutations.

## Key findings

- EGFR mutations are more common in female non-smokers, while KRAS mutations are more common in male smokers.
- EGFR-mutated patients treated with TKIs had significantly longer survival compared to others.
- Co-mutations are rare and may indicate resistance to treatment.

## Abstract

This study examines the genetic and clinical profiles of Vietnamese patients with non-small cell lung cancer (NSCLC), focusing on mutations in seven driver genes: EGFR, KRAS, NRAS, BRAF, ALK, ROS1, and PIK3CA. The goal is to identify mutation patterns and their correlations with clinical factors, thereby informing personalized treatment strategies.

A cross-sectional study of 299 NSCLC patients at the University Medical Center, Ho Chi Minh City (2019–2022) recorded demographics, smoking history, and tumor stage. Pre-treatment samples were analyzed via massively parallel sequencing, and survival analysis assessed the impact of EGFR/KRAS mutations on survival and TKI response.

Most patients (88.6 %) were diagnosed at stage IV. EGFR mutations were found in 43.5 % of cases, predominantly in female non-smokers, while KRAS mutations (15.4 %) were more common in male smokers. EGFR exon 19 deletions (46.3 %) and L858R (39.0 %) were the most frequent, with KRAS G12C (29.8 %) as the dominant variant. EGFR-mutant patients treated with TKIs had significantly longer survival (p = 0.027); however, no survival difference was observed between the EGFR- and KRAS-mutated groups. Co-mutations (3.7 %) were rare but may indicate resistance. Logistic regression confirmed EGFR mutations' association with female non-smokers and KRAS mutations with male smokers.

Genetic profiling in Vietnamese NSCLC patients reveals a high prevalence of actionable driver mutations, supporting the integration of routine molecular testing into NSCLC management. EGFR-mutated patients derive significant benefits from TKI therapy, underscoring the importance of personalized treatment strategies. Further research is needed to investigate resistance mechanisms and refine targeted therapeutic approaches.

•Most patients exhibit mutations, with 66.9 % having a mutation in a single gene and 3.7 % showing co-mutations.•Adenocarcinoma: most common histological type (93.3 %); Squamous Cell Carcinoma: 5.0 %.•EGFR mutations were present in 43.5 % of patients, mainly in female non-smokers, while KRAS mutations were found in 15.4 % of cases, primarily in male smokers.•No co-occurrence of EGFR and KRAS mutations was observed.•EGFR-mutated patients who received TKIs exhibited significantly prolonged survival (p = 0.027).

Most patients exhibit mutations, with 66.9 % having a mutation in a single gene and 3.7 % showing co-mutations.

Adenocarcinoma: most common histological type (93.3 %); Squamous Cell Carcinoma: 5.0 %.

EGFR mutations were present in 43.5 % of patients, mainly in female non-smokers, while KRAS mutations were found in 15.4 % of cases, primarily in male smokers.

No co-occurrence of EGFR and KRAS mutations was observed.

EGFR-mutated patients who received TKIs exhibited significantly prolonged survival (p = 0.027).

## Linked entities

- **Genes:** EGFR (epidermal growth factor receptor) [NCBI Gene 1956], KRAS (KRAS proto-oncogene, GTPase) [NCBI Gene 3845], NRAS (NRAS proto-oncogene, GTPase) [NCBI Gene 4893], BRAF (B-Raf proto-oncogene, serine/threonine kinase) [NCBI Gene 673], ALK (ALK receptor tyrosine kinase) [NCBI Gene 238], ROS1 (ROS proto-oncogene 1, receptor tyrosine kinase) [NCBI Gene 6098], PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) [NCBI Gene 5290]
- **Diseases:** non-small cell lung cancer (MONDO:0005233), adenocarcinoma (MONDO:0004970), Squamous Cell Carcinoma (MONDO:0005096)

## Full-text entities

- **Genes:** NRAS (NRAS proto-oncogene, GTPase) [NCBI Gene 4893] {aka ALPS4, CMNS, N-ras, NCMS, NRAS1, NS6}, KRAS (KRAS proto-oncogene, GTPase) [NCBI Gene 3845] {aka 'C-K-RAS, C-K-RAS, CFC2, K-RAS2A, K-RAS2B, K-RAS4A}, EGFR (epidermal growth factor receptor) [NCBI Gene 1956] {aka ERBB, ERBB1, ERRP, HER1, NISBD2, NNCIS}, PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) [NCBI Gene 5290] {aka CCM4, CLAPO, CLOVE, CWS5, HMH, MCAP}, BRAF (B-Raf proto-oncogene, serine/threonine kinase) [NCBI Gene 673] {aka B-RAF1, B-raf, BRAF-1, BRAF1, NS7, RAFB1}, ALK (ALK receptor tyrosine kinase) [NCBI Gene 238] {aka ALK1, CD246, NBLST3}, ROS1 (ROS proto-oncogene 1, receptor tyrosine kinase) [NCBI Gene 6098] {aka MCF3, ROS, c-ros-1}
- **Diseases:** tumor (MESH:D009369), NSCLC (MESH:D002289)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** L858R, G12C

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12156267/full.md

## References

55 references — full list in the complete paper: https://tomesphere.com/paper/PMC12156267/full.md

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Source: https://tomesphere.com/paper/PMC12156267