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Related Experiment Video

Updated: May 24, 2025

Author Spotlight: Advancements in Molecular Biomarker Testing for Non-Squamous Non-Small Cell Lung Cancer

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Published on: September 8, 2023

Molecular subtyping of stage I lung adenocarcinoma via molecular alterations in pre-invasive lesion progression.

Jun Shang^1,2,3,4, He Jiang³, Yue Zhao^1,2,4

¹Departments of Thoracic Surgery and State Key Laboratory of Genetic Engineering, Fudan University Shanghai Cancer Center, Shanghai, China.

Journal of Translational Medicine

|March 5, 2025

Summary

We identified two distinct molecular subtypes of stage I lung adenocarcinoma (LUAD) by analyzing key molecular alterations. This discovery helps identify high-risk LUAD patients for tailored treatments.

Keywords:

COL11A1 Lung adenocarcinoma Molecular subtypes Overfitting-resistant Pre/minimally invasive Prognosis THBS2 Unsupervised clustering

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Published on: November 5, 2019

Area of Science:

Oncology
Molecular Biology
Genomics

Background:

Lung adenocarcinoma in situ (AIS) and minimally invasive adenocarcinoma (MIA) are curable, but 20% of stage I LUAD patients have poor prognoses.
Key molecular differences between curable AIS/MIA and poor-prognosis stage I LUAD remain unclear.
This study investigates molecular alterations to distinguish LUAD subtypes.

Purpose of the Study:

To reveal molecularly and prognostically distinct subtypes of stage I LUAD.
To identify molecular drivers differentiating early-stage lung adenocarcinoma.
To develop a model for identifying high-risk stage I LUAD patients.

Main Methods:

Analyzed RNA and whole-exome sequencing data from 197 tumor-normal samples (AIS, MIA, invasive LUAD).
Utilized digital droplet PCR (ddPCR) and immunohistochemistry (IHC) for gene and protein expression analysis.
Validated findings using large-scale RNA-seq datasets (954 LUAD, including 541 stage I) and 12 published datasets (1,331 stage I LUAD).

Main Results:

Focal adhesion (FA) pathway was significantly perturbed at genomic and transcriptomic levels in invasive LUAD compared to AIS/MIA.
COL11A1 and THBS2 genes showed upregulation from AIS/MIA to stage I LUAD.
Unsupervised clustering identified two subtypes (S1, S2) of stage I LUAD based on COL11A1 and THBS2 expression, with S2 exhibiting more somatic alterations and activated cancer-associated fibroblasts (CAF).

Conclusions:

Two distinct molecular and prognostic subtypes (S1, S2) of stage I LUAD were identified.
The FA2 model (COL11A1, THBS2) effectively differentiates stage I LUAD subtypes.
This classification aids in identifying high-risk stage I LUAD patients for intensified treatment strategies.