Comparative genomics between matched solid and lepidic portions of semi-solid lung adenocarcinomas

Gavitt A. Woodard; Vivianne Ding; Christina Cho; Nathan R. Brand; Johannes R. Kratz; Kirk D. Jones; David M. Jablons

doi:10.1016/j.lungcan.2023.107211

Back

Comparative genomics between matched solid and lepidic portions of semi-solid lung adenocarcinomas

Journal article

Open access

Peer reviewed

Comparative genomics between matched solid and lepidic portions of semi-solid lung adenocarcinomas

Gavitt A. Woodard, Vivianne Ding, Christina Cho, Nathan R. Brand, Johannes R. Kratz, Kirk D. Jones and David M. Jablons

Lung cancer (Amsterdam, Netherlands), Vol.180, pp.107211-107211

06/01/2023

DOI: 10.1016/j.lungcan.2023.107211

PMCID: PMC10900430

PMID: 37121213

Files and links (1)

url

https://doi.org/10.1016/j.lungcan.2023.107211View

Published (Version of record) Open Access

Abstract

Background: Genetic changes that drive the transition from lepidic to invasive cancer development within a radiographic ground glass or semi-solid lung lesion (SSL) are not well understood. Biomarkers to predict the transition to solid, invasive cancer within SSL are needed.Methods: Patients with surgically resected SSL were identified retrospectively from a surgical database. Clinical characteristics and survival were compared between stage I SSL (n = 65) and solid adenocarcinomas (n = 120) resected during the same time period. Areas of normal lung, in situ lepidic, and invasive solid tumor were microdissected from within the same SSL specimens and next generation sequencing (NGS) and Affymetrix microarray of gene expression were performed.Results: There were more never smokers, Asian patients, and sub-lobar resections among SSL but no difference in 5-year survival between SSL and solid adenocarcinoma. Driver mutations found in both lepidic and solid invasive portion were EGFR (43%), KRAS (21%), and DNMT3A (5%). CEACAM5 was the most upregulated gene found in solid, invasive portions of SSL. Lepidic and invasive solid areas had many similarities in gene expression, however there were some significant differences with the gene SPP1 being a unique biomarker for the invasive component of a SSL.Conclusions: Common lung cancer driver mutations are present in in situ lepidic as well as invasive solid portions of a SSL, suggesting early development of driver mutations. CEACAM5 and SPP1 emerged as promising bio-markers of invasive potential in semi-solid lesions. Other studies have shown both genes to correlate with poor prognosis in lung cancer and their role in evolution of semi-solid lung lesions warrants further study.

Life Sciences & Biomedicine

Oncology

Respiratory System

Science & Technology

Details

Title: Subtitle: Comparative genomics between matched solid and lepidic portions of semi-solid lung adenocarcinomas
Creators: Gavitt A. Woodard - Leavitt Partners
Vivianne Ding - University of California, San Francisco
Christina Cho - Yale Cancer Center
Nathan R. Brand - University of California, San Francisco
Johannes R. Kratz - University of California, San Francisco
Kirk D. Jones - University of California, San Francisco
David M. Jablons - University of California, San Francisco
Resource Type: Journal article
Publication Details: Lung cancer (Amsterdam, Netherlands), Vol.180, pp.107211-107211
DOI: 10.1016/j.lungcan.2023.107211
PMID: 37121213
PMCID: PMC10900430
NLM abbreviation: Lung Cancer
ISSN: 0169-5002
eISSN: 1872-8332
Publisher: Elsevier
Number of pages: 9
Grant note: Yale Cancer Center Braude Foundation IRG 17-172-57 / Yale SPORE in Lung Cancer American Cancer Society International Lung Cancer Foundation
Language: English
Date published: 06/01/2023
Academic Unit: Internal Medicine
Record Identifier: 9984949509802771

Metrics

3 Record Views