---
title: "Chronic cigarette smoke drives distinct stem cell states that shape NSCLC subtypes"
id: "pubmed-42832683"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42832683"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42832683/"
doi: "10.1073/pnas.2604393123"
published_at: "2026-10-05T21:49:34.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Chronic cigarette smoke drives distinct stem cell states that shape NSCLC subtypes
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42832683
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42832683/)
- **DOI:** [10.1073/pnas.2604393123](https://doi.org/10.1073%2Fpnas.2604393123)
- **Published At:** 2026-10-05T21:49:34.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Chronic exposure to **cigarette smoke condensate (CSC)** creates persistent **chronic inflammation (CI)** that promotes non–small cell lung cancer (**NSCLC**) by inducing genetic and epigenetic changes in lung stem cells. - Using normal lung organoids (LOs), the study shows CSC exposure drives two separate **stem cell** populations into premalignant states with progressive epigenetic and transcriptomic abnormalities without acquisition of major driver mutations. - These premalignant stem cell states evolve toward an **immune-evasive** phenotype characterized by downregulation of inflammatory pathways and silencing of the PANoptosis regulator **Zbp1**, which reduces cell death signaling. - The two CSC-altered stem cell populations follow distinct trajectories and respond differently when canonical oncogenic events are introduced: expression of **KrasG12V** and loss of **Tp53**. - Introduction of oncogenic drivers produced rapid, one-step transformation of CSC-exposed organoids into two major NSCLC subtypes: **Kras** mutations triggered tumorigenesis predominantly from a bronchioalveolar stem cell–derived state producing adenocarcinomas, whereas **TP53** loss produced tumors from a basal stem cell–derived state resulting in squamous cell carcinomas. - CSC-induced downregulation of **Zbp1** and interferon signaling was further reduced in tumors with mutation-specific expression changes, most pronounced in Kras-mutant contexts according to the report. - The findings define unique transcriptomic profiles associated with CI-induced stem cell states and highlight cell death pathway–related genes as key modulators that potentiate oncogenic drivers to promote NSCLC. - The study suggests potential strategies to predict cancer risk and opportunities for early interception based on stem cell state, epigenetic changes, and death-pathway suppression. - Keywords in the source include chronic inflammation, epigenetic, non–small cell lung cancer, and stem cells. Details beyond the abstract (methods, sample sizes, and specific gene lists) were not reported in the source provided.
## Clinical Analysis & Structured Key Points
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Epub 2026 Oct 5. # Chronic cigarette smoke exposure induces distinct stem cell states driving genetic driver-specific non-small cell lung cancer subtypes [Na Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+N&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Raksha Padaki](https://pubmed.ncbi.nlm.nih.gov/?term=Padaki+R&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Sara-Jayne Thursby](https://pubmed.ncbi.nlm.nih.gov/?term=Thursby+SJ&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Ray-Whay Chiu Yen](https://pubmed.ncbi.nlm.nih.gov/?term=Yen+RC&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Leslie M Cope](https://pubmed.ncbi.nlm.nih.gov/?term=Cope+LM&cauthor_id=42832683)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-2 "Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-3 "Department of Biostatistics, Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Malcolm V Brock](https://pubmed.ncbi.nlm.nih.gov/?term=Brock+MV&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287.")[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-4 "Department of Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Edward Gabrielson](https://pubmed.ncbi.nlm.nih.gov/?term=Gabrielson+E&cauthor_id=42832683)[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-5 "Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Hariharan Easwaran](https://pubmed.ncbi.nlm.nih.gov/?term=Easwaran+H&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Stephen B Baylin](https://pubmed.ncbi.nlm.nih.gov/?term=Baylin+SB&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287.")[ 6 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-6 "Department of Epigenetics, Van Andel Research Institute, Grand Rapids, MI 49503."), [Michelle Vaz](https://pubmed.ncbi.nlm.nih.gov/?term=Vaz+M&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#full-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287.") Affiliations Expand ### Affiliations * 1 Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287. * 2 Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287. * 3 Department of Biostatistics, Johns Hopkins University School of Medicine, Baltimore, MD 21287. * 4 Department of Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287. * 5 Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287. * 6 Department of Epigenetics, Van Andel Research Institute, Grand Rapids, MI 49503. * PMID: **42832683** * DOI: [ 10.1073/pnas.2604393123 ](https://doi.org/10.1073/pnas.2604393123) Item in Clipboard # Chronic cigarette smoke exposure induces distinct stem cell states driving genetic driver-specific non-small cell lung cancer subtypes Na Wang et al. Proc Natl Acad Sci U S A. 2026. Show details Display options Display options Format Abstract PubMed PMID Proc Natl Acad Sci U S A Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Proc+Natl+Acad+Sci+U+S+A%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Proc+Natl+Acad+Sci+U+S+A%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42832683/) . 2026 Oct 20;123(42):e2604393123. doi: 10.1073/pnas.2604393123. Epub 2026 Oct 5. ### Authors [Na Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+N&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Raksha Padaki](https://pubmed.ncbi.nlm.nih.gov/?term=Padaki+R&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Sara-Jayne Thursby](https://pubmed.ncbi.nlm.nih.gov/?term=Thursby+SJ&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Ray-Whay Chiu Yen](https://pubmed.ncbi.nlm.nih.gov/?term=Yen+RC&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Leslie M Cope](https://pubmed.ncbi.nlm.nih.gov/?term=Cope+LM&cauthor_id=42832683)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-2 "Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-3 "Department of Biostatistics, Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Malcolm V Brock](https://pubmed.ncbi.nlm.nih.gov/?term=Brock+MV&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287.")[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-4 "Department of Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Edward Gabrielson](https://pubmed.ncbi.nlm.nih.gov/?term=Gabrielson+E&cauthor_id=42832683)[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-5 "Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Hariharan Easwaran](https://pubmed.ncbi.nlm.nih.gov/?term=Easwaran+H&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287."), [Stephen B Baylin](https://pubmed.ncbi.nlm.nih.gov/?term=Baylin+SB&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287.")[ 6 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-6 "Department of Epigenetics, Van Andel Research Institute, Grand Rapids, MI 49503."), [Michelle Vaz](https://pubmed.ncbi.nlm.nih.gov/?term=Vaz+M&cauthor_id=42832683)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42832683/#short-view-affiliation-1 "Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287.") ### Affiliations * 1 Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21287. * 2 Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287. * 3 Department of Biostatistics, Johns Hopkins University School of Medicine, Baltimore, MD 21287. * 4 Department of Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287. * 5 Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287. * 6 Department of Epigenetics, Van Andel Research Institute, Grand Rapids, MI 49503. * PMID: **42832683** * DOI: [ 10.1073/pnas.2604393123 ](https://doi.org/10.1073/pnas.2604393123) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID Linked Discoveries ## Abstract Cigarette smoke-induced chronic inflammation (CI) potentiates development of non-small cell lung cancer (NSCLC) by mediating genetic and epigenetic events. Using normal lung organoids (LOs), we define how chronic cigarette smoke condensate (CSC) exposure drives two separate stem cell populations to evolve premalignant states harboring progressive epigenetic and linked transcriptomic abnormalities in the absence of major driver mutations. These dynamics facilitate evolution of an immune evasive state with downregulation of inflammatory pathways and accompanying death signals mediated by epigenetic silencing of PANoptosis regulator, _Zbp1._ The stem cell populations evolve through distinct trajectories to respond differently to subsequent introduction of oncogenic mutations, KrasG12V and loss of Tp53, to induce one step transformation of CSC exposed organoids resulting in two major NSCLC subtypes. Kras mutations drive tumorigenesis primarily in a bronchioalveolar stem cell-derived state producing adenocarcinomas while TP53 loss drives tumorigenesis in a basal stem cell-derived state resulting in squamous cell carcinomas. CSC-induced downregulation of Zbp1 and interferon signaling is further potentiated in tumors with mutation-specific changes marked by decreased expression in Kras-mutant contexts. Our findings define unique transcriptomic profiles in CI-induced stem cell states and reveal a key role for cell death pathway-associated genes in potentiating oncogenic drivers to promote NSCLC. Together, our data suggest strategies to predict cancer risk and enable early interception. **Keywords:** chronic inflammation; epigenetic; non–small cell lung cancer; stem cells. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Competing interests statement:The authors declare no competing interest. ## MeSH terms * Animals Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Animals%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Animals) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42832683/) * Carcinoma, Non-Small-Cell Lung* / etiology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Carcinoma%2C+Non-Small-Cell+Lung%2Fetiology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Carcinoma%2C+Non-Small-Cell+Lung) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42832683/) * Carcinoma, Non-Small-Cell Lung* / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Carcinoma%2C+Non-Small-Cell+Lung%2Fgenetics%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Carcinoma%2C+Non-Small-Cell+Lung) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42832683/) * Carcinoma, Non-Small-Cell Lung* / pathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Carcinoma%2C+Non-Small-Cell+Lung%2Fpathology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Carcinoma%2C+Non-Small-Cell+Lung) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42832683/) * Cell Transformation, Neoplastic / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Transformation%2C+Neoplastic%2Fgenetics%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Transformation%2C+Neoplastic) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42832683/) * Epigenesis, Genetic Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Epigenesis%2C+Genetic%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Epigenesis%2C+Genetic) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42832683/) * Gene Expression Regulation, Neoplastic Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Gene+Expression+Regulation%2C+Neoplastic%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Gene+Expression+Regulation%2C+Neoplastic) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42832683/) * Humans Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Humans%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://ww
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