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Due to system maintenance, the application system, application review by the Data Access Committee will be unavailable during the following period.
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Following a change to our organizational structure effective April 1, 2026, this division has been renamed from the "Database Center for Life Science, Joint Support-Center for Data Science Research" to the "Database Division for Life Science (DBCLS), BioData Science Initiative (BSI), National Institute of Genetics (NIG)". Where the former name still appears in the guidelines, please read it as the new name.

Research ID

hum0414-v1Release info

Latest

Research title

Elucidation of molecular mechanisms of lung cancer development and progression based on genome analysis

Research overview

Aims
To analyze genomic aberrations and gene expression changes such as mutations, deletions, amplifications, and hypermethylation in human lung cancer cells at the somatic cell level, and to contrast these with clinicopathological information to elucidate the molecular mechanisms and characteristics of lung cancer development and progression at the genetic level.
Methods
Human small airway epithelial cells (SAEC) were immortalized via the expression of hTERT, a CDK4 mutant, and cyclin D1. After up to 35 days of 2D culture, SAECs expressing KRAS G12V (Control-ER-KRAS-G12V) showed a limited but significant anchorage-independent growth. These individual clones were named replication stress-tolerant cells (RSTC-2, RSTC-5, and RSTC-7). In this study, whole genome sequencing was performed on these five cell lines.
Participants/materials
SAEC and its derived cell lines
URL
N/A

Datasets

CartDataset IDType of dataAnalysis methodAccess criteriaDate published
DRA016800NGS (WGS)
  • WGS
Unrestricted-access2023-07-28

Data provider

Principal investigator
Bunsyo Shiotani
Affiliation
National Cancer Center Research Institute

Research projects

NameURL
Laboratory of Genome Stress Signaling
N/A

Grants

NameTitleProject number
KAKENHI Fund for the Promotion of Joint International Research (Fostering Joint International Research (B))
Elucidation of the mechanism underlying DNA replication stress response regulating genomic instability
  • 18KK0235
KAKENHI Grant-in-Aid for Scientific Research (B)
Elucidation of the mechanism underlying tumor initiation via DNA replication stress regulated by ATR
  • 18H03378
Core Research and Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST)
Development of an integrated cancer care system using artificial intelligence
  • JPMJCR1689
AIP Challenge PRISM Acceleration Support Program (AIP-PRISM), Japan Science and Technology Agency (JST)
Development of the innovative drug discovery system using artificial intelligence
  • JPMJCR18Y4

Related publications

TitleDOIDataset ID
An ATR-PrimPol pathway confers tolerance to oncogenic KRAS-induced and heterochromatin-associated replication stress.
https://doi.org/10.1038/s41467-023-40578-2 (opens in a new tab)