NBDC Research ID: hum0414.v1

 

SUMMARY

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

 

Dataset IDType of DataCriteriaRelease Date
DRA016800 NGS (WGS) Unrestricted-access 2023/07/25

*Release Note

*When the research results including the data which were downloaded from NHA/DRA, are published or presented somewhere, the data user must refer the papers which are related to the data, or include them in the acknowledgment. Learn more

 

MOLECULAR DATA

DRA016800

Participants/Materials

SAEC and its derived cell lines: 5 samples

    (SAEC, Control-ER-KRAS-G12V, RSTC-2, RSTC-5, RSTC-7)

Targets WGS
Target Loci for Capture Methods -
Platform Illumina [NovaSeq 6000]
Library Source DNA extracted from cell lines
Cell Lines SAEC (Lonza, Cat# CC-2547)
Library Construction (kit name) TruSeq DNA PCR-Free Library Prep Kit
Fragmentation Methods Ultrasonic fragmentation
Spot Type Paired-end
Read Length (without Barcodes, Adaptors, Primers, and Linkers) 150 bp
DDBJ Sequence Read Archive ID DRA016800
Total Data Volume 900 GB (fastq)
Comments (Policies) NBDC policy

 

DATA PROVIDER

Principal Investigator: Bunsyo Shiotani

Affiliation: National Cancer Center Research Institute

Project / Group Name: Laboratory of Genome Stress Signaling

URL: https://www.ncc.go.jp/en/ri/division/genome_stress_signaling/index.html

Funds / Grants (Research Project Number):

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

 

PUBLICATIONS

TitleDOIDataset ID
1 An ATR-PrimPol pathway confers tolerance to oncogenic KRAS-induced and heterochromatin-associated replication stress. doi: 10.1038/s41467-023-40578-2 DRA016800
2