{"id":"hum0414","version":1,"url":"https://humandbs.dbcls.jp/research/hum0414/v1","datePublished":"2023-07-25","versions":[{"version":1,"datePublished":"2023-07-25"}],"title":{"ja":"ゲノム解析に基づく肺がんの発生･進展の分子機構の解明","en":"Elucidation of molecular mechanisms of lung cancer development and progression based on genome analysis"},"summary":{"aims":{"ja":"ヒト肺がん細胞における変異・欠失・増幅・過メチル化等、体細胞レベルで生じたゲノム異常と遺伝子発現変動を解析し、それらを臨床病理学的情報と対比検討することで肺がんの発生・進展の分子機構及び特性を遺伝子レベルで明らかにすること。","en":"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":{"ja":"ヒト小気道上皮細胞（SAEC）は、hTERT・CDK4変異体・サイクリンD1の発現により不死化されている。KRAS G12Vを発現するSAEC（Control-ER-KRAS-G12V）を最大35日間2次元培養すると、限定的ではあるが有意な足場非依存性増殖を示す。これらのクローンをピックアップし、複製ストレス耐性細胞と名付けた（RSTC-2、RSTC-5、RSTC-7）。これらの細胞株に対して、全ゲノムシークエンスを実施した。","en":"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."},"targets":{"ja":"SAEC、Control-ER-KRAS-G12V、RSTC-2、RSTC-5、RSTC-7（計5株）","en":"SAEC and its derived cell lines"},"url":{"ja":null,"en":null}},"listingSummary":{"methods":{"ja":"配列決定","en":"Sequencing"},"targets":{"ja":"小気道上皮細胞株（SAEC）と派生細胞株：計5株\n（細胞株）","en":"SAEC and its derived cell lines: 5 samples\n(Cell-line)"},"typeOfData":{"ja":"NGS\n（WGS）","en":"NGS\n(WGS)"}},"releaseNote":{"ja":"小気道上皮細胞株（SAEC）とその派生細胞株から抽出したDNAを用いたwhole genome sequencing解析データをfastqファイルにて提供する。","en":"DNAs extracted from SAEC and its derived cell lines were used for whole genome sequencing analysis. Fastq file are provided."},"dataProviders":[{"name":{"ja":"塩谷 文章","en":"Bunsyo Shiotani"},"organization":{"name":{"ja":"国立がん研究センター研究所","en":"National Cancer Center Research Institute"}}}],"researchProjects":[{"name":{"ja":"ゲノムストレス応答学ユニット","en":"Laboratory of Genome Stress Signaling"},"url":{"ja":null,"en":null}}],"grants":[{"title":{"ja":"ゲノム不安定性を制御するDNA複製ストレス応答機構の解明","en":"Elucidation of the mechanism underlying DNA replication stress response regulating genomic instability"},"agency":{"ja":"科学研究費助成事業 国際共同研究加速基金（国際共同研究強化（B））","en":"KAKENHI Fund for the Promotion of Joint International Research (Fostering Joint International Research (B))"},"grantIds":["18KK0235"]},{"title":{"ja":"ATRによるDNA複製ストレス抵抗性を介した発がん制御機構の解明","en":"Elucidation of the mechanism underlying tumor initiation via DNA replication stress regulated by ATR"},"agency":{"ja":"科学研究費助成事業 基盤研究（B）","en":"KAKENHI Grant-in-Aid for Scientific Research (B)"},"grantIds":["18H03378"]},{"title":{"ja":"イノベーション創発に資する人工知能基盤技術の創出と統合化","en":"Development of an integrated cancer care system using artificial intelligence"},"agency":{"ja":"国立研究開発法人科学技術振興機構（JST） 戦略的創造研究推進事業（CREST）","en":"Core Research and Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST)"},"grantIds":["JPMJCR1689"]},{"title":{"ja":"人工知能技術を活用した革新的ながん創薬システムの開発","en":"Development of the innovative drug discovery system using artificial intelligence"},"agency":{"ja":"国立研究開発法人科学技術振興機構（JST） AIPチャレンジPRISM加速支援（AIP-PRISM）","en":"AIP Challenge PRISM Acceleration Support Program (AIP-PRISM), Japan Science and Technology Agency (JST)"},"grantIds":["JPMJCR18Y4"]}],"relatedPublications":[{"title":"An ATR-PrimPol pathway confers tolerance to oncogenic KRAS-induced and heterochromatin-associated replication stress.","doi":"https://doi.org/10.1038/s41467-023-40578-2","datasets":["DRA016800"]}],"datasets":["DRA016800"],"controlledAccessUsers":[]}