The New Way to Define Key Oncogenic Drivers of Small Cell Lung Cancer
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Small-cell lung cancer (SCLC) continues to be the deadliest of all lung cancer types. Its high mortality is largely attributed to the unchangeable development of resistance to standard chemo/radiotherapies, which have remained invariable for the past 30 years, underlining the need for new therapeutic approaches. Recent studies of SCLC genome revealed a large number of somatic alterations and identified remarkable heterogeneity of the frequent mutations except for the loss of both RB and P53 tumor suppressor genes (TSGs). Identifying the somatic alterations scattered throughout the SCLC genome will help to define the underlying mechanism of the disease and pave the way for the discovery of therapeutic vulnerabilities associated with genomic alterations. The new technique made it possible to determine the underlying mechanism for the discovery of therapeutic targets. To these ends, the techniques have been focused on understanding the molecular determinants of SCLC.
Abstract
Small-cell lung cancer (SCLC) continues to be the deadliest of all lung cancer types. Its high mortality is largely attributed to the unchangeable development of resistance to standard chemo/radiotherapies, which have remained invariable for the past 30 years, underlining the need for new therapeutic approaches. Recent studies of SCLC genome revealed a large number of somatic alterations and identified remarkable heterogeneity of the frequent mutations except for the loss of both RB and P53 tumor suppressor genes (TSGs). Identifying the somatic alterations scattered throughout the SCLC genome will help to define the underlying mechanism of the disease and pave the way for the discovery of therapeutic vulnerabilities associated with genomic alterations. The new technique made it possible to determine the underlying mechanism for the discovery of therapeutic targets. To these ends, the techniques have been focused on understanding the molecular determinants of SCLC.
참고문헌 (33)
- Augert A, "Small cell lung cancer exhibits frequent inactivating mutations in the histone methyltransferase KMT2D", MLL2: CALGB 151111 (alliance), 2017, pp.12, 704~713
- Balanis NG, "Pan-cancer convergence to a small-cell neuroendocrine phenotype that shares susceptibilities with hematological malignancies", Cancer Cell, 36, pp.17~34.E7 (2019)
- Byers LA, "Small cell lung cancer: Where do we go from here?", Cancer, 121, pp.664~672 (2015)
- Cardnell RJ, "Protein expression of TTF1 and cMYC define distinct molecular subgroups of small cell lung cancer with unique vulnerabilities to aurora kinase inhibition, DLL3 targeting, and other targeted therapies", Oncotarget, 8, pp.73419~73432 (2017)
- Chalishazar MD, "MYCdriven small-cell lung cancer is metabolically distinct and vulnerable to arginine depletion", Clin Cancer Res, 25, pp.5107~5121 (2019)
- Cong L, "Multiplex genome engineering using CRISPR", Cas systems, 2013, pp.339, 819~823
- Friedel RH, "EUCOMM—The European conditional mouse mutagenesis program", Brief Funct Genomics Proteomics, 6, pp.180~185 (2007)
- Gay CM, "Patterns of transcription factor programs and immune pathway activation define four major subtypes of SCLC with distinct therapeutic vulnerabilities", Cancer Cell, 39, pp.346~360.E7 (2021)
- George J, "Comprehensive genomic profiles of small cell lung cancer", Nature, 524, pp.47~53 (2015)
- Hansen GM, "Large-scale gene trapping in C57BL", 6N mouse embryonic stem cells, 2008, pp.18, 1670~1679
- Jia D, "Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition", Cancer Discov, 8, pp.1422~1437 (2018)
- Kim DW, "Genetic requirement for Mycl and efficacy of RNA Pol I inhibition in mouse models of small cell lung cancer", Genes Dev, 30, pp.1289~1299 (2016)
- Kim KB, "KIX domain determines a selective tumorpromoting role for EP300 and its vulnerability in small cell lung cancer", Sci Adv, 8, pp.eabl4618~ (2022)
- Kim KB, "WNT5A–RHOA signaling is a driver of tumorigenesis and represents a therapeutically actionable vulnerability in small cell lung cancer", Cancer Res, 82, pp.4219~4233 (2022)
- Kim KB, "FGFR1 is critical for RBL2 loss–driven tumor development and requires PLCG1 activation for continued growth of small cell lung cancer", Cancer Res, 80, pp.5051~5062 (2020)
- Lally BE, "Small cell lung cancer:Have we made any progress over the last 25 years?", Oncologist, 12, pp.1096~1104 (2007)
- Lewis DR, "US lung cancer trends by histologic type", Cancer, 120, pp.2883~2892 (2014)
- Mali P, "RNAguided human genome engineering via Cas9", Science, 339, pp.823~826 (2013)
- Mollaoglu G, "MYC drives progression of small cell lung cancer to a variant neuroendocrine subtype with vulnerability to Aurora kinase inhibition", Cancer Cell, 31, pp.270~285 (2017)
- Ng SR, "CRISPR-mediated modeling and functional validation of candidate tumor suppressor genes in small cell lung cancer", Proc Natl Acad Sci USA, 117, pp.513~521 (2020)
- Oberg K, "Consensus on biomarkers for neuroendocrine tumour disease", Lancet Oncol, 16, pp.E435~E446 (2015)
- 박지영, "Epidemiology of Lung Cancer in Korea: Recent Trends", Tuberculosis and Respiratory Diseases, 79(2), pp.58~69 (2016), 대한결핵및호흡기학회
- Peifer M, "Integrative genome analyses identify key somatic driver mutations of small-cell lung cancer", Nat Genet, 44, pp.1104~1110 (2012)
- Rogers ZN, "Mapping the in vivo fitness landscape of lung adenocarcinoma tumor suppression in mice", Nat Genet, 50, pp.483~486 (2018)
- Rudin CM, "Small-cell lung cancer", Nat Rev Dis Primers, 7, pp.3~ (2021)
- Rudin CM, "Comprehensive genomic analysis identifies SOX2 as a frequently amplified gene in small-cell lung cancer", Nat Genet, 44, pp.1111~1116 (2012)
- Russell WC, "Update on adenovirus and its vectors", J Gen Virol, 81, pp.2573~2604 (2000)
- Schaffer BE, "Loss of p130 accelerates tumor development in a mouse model for human small-cell lung carcinoma", Cancer Res, 70, pp.3877~3883 (2010)
- Torre LA, "Lung Cancer and Personalized Medicine: Current Knowledge and Therapies", pp.1~19 (2016), Springer
- Walrath JC, "Genetically engineered mouse models in cancer research", Adv Cancer Res, 106, pp.113~164 (2010)
- Weinstein JN, "The Cancer Genome Atlas Pan-Cancer analysis project", Nat Genet, 45, pp.1113~1120 (2013)
- Xue W, "CRISPR-mediated direct mutation of cancer genes in the mouse liver", Nature, 514, pp.380~384 (2014)
- Yin H, "Genome editing with Cas9 in adult mice corrects a disease mutation and phenotype", Nat Biotechnol, 32, pp.551~553 (2014)
