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The telomere maintenance mechanism spectrum and its dynamics in gliomas

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dc.contributor.authorKim, Sojin-
dc.contributor.authorChowdhury, Tamrin-
dc.contributor.authorYu, Hyeon Jong-
dc.contributor.authorKahng, Jee Ye-
dc.contributor.authorLee, Chae Eun-
dc.contributor.authorChoi, Seung Ah-
dc.contributor.authorKim, Kyung-Min-
dc.contributor.authorKang, Ho-
dc.contributor.authorLee, Joo Ho-
dc.contributor.authorLee, Soon-Tae-
dc.contributor.authorWon, Jae-Kyung-
dc.contributor.authorKim, Kyung Hyun-
dc.contributor.authorKim, Min-Sung-
dc.contributor.authorLee, Ji Yeoun-
dc.contributor.authorKim, Jin Wook-
dc.contributor.authorKim, Yong-Hwy-
dc.contributor.authorKim, Tae Min-
dc.contributor.authorChoi, Seung Hong-
dc.contributor.authorPhi, Ji Hoon-
dc.contributor.authorShin, Young-Kyoung-
dc.contributor.authorKu, Ja-Lok-
dc.contributor.authorLee, Sungyoung-
dc.contributor.authorYun, Hongseok-
dc.contributor.authorLee, Hwajin-
dc.contributor.authorKim, Dokyoung-
dc.contributor.authorKim, Kyoungmi-
dc.contributor.authorHur, Junho K.-
dc.contributor.authorPark, Sung-Hye-
dc.contributor.authorKim, Seung-Ki-
dc.contributor.authorPark, Chul-Kee-
dc.date.accessioned2022-09-16T11:20:51Z-
dc.date.available2022-09-16T20:21:56Z-
dc.date.issued2022-08-11-
dc.identifier.citationGenome Medicine, 14(1):88ko_KR
dc.identifier.issn1756-994X-
dc.identifier.urihttps://doi.org/10.1186/s13073-022-01095-x-
dc.identifier.urihttps://hdl.handle.net/10371/184477-
dc.description.abstractBackground : The activation of the telomere maintenance mechanism (TMM) is one of the critical drivers of cancer cell immortality. In gliomas, TERT expression and TERT promoter mutation are considered to reliably indicate telomerase activation, while ATRX mutation and/or loss indicates an alternative lengthening of telomeres (ALT). However, these relationships have not been extensively validated in tumor tissues.
Methods : Telomerase repeated amplification protocol (TRAP) and C-circle assays were used to profile and characterize the TMM cross-sectionally (n = 412) and temporally (n = 133) across glioma samples. WES, RNA-seq, and NanoString analyses were performed to identify and validate the genetic characteristics of the TMM groups.
Results : We show through the direct measurement of telomerase activity and ALT in a large set of glioma samples that the TMM in glioma cannot be defined solely by the combination of telomerase activity and ALT, regardless of TERT expression, TERT promoter mutation, and ATRX loss. Moreover, we observed that a considerable proportion of gliomas lacked both telomerase activity and ALT. This telomerase activation-negative and ALT negative group exhibited evidence of slow growth potential. By analyzing a set of longitudinal samples from a separate cohort of glioma patients, we discovered that the TMM is not fixed and can change with glioma progression.
Conclusions : This study suggests that the TMM is dynamic and reflects the plasticity and oncogenicity of tumor cells. Direct measurement of telomerase enzyme activity and evidence of ALT should be considered when defining TMM. An accurate understanding of the TMM in glioma is expected to provide important information for establishing cancer management strategies.
ko_KR
dc.description.sponsorshipThis research was supported by the Bio & Medical Technology Development Program of the National Research Foundation (NRF), funded by the Ministry of Science & ICT (NRF-2018M3A9H3021707), and the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (HI21C0239).ko_KR
dc.language.isoenko_KR
dc.publisherBMCko_KR
dc.subjectGlioma-
dc.subjectTelomere maintenance mechanism-
dc.subjectTERT-
dc.subjectALT-
dc.titleThe telomere maintenance mechanism spectrum and its dynamics in gliomasko_KR
dc.typeArticleko_KR
dc.identifier.doi10.1186/s13073-022-01095-xko_KR
dc.citation.journaltitleGenome Medicineko_KR
dc.language.rfc3066en-
dc.rights.holderThe Author(s)-
dc.date.updated2022-08-14T03:14:56Z-
dc.citation.number1ko_KR
dc.citation.startpage88ko_KR
dc.citation.volume14ko_KR
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