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Rapid PTEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy [ATAC-Seq]

ABSTRACT: This study examines the reorganization of transcriptionally active chromatin that underlies the adaptive response of glioblastoma cells to radiotherapy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE211148 | GEO | 2023/12/01

REPOSITORIES: GEO

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Rapid PTEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy [ChIP-Seq]

Project description:This study examines the reorganization of transcriptionally active chromatin that underlies the adaptive response of glioblastoma cells to radiotherapy.

2023-12-01 | GSE211147 | GEO

Rapid PTEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy [RNA-seq]

Project description:Using a combination of ChIP-, ATAC-, RNA-seq, and CUT&RUN in model systems of diffuse intrinsic pontine glioma and other pediatric high-grade gliomas, we observe a rapid genome-wide reorganization of active chromatin within hours of exposure to therapeutic ionizing radiation. This redistribution facilitates PTEFb-mediated pause-release of Pol II to drive nascent transcriptional induction of canonical DNA damage response programs. Concurrent inhibition of PTEFb imparts a transcription elongation defect, disrupting this chromatin reorganization and blunting transcriptional induction. Functionally, concurrent PTEFb inhibition abrogates key adaptive programs such as DNA damage repair and cell cycle regulation. This combination demonstrates a potent, synergistic therapeutic potential agnostic of glioma subtype, leading to a marked induction of tumor cell apoptosis and prolongation of xenograft survival.

2024-04-16 | GSE263946 | GEO

Rapid PTEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy [CUT&RUN]

Project description:Using a combination of ChIP-, ATAC-, and RNA-seq in model systems of diffuse intrinsic pontine glioma and other pediatric high-grade gliomas, we observe a rapid genome-wide reorganization of active chromatin within hours of exposure to therapeutic ionizing radiation. This redistribution facilitates PTEFb-mediated pause-release of Pol II to drive nascent transcriptional induction of canonical DNA damage response programs. Concurrent inhibition of PTEFb imparts a transcription elongation defect, disrupting this chromatin reorganization and blunting transcriptional induction. Functionally, concurrent PTEFb inhibition abrogates key adaptive programs such as DNA damage repair and cell cycle regulation. This combination demonstrates a potent, synergistic therapeutic potential agnostic of glioma subtype, leading to a marked induction of tumor cell apoptosis and prolongation of xenograft survival.

2024-04-15 | GSE227795 | GEO

Rapid PTEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy [ATAC-Seq]

2024-04-12 | GSE227792 | GEO

Rapid PTEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy [ChIP-Seq]

2024-04-15 | GSE227796 | GEO

Rapid PTEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-12 | GSE227797 | GEO

Rapid PTEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-12-01 | GSE211149 | GEO

Rapid Monocyte Recruitment Dictates the Therapeutic Efficacy of Focal Radiotherapy

Project description:The recruitment of monocytes and their differentiation into immunosuppressive cells is associated with the negative outcome of non-conformal radiotherapy (RT). However, non-conformal RT is irrelevant in the clinic, and little is known about the role of monocytes following radiotherapy modes used in patients, such as conformal radiotherapy (CRT). Here, we investigated the acute immune infiltration post-CRT. Contrary to non-conformal RT approaches, we found that CRT induces a rapid and robust recruitment of monocytes to the tumor that minimally differentiate into tumor-associated macrophages (TAM) or dendritic cells (DC), but instead upregulate major histocompatibility complex II (MHCII) and costimulatory molecules. We establish that these large numbers of infiltrating monocytes are responsible for increasing type I interferon in the tumor microenvironment (TME), activation of CD8+ T cells and the reduction in tumor burden. Importantly, we demonstrate that rapid monocyte infiltration to the TME is hindered when RT inadvertently affects healthy tissues. Our results unravel a positive role of monocytes during clinically relevant modes of RT and demonstrate that limiting exposure of healthy tissues to radiation has a positive therapeutic effect on the overall immune response within the tumor.

2022-06-30 | MSV000089775 | MassIVE

Impaired reorganization of centrosome structure underlies human congenital dilated cardiomyopathy

Project description:Impaired reorganization of centrosome structure underlies human congenital dilated cardiomyopathy

| PRJNA767002 | ENA

Cancer cells enter an adaptive persistence to survive radiotherapy and repopulate tumor 1

Project description:Tumor cell repopulation represents a critical factor in the failure of radiotherapy. Analogous to the concept of “drug-tolerant persistence (DTP)” in stress of chemo- or targeted therapy, here, we show that cancer cells enter a “radiation-tolerant persistence (RTP)” to survive radiotherapy and repopulate tumor. These RTP cells exhibit a distinct phenotype characterized by enlargement of cell sizes and nucleus, complex karyotype, cell cycle arrest and engagement of quiescence. A fraction of RTPs unexpectedly give birth to mitotic-competent progeny cells via a viral budding-mimicking cell division. To gain insight into the molecular mechanisms how RTPs generating progenies and repopulating tumors, we applied single cell SMART RNA-sequencing and 10x RNA-sequencing to different status of human colorectal cancer cells HCT116 before and exposed to irradiation. For the first time, we profiled two transitional transcriptional waves throughout budding process and characterized two gene panels associated with budding of RTPs, illustrating the therapeutic potential for blocking tumor repopulation after radiation.

2023-01-06 | GSE221180 | GEO

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