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Understanding the early molecular changes associated with radiation therapy – a preliminary bulk RNA sequencing study

ABSTRACT: Understanding the early molecular changes associated with radiation therapy – a preliminary bulk RNA sequencing study

PROVIDER: PRJNA1165829 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30813600.fastq.gz	Fastqsanger.gz
	SRR30813601.fastq.gz	Fastqsanger.gz
	SRR30813602.fastq.gz	Fastqsanger.gz
	SRR30813603.fastq.gz	Fastqsanger.gz
	SRR30813604.fastq.gz	Fastqsanger.gz

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Understanding the early molecular changes associated with radiation therapy – a preliminary bulk RNA sequencing study

Project description:Introduction Cancer is the second leading cause of death in the United States, with breast cancer being the most commonly diagnosed new cancer in women. Radiation therapy provides well-documented survival and recurrence benefits; however, it can lead to significant adverse effects, such as radiation-induced fibrosis (RIF), which can cause pain and result in poor aesthetic outcomes. The biological mechanisms underlying RIF are not entirely understood and require further investigation to identify potential intervention avenues. In this study, we investigated the biological response to radiotherapy by analyzing non-irradiated and irradiated tissues from breast cancer patients. Materials and methods We collected tissue from breast cancer patients who underwent unilateral radiation and bilateral breast reconstruction. At the time of final reconstruction (post-radiation), samples were collected from both non-irradiated and irradiated reconstruction sites. These samples were analyzed using bulk RNA sequencing, histology, and immunohistochemistry (IHC). Results In fibrous tissue capsules, CLCA2, COL4A5, and COL6A6 were differentially expressed and may be related to reduced micro-vascularization. CXCL9 and PTCHD4 were upregulated within the skin, possibly conferring an increased immune response, while multiple keratin-related genes (KRT6B, KRT17, KRT25, KRT28, and KRT75) were downregulated. In irradiated muscle tissue, there was increased expression of CXCL10 and downregulation of DCD. These results were confirmed using IHC. Conclusions This study highlights the utility of bulk RNA sequencing studies in conjunction with IHC to identify target genes and biological processes responsible for RIF in tissues at final breast reconstruction. Due to the sample size limitation, further research is warranted to understand the role of keratin and collagen genes in regulating epidermal changes, vascularity, and fibrosis.

2024-09-27 | GSE278183 | GEO

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Deep proteomic and phosphoproteomic profiling of DIPG responses to radiation therapy

Project description:Different DIPG tumor models have different responses to radiation therapy, which can be identified by quantitative proteomics/phospho-proteomics approach

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BDNF augmentation reverses cranial radiation therapy-induced cognitive decline and neurodegenerative consequences

Project description:Spatial transcriptomic profiling was conducted on hippocampal brain sections from mice across four experimental combinations: cranial radiation therapy(RT) with Riluzole (label as Ir-Rz), cranial radiation therapy with vehicle (label as Ir-Veh), control with Riluzole (label as Ctl-Rz), and control with vehicle (label as Ctl-Veh).

2024-11-30 | GSE282950 | GEO

RNAseq analysis of chemotherapy and radiation therapy-naïve breast tumors

Project description:Assessment of chemo- and radiation therapy-naïve biopsy-confirmed invasive human breast tumors by RNAseq.

2017-07-08 | GSE100925 | GEO

Protein difference of breast cancer tissue in mice after radiation therapy and without radiation

Project description:In this study, radiation therapy was performed on mouse breast cancer spontaneous gene mice (MMTV-PyMT) to obtain radiation therapy model of breast cancer mice. To simulate clinical breast cancer radiotherapy and study the differential proteins of breast cancer radiotherapy resistance. MMTV-PyMT mice were randomly divided into two groups, and the radiotherapy group was given the same dose 5 times (3GY, once every 2 days) when the breast cancer tumor grew to an appropriate size (200mm3). The protein extracted from mouse tumor was analyzed by mass spectrometry.

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Myeloid MyD88 restricts CD8+ T cell response to radiation therapy in pancreatic cancer [sequencing]

Project description:Radiation therapy induces immunogenic cell death in cancer cells, whereby apoptotic cells release endogenous adjuvants that are sensed by immune cells to direct adaptive immune responses. Toll-like receptors (TLRs) expressed on several immune subtypes recognize these products to direct downstream responses in part via the adapter protein MyD88. Here we use lineage specific deletion of Myd88 to interrogate its contribution to the immune response to radiation therapy in distinct immune populations in pancreatic cancer. While Myd88 deletion in Itgax- and Lck-expressing immune populations had little discernable effects on response to radiation therapy, Lyz2-specific loss of Myd88 rendered tumors more susceptible to radiation therapy dependent on CD8+ T cells. scRNAseq revealed gene signatures in myeloid and dendritic cells indicative of enhanced type I and II interferon responses. Together, these data implicate MyD88 signaling in myeloid cells as a critical source of immunosuppression that hinders adaptive immune tumor control following radiation therapy.

2023-08-28 | GSE176011 | GEO

Myeloid MyD88 restricts CD8+ T cell response to radiation therapy in pancreatic cancer [Nanostring]

2023-08-28 | GSE176014 | GEO

Imaging Studies of Local Responses of Prostate Cancer to Radiation Therapy

Project description:Patients receiving radiation therapy for prostate cancer received a multiparametric MRI and MRI/ultrasound-fusion targeted biopsy. Patients received a second mpMRI six months after radiation therapy. The goal of this study was to generate gene expression profiles of prostate cancer tumor tissue prior to treatment, and compare the gene expression profiles of those patients based on imaging response or time to biochemical recurrence.

2025-08-25 | GSE129274 | GEO

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