Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Examination of Generational Impacts of Adolescent Chemotherapy: Ifosfamide and Potential for Epigenetic Transgenerational Inheritance

ABSTRACT: Examination of Generational Impacts of Adolescent Chemotherapy: Ifosfamide and Potential for Epigenetic Transgenerational Inheritance

PROVIDER: PRJNA897002 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22149500_1.fastq.gz	Fastqsanger.gz
	SRR22149500_2.fastq.gz	Fastqsanger.gz
	SRR22149501_1.fastq.gz	Fastqsanger.gz
	SRR22149501_2.fastq.gz	Fastqsanger.gz
	SRR22149502_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 68

Similar Datasets

Examination of Generational Impacts of Adolescent Chemotherapy: Ifosfamide and Potential for Epigenetic Transgenerational Inheritance

Project description:The current study was designed to use a rodent model to determine if exposure to the chemotherapy drug ifosfamide during puberty can induce altered phenotypes and disease in the grand-offspring of exposed individuals through epigenetic transgenerational inheritance. Numerous toxicant exposures during critical developmental windows can have generational impacts through this non-genetic inheritance mechanism. Pathologies such as delayed pubertal onset, kidney disease and multiple pathologies were observed to be significantly more frequent in the F1 generation offspring of ifosfamide lineage females. The F2 generation grand-offspring ifosfamide lineage males had transgenerational pathology phenotypes of early pubertal onset and reduced testis pathology. Reduced levels of anxiety were observed in both males and females from the exposure lineage in the transgenerational F2 generation grand-offspring. Differential DNA methylated regions (DMRs) were also identified in chemotherapy and control lineages sperm in the F1 and F2 generations. The transgenerational alterations in sperm epigenetics provides a molecular mechanism for the ancestral impacts of chemotherapy. Therefore, chemotherapy exposure can impact pathology and disease susceptibility in subsequent generations.

2022-11-30 | GSE217141 | GEO

Glyphosate Induced Epigenetic Transgenerational Inheritance of Pathologies and Sperm Epimutations: Generational Toxicology

Project description:Glyphosate Induced Epigenetic Transgenerational Inheritance of Pathologies and Sperm Epimutations: Generational Toxicology

| PRJNA486088 | ENA

Examination of generational impacts of adolescent chemotherapy: Ifosfamide and potential for epigenetic transgenerational inheritance.

Project description:The current study was designed to use a rodent model to determine if exposure to the chemotherapy drug ifosfamide during puberty can induce altered phenotypes and disease in the grand-offspring of exposed individuals through epigenetic transgenerational inheritance. Pathologies such as delayed pubertal onset, kidney disease, and multiple pathologies were observed to be significantly more frequent in the F1 generation offspring of ifosfamide lineage females. The F2 generation grand-offspring ifosfamide lineage males had transgenerational pathology phenotypes of early pubertal onset and reduced testis pathology. Reduced levels of anxiety were observed in both males and females in the transgenerational F2 generation grand-offspring. Differential DNA methylated regions (DMRs) in chemotherapy lineage sperm in the F1 and F2 generations were identified. Therefore, chemotherapy exposure impacts pathology susceptibility in subsequent generations. Observations highlight the importance that prior to chemotherapy, individuals need to consider cryopreservation of germ cells as a precautionary measure if they have children.

| S-EPMC9708925 | biostudies-literature

Environmental Induced Epigenetic Transgenerational Inheritance of Pathology: Systems Epigenetics in Disease Etiology and Generational Toxicology

Project description:Several epigenome-wide association studies (EWAS) have been shown to identify epigenetic alterations (i.e., epimutations) associated with diseases. The sperm epimutations potentially involved in the transgenerational inheritance of specific pathologies have been identified. Transgenerational sperm epimutations associated with kidney, prostate, puberty, testis, obesity, and multiple pathologies have been identified for a variety of environmental toxicants including dioxin, plastics, pesticides, glyphosate, methoxychlor, atrazine, and jet fuel. The transgenerational sperm epimutations for exposure and disease-specific epimutations have been identified in these EWAS studies. The current study used the information from these previous toxicant-induced epigenetic transgenerational inheritance EWAS rat studies and adds a comparable control group, rats that have not been exposed to any particular toxicant. Two additional control groups were collected and are presented here.

2022-04-27 | GSE198452 | GEO

Epigenetic Transgenerational Inheritance of Testis Pathology and Sertoli Cell Epimutations: Generational Origins of Male Infertility

Project description:Environmental toxicant induced epigenetic transgenerational inheritance has been shown to affect testis pathology and sperm count. Sertoli cells have an essential role in spermatogenesis by providing physical and nutritional support for developing germ cells. The current study was designed to further investigate the transgenerational epigenetic changes in the rat Sertoli cell epigenome that are associated with the onset of testis disease.

2018-11-08 | GSE118306 | GEO

Environmental Induced Epigenetic Transgenerational Inheritance of Pathology: Systems Epigenetics in Disease Etiology and Generational Toxicology

Project description:Environmental Induced Epigenetic Transgenerational Inheritance of Pathology: Systems Epigenetics in Disease Etiology and Generational Toxicology

| PRJNA815328 | ENA

Epigenetic Transgenerational Inheritance of Testis Pathology and Sertoli Cell Epimutations: Generational Origins of Male Infertility

Project description:Epigenetic Transgenerational Inheritance of Testis Pathology and Sertoli Cell Epimutations: Generational Origins of Male Infertility

| PRJNA485141 | ENA

Transgenerational inheritance of chronic adolescent stress: Effects of stress response and the amygdala transcriptome

Project description:Transgenerational inheritance of chronic adolescent stress: Effects of stress response and the amygdala transcriptome

| PRJNA427314 | ENA

The chromatin modifiers SET-25 and SET-32 are required for initiation but not long-term maintenance of transgenerational epigenetic inheritance

Project description:Some epigenetic modifications are inherited from one generation to the next, providing a potential mechanism for the inheritance of environmentally acquired traits. Transgenerational inheritance of RNA interference phenotypes in C. elegans provides an excellent model to study this phenomenon, and whilst studies have implicated both chromatin modifications and small RNA pathways in heritable silencing their relative contributions remain unclear. Here we demonstrate that the histone methyltransferases SET-25 and SET-32 are required for the establishment of a transgenerational silencing signal, but not for long-term maintenance of this signal between subsequent generations suggesting that transgenerational epigenetic inheritance is a multi-step process, with distinct genetic requirements for establishment and maintenance of heritable silencing. Furthermore, small RNA sequencing reveals that the abundance of secondary siRNA (thought to be the effector molecules of heritable silencing) does not correlate with silencing phenotypes. Together, our results suggest that the current mechanistic models of epigenetic inheritance are incomplete.

2018-10-30 | PXD008754 | Pride

Transgenerational Adaptation to Hypoxia

Project description:Adaptation to environmental stresses is crucial for survival. Transgenerational epigenetic inheritance allows organisms to respond to irregular conditions, alert their naïve descendants that stresses could still be present, and for distant descendants to eventually return to a basal state after several generations without the stress. However, it is still unclear whether organisms adapt on a transgenerational scale after repeated generational exposures to the same environmental stress. We recently found that C. elegans exposed to hypoxia in the parental (P0) generation: increased longevity in the P0 generation, caused an intergenerational reduction in lipids, and elicited a transgenerational reduction in fertility (P0-F2) that was dependent on small RNAs that were transmitted from parents to their naïve children. Here, we find that exposure of subsequent generations of C. elegans to hypoxia caused a transgenerational adaptation such that C. elegans that had repeated generational exposure to hypoxia failed to display hypoxia induced phenotypes. We show that upon two repeated generational exposures to hypoxia, C. elegans no longer display an increase in lifespan, and after four repeated generational exposures to hypoxia, C. elegans no longer display a decrease in reproduction. Transgenerational adaptation of the reproduction phenotype is dependent on the putative H3K27 trimethytransferase PRC2 complex and we identified critical genes that adapted on a transgenerational timeframe to repeated hypoxia exposure. Our findings reveal that transgenerational adaptation occurs and suggest that H3K27me3 is a critical modification for adapting to repeated generational stresses.

2025-09-19 | GSE255871 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data