CIDR: Detroit Research on Cancer Survivors (ROCS) and Disparities and Cancer Epidemiology- Colorectal Cancer (DANCE)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA902083 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Detroit Research on Cancer Survivors (ROCS) and Disparities and Cancer Epidemiology- Colorectal Cancer (DANCE)
| PRJNA902082 | ENA
Project description:Cancer-related fatigue is one of the most frequent complaints among breast cancer survivors, with a major negative impact on general life. However, the etiology behind this syndrome is still unraveled. Gene expression analysis was performed on whole blood samples from breast cancer survivors classified as either fatigued or non-fatigued at two consecutive time points. The analysis identified several gene sets concerning plasma and B cell pathways as different between the fatigue and non-fatigue groups, suggesting that a deregulation in these pathways might underlie the fatigue syndrome. The fatigue group also showed a higher mean level of leucocytes, lymphocytes and neutrophiles compared with the non-fatigue group, thus further implicating the immune system in the biology behind the fatigue syndrome. Keywords: Blood RNA and late side effects Breast cancer survivors treated with adjuvant radiotherapy at The Norwegian Radium Hospital between 1998 and 2002 were invited to participate in a study assessing late treatment effects in breast cancer survivors. In the present study, gene expression analysis was performed on whole blood samples from breast cancer survivors with and without persistent fatigue, to look for different expression patterns that might shed light on the biology behind cancer-related fatigue.
2009-07-01 | E-GEOD-14786 | biostudies-arrayexpress
Project description:In this study RNA-Seq was performed in anthracycline- exposed childhood cancer survivors who had cardiomyopathy (cases) matched to those without cardiomyopathy (controls) to understand the pathogenesis of anthrcaycline-related cardiomyopathy
2023-01-31 | GSE218276 | GEO
Project description:SUMMARY Non-Hispanic Black/African American (Black/AA) men in the United States have disproportionally higher incidence and mortality rates of lung cancer compared to non-Hispanic White (NHW) men. Biological factors are believed to play critical roles in driving the disparities. Nevertheless, large-scale genomic studies fail to identify significant somatic differences in lung cancer driver genes contributing to the disparities. Elevated expression of protein arginine methyltransferases (PRMTs) correlating with poorer prognosis is observed in many cancer types. Here, we observed a higher PRMT6 expression in lung cancer of Black/AA men compared to NHW men. PRMT6 formed a heteromer complex with PRMT1 to catalyze arginine methylation of interleukin enhancer-binding factor 2 essential for cell proliferation. Disrupting PRMT1/PRMT6 heteromer complex by a competitive peptide reduced cell proliferation in non-small cell lung cancer cell lines and lung cancer patient-derived organoids. This work implicates that PRMT1/PRMT6 heteromer complex contributes to poorer lung cancer outcomes in Black/AA men vs. NHW men that could serve as a target to eliminate cancer health disparities.
2023-12-15 | MSV000093674 | MassIVE
Project description:Analysis of breast cancer survivors' gut microbiota after lifestyle intervention, during the COVID-19 lockdown, by 16S sequencing of fecal samples.
2023-01-13 | E-MTAB-12486 | biostudies-arrayexpress
Project description:Cancer-related fatigue is one of the most frequent complaints among breast cancer survivors, with a major negative impact on general life. However, the etiology behind this syndrome is still unraveled. Gene expression analysis was performed on whole blood samples from breast cancer survivors classified as either fatigued or non-fatigued at two consecutive time points. The analysis identified several gene sets concerning plasma and B cell pathways as different between the fatigue and non-fatigue groups, suggesting that a deregulation in these pathways might underlie the fatigue syndrome. The fatigue group also showed a higher mean level of leucocytes, lymphocytes and neutrophiles compared with the non-fatigue group, thus further implicating the immune system in the biology behind the fatigue syndrome. Keywords: Blood RNA and late side effects
2009-07-01 | GSE14786 | GEO
Project description:Characterisation of VDR signaling in prostate cancer health disparities
| PRJNA925935 | ENA
Project description:Long-term toxicities caused by cancer treatments have recently gained increasing recognition due to a steadily growing population of cancer survivors. Radiotherapy (RT) is a common treatment known to unintentionally harm surrounding normal tissues including the skin, hindering wound healing even years after treatment. Our study aimed to elucidate the underlying mechanisms of these late-onset adverse effects caused by RT. By comparing paired skin biopsies from previously irradiated (RT+) and non-irradiated (RT-) sites in breast cancer survivors who underwent RT years ago, we discovered compromised wound healing capacity and impaired fibroblast functions in the RT+ skin. By employing ATAC-seq, we identified altered chromatin landscapes in RT+ fibroblasts, pinpointing THBS1 as a crucial epigenetically primed wound repair-related gene. Further confirmation of THBS1's significance during wound repair came from single-cell RNA-sequencing and spatial transcriptomic analysis of human wounds. Remarkably, heightened and sustained THBS1 expression was observed in RT+ fibroblasts in both mouse and human radiation wound models, leading to impaired fibroblast motility and contractility. Encouragingly, our study found that treatment with anti-THBS1 antibodies promoted ex vivo wound closure in RT+ skin from breast cancer survivors. These findings indicate that dermal fibroblasts retain a long-term radiation memory recorded in the form of epigenetic changes. Targeting this maladaptive epigenetic memory shows promise for mitigating the late-onset adverse effects caused by RT, offering potential solutions to improve the quality of life for cancer survivors.
2024-08-02 | GSE254756 | GEO
Project description:Long-term toxicities caused by cancer treatments have recently gained increasing recognition due to a steadily growing population of cancer survivors. Radiotherapy (RT) is a common treatment known to unintentionally harm surrounding normal tissues including the skin, hindering wound healing even years after treatment. Our study aimed to elucidate the underlying mechanisms of these late-onset adverse effects caused by RT. By comparing paired skin biopsies from previously irradiated (RT+) and non-irradiated (RT-) sites in breast cancer survivors who underwent RT years ago, we discovered compromised wound healing capacity and impaired fibroblast functions in the RT+ skin. By employing ATAC-seq, we identified altered chromatin landscapes in RT+ fibroblasts, pinpointing THBS1 as a crucial epigenetically primed wound repair-related gene. Further confirmation of THBS1's significance during wound repair came from single-cell RNA-sequencing and spatial transcriptomic analysis of human wounds. Remarkably, heightened and sustained THBS1 expression was observed in RT+ fibroblasts in both mouse and human radiation wound models, leading to impaired fibroblast motility and contractility. Encouragingly, our study found that treatment with anti-THBS1 antibodies promoted ex vivo wound closure in RT+ skin from breast cancer survivors. These findings indicate that dermal fibroblasts retain a long-term radiation memory recorded in the form of epigenetic changes. Targeting this maladaptive epigenetic memory shows promise for mitigating the late-onset adverse effects caused by RT, offering potential solutions to improve the quality of life for cancer survivors.
2024-08-02 | GSE254753 | GEO