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Genomic comparison of post-radiation versus sporadic sarcomas

ABSTRACT: Genomic comparison of post-radiation versus sporadic sarcomas

PROVIDER: PRJNA646742 | ENA |

REPOSITORIES: ENA

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Genomic comparison of post-radiation versus sporadic sarcomas

Project description:Post-radiation sarcomas are rare secondary cancers arising from radiation therapies. To date, few genetic specificities have been described for such malignancies and the oncogenesis of sarcomas with complex genetics (both sporadic and post-radiation) remains largely misunderstood. We performed genomic analyses on both sporadic and post-radiation sarcomas to study their copy-number alterations. This analysis is described in Lesluyes et al. 2019 (PMID: 31243333).

2020-07-17 | GSE154591 | GEO

Transcriptome characterization of radiation-induced sarcomas

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Proteomics analysis of primary mouse sarcomas post radiation therapy

Project description:- We revealed that inhibition of glutamine metabolism via genetic deletion or pharmacological inhibition of glutaminase (Gls1) radiosensitizes primary sarcomas in vivo. To delineate the potential mechanism(s) of radiosensitization post radiation therapy (RT), we performed proteomic analysis of Gls1+/+ and Gls1fl/flsarcomas 48 hours post 10 Gy RT. We found that 490 and 217 proteins were differentially expressed in Gls1fl/flsarcomas post 0 Gy and 10 Gy compared to Gls1+/+ sarcomas, respectively. Hallmark pathway analysis revealed that Gls1 deletion with or without RT decreased the expression of protein related to proliferation and translation (E2F targets and G2M checkpoint). Interestingly, Gls1 deletion post-RT increased innate immune response marked by elevated interferon-alpha, interferon-gamma, and natural killer (NK) cell responses. Flow cytometry analysis further validated these findings and showed significantly elevated NK cells, but not dendritic and myeloid cells in primary Gls1-deficient sarcomas compared to Gls1-proficient sarcomas post-RT. Collectively, proteomic and flow cytometry datasets suggested that innate immune response is partly accountable for radiosensitizing Gls1-deficient sarcomas.

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Selective DNA-PK inhibition enhances chemotherapy and ionizing radiation activity in soft-tissue sarcomas

Project description:Purpose: Patients with advanced soft-tissue sarcomas (STSs) exhibit a poor prognosis and have few therapeutic options. DNA-dependent protein kinase catalytic subunit (DNA-PK) is a multifunctional serine—threonine protein kinase that plays a crucial role in DNA double-strand damage repair via nonhomologous end joining (NHEJ). Experimental design: To investigate the therapeutic potential of DNA-PK targeting in STS, we first evaluated the prognostic value of DNA-PK expression in two large cohorts of patients with STS. We then used the potent and selective DNA-PK inhibitor AZD7648 compound to investigate the antitumor effect of the pharmacological inhibition of DNA-PK in vitro via MTT, apoptosis, cell cycle, and proliferation assays. In vivo studies were performed with patient-derived xenograft models to evaluate the effects of AZD7648 in combination with chemotherapy or ionizing radiation on tumor growth. The mechanisms of sensitivity and resistance to DNA-PK inhibition were investigated by using a genome-wide CRISPR-Cas9 positive screen. Results: DNA-PK overexpression is significantly associated with poor prognosis in patients with sarcomas. Selective pharmacological inhibition of DNA-PK strongly synergizes with radiation- and doxorubicin-based regimen in sarcoma models. By using a genome-wide CRISPR-Cas9 positive screen, we identified genes involved in sensitivity to DNA-PK inhibition. Conclusion: DNA-PK inhibition deserves clinical investigation to improve response to current therapies in patients with sarcoma

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