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Targeting cancer stem cells with differentiation agents as an alternative to genotoxic chemotherapy for the treatment of malignant testicular germ cell tumors

ABSTRACT: Targeting cancer stem cells with differentiation agents as an alternative to genotoxic chemotherapy for the treatment of malignant testicular germ cell tumors

PROVIDER: PRJNA706696 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13858561.fastq.gz	Fastqsanger.gz
	SRR13858562.fastq.gz	Fastqsanger.gz
	SRR13858563.fastq.gz	Fastqsanger.gz
	SRR13858564.fastq.gz	Fastqsanger.gz
	SRR13858565.fastq.gz	Fastqsanger.gz

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Targeting cancer stem cells with differentiation agents as an alternative to genotoxic chemotherapy for the treatment of malignant testicular germ cell tumors

Project description:Testicular germ cell tumors (TGCTs) are exceptionally sensitive to genotoxic chemotherapy, resulting in a high cure rate for the young men presenting with these malignancies. However, this treatment is associated with significant toxicity, and a subset of malignant TGCTs demonstrate chemoresistance. Mixed non-seminomas often contain pluripotent embryonal carcinoma (EC) cells, the cancer stem cells (CSCs) of these tumors. We hypothesized that differentiation therapy, a treatment strategy which aims to induce differentiation of tumor-propagating CSCs to slow tumor growth, could effectively treat mixed non-seminomas without significant toxicity. The FDA-approved anti-psychotic thioridazine and the agricultural antibiotic salinomycin are two drugs previously found to selectively target CSCs, and here we report that these agents differentiate EC cells in vitro and greatly reduce their tumorigenic potential in vivo. Using a novel transformed induced pluripotent stem cell allograft model and a human xenograft model, we show that thioridazine extends the survival of tumor-bearing mice and can reduce the number of pluripotent EC cells within tumors. These results suggest that thioridazine could be repurposed as an alternative TGCT treatment that avoids the toxicity of conventional chemotherapeutics.

2021-04-23 | GSE168261 | GEO

KSR1 and genotoxic agents in MCF7 (SILAC-MS)

Project description:We use KSR1 overexpression and exposure to doxorubin or etoposide in MCF7 cells to reveal a comprehensive repertoire of thousands of proteins identified in each dataset and compare the unique proteomic profile as well as functional connections modulated by KSR1 after doxorubicin (Doxo-KSR1) or etoposide (Etop-KSR1) stimulus. From the up-regulated top hits, several proteins, including STAT1, ISG15 and TAP1 were also found to be positively associated with KSR1 expression in patient samples. Moreover, high KSR1 expression, as well as high abundance of these proteins, is correlated with better survival in breast cancer patients who underwent chemotherapy. Our data exemplify a broad functional network conferred by KSR1 with genotoxic agents and highlight its implication in predicting chemotherapy response in breast cancer.

2022-03-02 | PXD002233 | Pride

Targeting Cancer Stem Cells with Differentiation Agents as an Alternative to Genotoxic Chemotherapy for the Treatment of Malignant Testicular Germ Cell Tumors.

Project description:Testicular germ cell tumors (TGCTs) are exceptionally sensitive to genotoxic chemotherapy, resulting in a high cure rate for the young men presenting with these malignancies. However, this treatment is associated with significant toxicity, and a subset of malignant TGCTs demonstrate chemoresistance. Mixed nonseminomas often contain pluripotent embryonal carcinoma (EC) cells, the cancer stem cells (CSCs) of these tumors. We hypothesized that differentiation therapy, a treatment strategy which aims to induce differentiation of tumor-propagating CSCs to slow tumor growth, could effectively treat mixed nonseminomas without significant toxicity. The FDA-approved antipsychotic thioridazine and the agricultural antibiotic salinomycin are two drugs previously found to selectively target CSCs, and here we report that these agents differentiate EC cells in vitro and greatly reduce their tumorigenic potential in vivo. Using a novel transformed induced pluripotent stem cell allograft model and a human xenograft model, we show that thioridazine extends the survival of tumor-bearing mice and can reduce the number of pluripotent EC cells within tumors. These results suggest that thioridazine could be repurposed as an alternative TGCT treatment that avoids the toxicity of conventional chemotherapeutics.

| S-EPMC8122873 | biostudies-literature

Depletion of the Chromatin Remodeler CHD4 Sensitizes AML Blasts to Genotoxic Agents and Reduces Tumor Formation

Project description:Depletion of CHD4 sensitizes AML cells but not normal CD34+ progenitors to genotoxic agents by relaxing chromatin and impairing DSB repair. Depletion of CHD4 modulates expression of AML cell genes that regulate tumor formation in vivo and colony formation in vitro.

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Clonal Analyses of Refractory Testicular Germ Cell Tumors

Project description:We used DNA content-based flow cytometry to distinguish and isolate nuclei of clonal tumor populations from primary and metastatic refractory testicular germ cell tumors (TGCTs) tissues. We then interrogated each sorted tumor populationwith whole genome aCGH and next generation sequencing (NGS). we have explored the clonal basis of refractory TGCT by investigating distinct tumor populations that were present in each tumor. Notably this included resected primary tissues and treatment refractory metastases that arose after high dose chemotherapy. These results provide new knowledge regarding the role of clonal selection and selected genomic lesions in the resistance to chemotherapy in TGCT within this exceptional cohort.

2019-02-26 | GSE123464 | GEO

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Project description:RNA-seq analysis of two Testicular Germ Cell Cancers (TGCC) of patients with chemotherapy-resistant disease. Purpose of the study was to resolve the early development and progression of the disease by whole genome sequencing, RNA-seq and methylation profiling of the primary tumor, and the targeted sequencing of purified tumor components (embryonal carcinoma (EC), teratoma (TE), and yolk sac tumor (YST), precursor lesion (Germ Cell Neoplasia In Situ (GCNIS)), and metastases. Whole genome sequencing for the two patients, T6107 and T3209, have been deposited with the European Nucleotide Archive under project accession number PRJEB20644 / study accession ERP022815 ( http://www.ebi.ac.uk/ena/data/search?query=ERP022815 ).

2019-02-11 | E-MTAB-5746 | biostudies-arrayexpress

Transcription profiling of human acute myeloid leukemia cells before and early after the start of conventional genotoxic chemotherapy

Project description:The molecular changes in vivo in acute myeloid leukemia cells early after start of conventional genotoxic chemotherapy are incompletely understood, and it is not known if early molecular modulations reflect clinical response. The gene expression was examined by whole genome 44k oligo microarrays in peripheral blood leukocytes collected from seven leukemia patients before treatment, 2-4 h and 18-24 h after start of chemotherapy and validated by real-time quantitative PCR.

2009-02-04 | E-TABM-632 | biostudies-arrayexpress

Genetic Effect of Chemotherapy Exposure in Children of Testicular Cancer Survivors

Project description:Genetic Effect of Chemotherapy Exposure in Children of Testicular Cancer Survivors

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IRF3 drives replication stress signaling and determines sensitivity to genotoxic agents in triple-negative breast cancer cells

Project description:Interferon-β signaling has been shown to play important roles in anti-virus as well as anti-tumor immunity. We here report that the key transcription factor in type I interferon signaling, IRF3, as well as downstream interferon-β are able to induce replication stress signaling in triple-negative breast cancer cells. IRF3 overexpression sensitizes triple-negative breast cancer cells to several genotoxic agents. Addition of IFN-β, a key downstream cytokine of IRF3,reduced replication fork speed and activated ATR-CHK1 signaling. Conversely, type I interferon-neutralizing antibodies or nucleosides supplementation rescued IRF3-induced replication stress.

2024-05-01 | GSE263947 | GEO

aCGH from mouse gPAK testicular teratocarcinomas

Project description:Testicular germ cell tumors are among the most responsive solid cancers to conventional chemotherapy. To elucidate the underlying mechanisms, we developed a mouse testicular germ cell tumor model in which germ cell-specific oncogenic Kras activation and tumor suppressor Pten inactivation was driven by CRE-mediated recombination. The resulting mice rapidly developed malignant, metastatic testicular cancers composed of both teratoma and embryonal carcinoma, the latter of which exhibited stem cell characteristics, including expression of the pluripotency factor OCT4. As part of our analysis of mouse gPAK testicular tumors, as well as comparison to benign 129-Dnd1Ter/Ter testicular teratomas, we used NimbleGen Mouse CGH 3x720k Whole-Genome Tiling Arrays to assess copy number variations in this novel genetically engineered mouse model of malignant, metastatic testicular cancer.

2017-11-14 | GSE70746 | GEO

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