Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of BMN/PAZA combination therapy on lung cancer cells

ABSTRACT: To investigate the BMN/PAZA combination in DNA repair and epigenetic regulation. Dose effect is considered.

ORGANISM(S): Mus musculus

PROVIDER: GSE245266 | GEO | 2024/05/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of BMN/PAZA combination therapy on lung cancer cells

Project description:Effect of BMN/PAZA combination therapy on lung cancer cells

| PRJNA1027481 | ENA

Endometrial profile of low-dose estradiol and tamoxifen combination therapy

Project description:Combination therapy with estrogen and a selective estrogen receptor modulator (SERM) is a promising approach to safely alleviate important side effects related to estrogen deficiency in women at high risk for breast cancer. Data related to endometrial safety of estrogen+SERM co-therapies are limited, however. The primary goal of this study was to evaluate the endometrial profile of low-dose E2 and Tam alone and in combination. In this study 16 postmenopausal female cynomolgus macaques were randomized to receive placebo, low-dose micronized estradiol (E2, 0.25 mg/1800 kcal), the SERM tamoxifen (Tam, 20 mg/1800 kcal), or E2+Tam in a parallel-arm design. Endometrial samples were collected after 4 months of treatment and used for microarray analysis.

2010-05-06 | E-GEOD-14518 | biostudies-arrayexpress

Dual Inhibition of DNA methylation and PARP Increases Anti-tumor Efficacy in SETD2 Deficient Kidney Cancer

Project description:Purpose: SETD2 deficiency, a driving force of depleted levels of H3K36me3 due to impaired methyltransferase activity, plays an important role in diverse forms of cancer, most notably in aggressive and metastatic clear cell renal cell carcinomas (ccRCC). Developing novel treatment schema targeting SETD2-compromised cancer cells are urgently needed. Methods: Human kidney cancer cell lines with or without SETD2 deficiency were treated with a DNA Hypomethylating Agent (HMA), a poly(ADP-ribose) polymerase inhibitor (PARPi), and both (HMA + PARPi) in combination in both in vitro and in vivo settings. Cell inhibition, Comet, flow cytometry, western blot, and RNA-sequencing (RNA-seq) gene expression assays as well as bioinformatic analyses were performed to explore the underlying mechanism action. Results: By taking advantage of involvement of SETD2 in DNA methylation and DNA repair, we found the combination treatment of an HMA (5-Aza-CdR/DAC) and a PARPi (Talazoparib/BMN-673) generated increased cytotoxicity in in vitro SETD2-deficient RCC cell lines than in SETD2-proficient cell lines. Furthermore, our results also demonstrate synergetic anti-tumor effects in SETD2 deficiency RCC cell lines when treated with DAC and BMN-673 that include apoptotic induction, increased DNA damage, insufficient DNA damage repair, upregulation of immune responses by STING and transposable elements (TEs), as well as increased genomic instability. Finally, the combination treatment for SETD2-deficient RCCs was also validated using in vivo mouse models. Conclusion: SETD2 deficiency creates a vulnerable epigenetic status to generate efficacious anti-tumor effects via the combination treatment of DAC and BMN-673 in human and mouse RCC systems, making it a precise medicine-based approach for SETD2-compromised cancers.

2023-08-29 | GSE223893 | GEO

Toxicogenomics profiling of bone marrow from rats treated with topotecan in combination with oxaliplatin: a mechanistic strategy to inform combination toxicity.

Project description:Combinations of anticancer agents may have synergistic anti-tumor effects, but enhanced hematological toxicity often limit their clinical use. We examined whether M-bM-^@M-^\microarray profilesM-bM-^@M-^] could be used to compare early molecular responses following a single dose of agents administered individually with that of the agents administered in a combination. Six patterns of co-expressed genes were detected at the 1-hour time point which indicate regulatory expression of genes dependent on the order of the administration. When topotecan is given first, several signal transduction transcription factors associated with cancer or inactivation of a tumor suppressor were co-regulating gene expression. These results suggest alterations in histone biology, chromatin remodeling, DNA repair, bone regeneration, and respiratory and oxidative phosphorylation are among the prominent pathways modulated in bone marrow from animals treated with an oxaliplatin/topotecan combination. mRNA responses were compared within bone marrow of Sprague-Dawley rats after a single 30-minute treatment with topotecan at 4.7 mg/kg or oxaliplatin at 15 mg/kg alone to that of sequentially administered combination therapy or vehicle control Please note that one of the 'Bone Marrow_Oxaliplatin _Vehicle 1' sample (1344-05H_4M 40) was considered an outlier and thus, was excluded from data analysis and GEO records.

2015-01-21 | E-GEOD-63902 | biostudies-arrayexpress

Endometrial profile of low-dose estradiol and tamoxifen combination therapy

2009-02-03 | GSE14518 | GEO

Nobelitin and Sorafenib Combination Therapy

Project description:Nobelitin and Sorafenib Combination Therapy

| PRJNA1029033 | ENA

Overcoming clinical resistance to EZH2 inhibition using rational epigenetic combination therapy

Project description:Overcoming clinical resistance to EZH2 inhibition using rational epigenetic combination therapy

| PRJNA882766 | ENA

Overcoming clinical resistance to EZH2 inhibition using rational epigenetic combination therapy

Project description:Overcoming clinical resistance to EZH2 inhibition using rational epigenetic combination therapy

| PRJNA928835 | ENA