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Radiation enhances melanoma response to immunotherapeutic and synergizes with benzodiazepines to promote improved anti-tumor activity

ABSTRACT: Radiation enhances melanoma response to immunotherapeutic and synergizes with benzodiazepines to promote improved anti-tumor activity

PROVIDER: PRJNA543883 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR9097550_1.fastq.gz	Fastqsanger.gz
	SRR9097550_2.fastq.gz	Fastqsanger.gz
	SRR9097551_1.fastq.gz	Fastqsanger.gz
	SRR9097551_2.fastq.gz	Fastqsanger.gz

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Radiation enhances melanoma response to immunotherapeutic and synergizes with benzodiazepines to promote improved anti-tumor activity

Project description:The RNA-Seq data of 17 brain metastatic samples short-read sequences were aligned to the hg19 human reference genome using STAR (v 2.4.1a). featureCounts was used to count the reads of the mapped bam files. SAMseq was used to conduct differential expression analysis among the two treatment groups. SAMseq was utilized as it accounts for potential correlation in expression among genes and its permutation-based testing method was deemed more appropriate for a smaller sample size. After identifying the differentially expressed genes (FDR cut-off, 0.05), expression levels were normalized with the samr R package before being log2 transformed. This data was utilized to generate a heatmap with the patients sorted with supervised clustering based upon their immunotherapy/radiation groups and the gene dendrogram was created with Pearson’s Correlation Coefficient and with the Ward D2 linkage method. Differentially expressed genes (FDR<0.05[KD1] ) were subjected to pathway analysis using MetaCore.

2019-05-21 | GSE131521 | GEO

Peptide Vaccines in Melanoma: Chemical Approaches towards Improved Immunotherapeutic Efficacy.

Project description: Not available

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MEK-PARP co-targeting enhances radiation response in rectal cancer.

Project description:Locally advanced rectal cancer is usually treated by neoadjuvant chemoradiotherapy. However, tumor response rates to this treatment vary greatly. Thus, most patients do not reach a complete remission and have to undergo tumor resection. In the present study, we introduce a patient-derived rectal cancer organoid platform that reflects clinical radiosensitivity and use this to screen 1596 drug-radiation combinations. We identify inhibitors of RAS-MAPK signaling, especially MEK inhibitors, strongly synergizing with radiation response. Mechanistically, MEK inhibitors suppressed radiation-induced activation of RAS-MAPK signaling, and selectively downregulated the homologous recombination DNA repair pathway component RAD51, thereby achieving radio-enhancement. Through testing drug-drug-radiation combinations in organoids and cell lines, we identified synergism between PARP and MEK inhibitors to further enhance the effect of radiation. Our data support clinical testing of combined MEK and PARP inhibition with radiotherapy in locally advanced rectal cancers.

2025-05-26 | PXD063024 | Pride

Synthetic RIG-I agonist-mediated cancer immunotherapy synergizes with MAP-Kinase inhibition against BRAF mutated melanoma

Project description:The implementations of targeted molecular therapies and immunotherapy in melanoma vastly improved the therapeutic outcome in patients with limited efficacy of surgical intervention. Nevertheless, a large fraction of melanoma patients still remains refractory or acquires resistance to these new forms of treatment, illustrating a need for improvement. Here we report that the clinically relevant combination of MAP kinase inhibitors Dabrafenib and Trametinib synergizes with RIG-I agonist-induced immunotherapy to kill BRAF-mutated human and mouse melanoma cells. Kinase inhibition did not compromise the agonist-induced innate immune response of the RIG-I pathway in host immune cells. In a melanoma transplantation mouse model, the triple therapy outperformed the individual therapies. Our study suggests that targeted activation of RIG-I with its synthetic ligand 3pRNA could vastly improve tumor control in a substantial fraction of melanoma patients receiving MAP kinase inhibitors.

2024-07-26 | GSE268982 | GEO

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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Synthetic RIG-I agonist-mediated cancer immunotherapy synergizes with MAP-Kinase inhibition against BRAF mutated melanoma [YUMM1.7]

2024-06-04 | GSE269008 | GEO

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Combined MEK and PARP inhibition enhances radiation response in rectal cancer

Project description:Rectal cancer is most frequently diagnosed at a locally advanced stage and treated by neoadjuvant chemoradiation. Current efforts to improve treatment outcome are focused on intensifying neoadjuvant chemotherapy, which is however associated with higher levels of toxicity. To discover alternative strategies, we established patient-derived rectal cancer organoids (PDOs) that reflect clinical radiosensitivity and used these organoids to screen 1596 drug-radiation combinations. We found that inhibitors of RAS-MAPK signaling, especially MEK inhibitors, strongly enhance radiation response. Mechanistically, MEK inhibitors suppressed radiation-induced activation of RAS-MAPK signaling, and selectively downregulated RAD51, a key component of the homologous recombination DNA repair pathway. Through testing drug-drug-radiation combinations in organoids and cell lines, we identified that a combined PARP and MEK inhibition can further enhance radiosensitivity of colorectal cancers, which was confirmed in mouse xenograft models. Our data support clinical testing of MEK and PARP combination therapy with radiation in locally advanced rectal cancers as an alternative to chemoradiation Microarrays were used to investigate the effect of radiation treatment on gene expression in three patient-derived colorectal cancer organoid lines.

2025-04-23 | GSE294953 | GEO

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