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DDX54 inhibition enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden [bulk RNA-seq]

ABSTRACT: DDX54 inhibition enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden [bulk RNA-seq]

PROVIDER: PRJNA1203199 | ENA |

REPOSITORIES: ENA

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	SRR31831921.fastq.gz	Fastqsanger.gz

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DDX54 inhibition enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden

Project description:High tumor mutational burden (TMB) is a predictive biomarker for the responsiveness of cancer to immune checkpoint inhibitor therapy that indicates whether immune cells can sufficiently recognize cancer cells as non-self. However, about 30% of all cancers from The Cancer Genome Atlas are classified as immune-desert tumors lacking T cell infiltration despite high TMB. Since the underlying mechanism of these immune-desert tumors has yet to be unraveled, there is a pressing need to transform such immune-desert tumors into immune-inflamed tumors and thereby enhance their responsiveness to anti-PD1 therapy. Here, we present a systems framework for identifying immuno-oncotargets, based on analysis of gene regulatory networks, and validating the effect of these targets in transforming immune-desert into immune-inflamed tumors. In particular, we identify DEAD-box helicases 54 (DDX54) as a master regulator of immune escape in immune-desert lung cancer with high TMB, and show that knockdown of DDX54 can increase immune cell infiltration and lead to improved sensitivity to anti-PD1 therapy.

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DDX54 inhibition enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden [Xenium]

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DDX54 inhibition enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden

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