Roland Rad

This study shows that different colorectal cancer genotypes create distinct microbial ecosystems and that microbiota dependence decreases as tumors progress.

This study uses an in ovo model to show that the CAM platform supports tumor-stroma coevolution in pancreatic cancer, preserving patient-specific features and enabling functional analysis of stromal interactions.

This paper generates cross-species single-cell atlases of pancreatic cancer to study progression, therapy response, and immune evasion across human and mouse models.

This study identifies SMAC as a regulator of cancer cell growth, inflammation, and mitochondrial integrity, showing its role in both apoptotic and non-apoptotic contexts.

The paper re-analyzes a lncRNA screen using Cas13d and finds that off-target effects caused many false-positive results, undermining the study's conclusions.

The paper shows that Treg cells use IFNγ and IL-10 to promote intestinal stem cell growth and repair after injury.

The paper identifies 27 cyclic dinucleotides that activate STING, showing STING's preference for 2'3'-linked nucleotides and its ability to respond to non-hydrolysable isomers.

This study shows that ATM-deficient pancreatic cancers reprogram the tumor microenvironment via TGF-β-driven myCAF enrichment, and targeting this stromal axis with chemotherapy improves therapeutic efficacy.

This study shows caspase-3 cleaves activated MAVS to suppress spontaneous innate immune signaling in non-apoptotic cells.

This study compares genomic and phenotypic stability of pediatric Ewing sarcoma cell lines to adult carcinoma cell lines over 12 months of culture.

This study identifies KRAS mutation as a driver of invasive gastro-esophageal adenocarcinoma in a mouse model, showing its synergistic role with Tp53 or Rb1 loss and potential as a therapeutic target.

This study identifies RNF43 mutations as a driver of colitis-associated cancer by showing their role in promoting inflammation and dysbiosis in mouse models and human patients.

Concurrent multi-omics of SARS-CoV-2 and SARS-CoV in A549 cells, integrated by network diffusion, maps shared and virus-specific host perturbations and nominates antiviral drug hotspots.