BTBD7 (BTB Domain Containing 7)

A-to-I RNA edited POLA2 attained carcinogenesis in PCa by impeding immune infiltration, fortifying glycolysis and upregulating BTBD7, indicating that edited POLA2 has the potential to become a tool for gene therapy.

Pre-analytic evaluation of the manufacturer's recommended 20% tumor content cut-off is essential to ensure valid results. The Idylla MSI assay offers several advantages over other PCR-based assays including minimal hands-on time, rapid turn-around-time, no requirement for a paired normal sample and the use of FFPE directly without an extraction step.

P1/2, N=50, Completed, University of the Sunshine Coast Mind and Neuroscience Thompson Institute | Suspended --> Completed

P2, N=25, Terminated, Thompson Institute, University of the Sunshine Coast | Recruiting --> Terminated

MFGE8 promoted cell proliferation, EMT progress, and tumor growth of gastric cancer by activating the IL-6/JAK/STAT3 signaling.

Additionally, the suppressed Rho/ROCK2 pathway conferred by circZCCHC2 knockdown could be restored by inhibiting miR-936 expression. Collectively, our findings reveal that circZCCHC2 plays an oncogenic role of in HCC progression by modulating the miR-936/BTBD7/Rho/ROCK2 pathway.

The Idylla MSI Test was successfully technically validated as an adequate tool for the evaluation of the MSI status in CRC.

Idylla™ MSI assayshows higher sensitivity than Pro-mega™ MSI analysis, in detecting MSI-H in MMRd EC. Promega™ misses isolated losses of MMR proteins. Probably, the selection criteria for MSI-H in Promega™ (more than one gene mutated) is the reason of the low agreement.

This is the first large-scale whole-genome sequencing for DFSP, and our findings describe the comprehensive genomic landscape, highlighting the molecular complexity and genomic aberrations of DFSP. Our findings also provide novel potential diagnostic and therapeutic targets for this disease. What is already known about this topic? Chromosomal translocation between chromosome 17 and chromosome 22 is the main feature in the pathogenesis of dermatofibrosarcoma protuberans (DFSP). What does this study add? We describe the comprehensive genomic landscape of DFSP, highlighting the molecular complexity and genomic aberrations. Our findings provide novel potential diagnostic and therapeutic targets for this disease. What is the translational message? Our study revealed novel molecular subtypes of DFSP based on genetic mutations, which benefits precision diagnosis. We also found oncogene amplification, including AKT1 and SPHK1, which provides novel potential target molecules for further DFSP treatment. In addition to gene fusion of COL1A1-PDGFβ, we identified a novel gene fusion of SLC2A5-BTBD7 in DFSP, which is a novel potential diagnostic and therapeutic target for this disease.

BC cells were treated with different concentrations of doxorubicin, cisplatin, and fulvestrant, and the cell survival was evaluated. EVs carrying miR-887-3p could target BTBD7 and activate the Notch1/Hes1 signaling pathway, thereby promoting BC cell drug resistance. This study may offer novel insights into BC treatment.

Further investigation showed that KBTBD7 enhanced ubiquitin-dependent degradation of PTEN, thus activating EGFR/PI3K/AKT signaling and promoting NSCLC cell proliferation and invasion by regulating CCNE1, CDK4, P27, ZEB-1, Claudin-1, ROCK1, MMP-9, and E-cadherin protein levels. Our results indicate that KBTBD7 may be a potential therapeutic target for the treatment of NSCLC.

Our findings support that the Idylla MSI assay provides a rapid, reliable, and ease-to-use solution to MSI detection in Chinese CRC patients with high sensitivity and specificity. The inconsistent cases between IHC and PCR-based approaches need a further analysis.