ETV3 (ETS Variant Transcription Factor 3)

Mechanistically, hypermethylation at cg08640619 disrupts RUNX2 binding, leading to inhibition of KIRREL1 and ETV3. Our study provides a comprehensive platform for understanding how genetic and epigenetic variants disrupt transcriptional programs in CRC, offering insights into disease susceptibility and identifying potential diagnostic and therapeutic targets.

Limitations include sample size constraints for methylation integration. Future studies should validate these findings in prospective clinical trials.

Our findings demonstrate that machine learning-driven survival models, particularly RSF, can effectively identify NSCLC patients who may benefit from ACT. This approach supports data-driven, individualized chemotherapy decision-making and contributes to advancing personalized treatment strategies in early-stage NSCLC.

We report a rare case of cutaneous IDCT with ETV3::NOAC2 rearrangement providing further evidence to its association with this condition. With its ease of administration and minimal side effects, PUVA therapy can be successfully used to treat cutaneous forms of IDCT.

Four months later, his ICH skin eruptions, eczematous plaques, and lymphoadenopathy gradually regressed. Our case supports the notion that the detection of ETV3-NCOA2 translocation can be useful for diagnosis of ICH.

Age at diagnosis and any nodal involvement at diagnosis predicted inferior overall survival, but BRAF/RAS pathway alterations did not impact outcome. These data have implications for the diagnostic evaluation, classification, and therapeutic management of IDCH.

Then, using the drug repurposing method with the Connectivity Map CLUE Query tools, potential drugs such as Forskolin, Gestrinone, Cediranib, Apicidine, and Everolimus, which showed a highly negative correlation with the expression levels of the selected genes, were identified. This study provides a method to develop new approaches to diagnosing and treating gastric cancer by comparing the transcriptome profiles of patients gastric cancer and performing a feature engineering-assisted drug repurposing analysis based on cancer data.

MM patients carrying with higher 1q21+ copies expressed higher level of ETV3 genes, which indicated a worse prognosis. Knocking down ETV3 on myeloma cells reduced their proliferation ability and enhanced their sensitivity to selinexor. PKN1 might involved in this process.

Furthermore, in the same cell line we identified PBX1-mediated overexpression of RIOK2 which inhibited ETS1 and activated JAK2 expression. Collectively, we codified normal ETS gene activities in lymphopoiesis and identified oncogenic ETS members in HL.

Offered therapies included ibrutinib for DLBCL with a CD78B mutation, romidepsin for T cell lymphoma with a TET2 mutation, and ruxolitinib for T cell lymphoma with JAK2 fusion...Identified resistance mutations included alterations in BTK , PLCG2 , and BCL2 genes, which led to changes in therapy from a BTK inhibitor to venetoclax or vice versa...Conclusion Comprehensive genomic profiling of non-myeloid hematologic malignancies identified variants of clinical significance in 72% of patients and led to changes in practice in 22% of patients. CGP was often sent late in the clinical course.