[Alternative Splicing Detection as Biomarker Candidates for XXXX Diagnosis and Treatment with Establishment of Clinical Biobank in Chiba University].

@entity1 @entity981 @entity19 @entity5 @entity186 @entity1820 @entity6732 @entity105 @entity11511 @entity71922
Alternative splicing is a fundamental process of gene regulation that contributes to protein diversity, a common phenomenon in the @entity1 genome. Alternative splicing events not only happen in the normal gene regulation process, but are also closely related to certain diseases, including @entity5 . In this review, we briefly demonstrate the proof of concept (POC) of the relationship between alternative splicing and DNA damage, and describe the associations among alternative splicing and @entity5 pathogenesis, DNA damage, and @entity1820 . We discuss whether alternative splicing leads to genetic instability, which is considered to be a driving force for tumorigenesis. @entity71922 is a c-myc transcriptional suppressor. A splice variant of FIR that lacks exon 2 in the transcriptional repressor domain ( @entity71922 exon2), upregulates c-myc transcription by inactivating wild-type FIR. FIR+/- m @entity19 exhibited marked c-myc mRNA upregulation, particularly in the peripheral blood (PB), without any significant pathogenic phenotype. Because the single knockout of T @entity186 generates t @entity6732 FIR+/-T @entity186 /- m @entity19 developed T @entity11511 (T @entity981 with increased organ or bone marrow invasion and showed a poor prognosis. After describing the POC of alternative splicing of FIR in DNA damage and c @entity105 clinical application for c @entity5 diagnosis and treatment by FIR/F @entity71922 exon2 was briefly summarized. Chiba University has prepared a biobank to support studies to develop biomarker detection, molecular diagnosis, and "Omics" research. In conclusion, alternative splicing of FIR, generating FI @entity71922 xon2, potentially contributes to not only colorectal car @entity105 ut also leukemogenesis, and a better understanding of the role and mechanism of alternative splicing in tumorigenesis may reveal new directions for can @entity5 omarker detection.
