Page 41 - SDIR5 Abstract book 21 12 2021.
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POSTER PRESENTATIONS




               POSTER SESSION


               P1




                   Pan-cancer analysis of the role of flap endonuclease 1 (FEN1) in human various tumors

                                                             1,2
                                                                           2
                                                Hongling Yuan , Zekiye Altun
                   1 İzmir International BioMedicine and Genome Institute, Dokuz Eylul University; İzmir,  Department of Basic
                                                                                        2
                                  Oncology, Institute of Oncology, Dokuz Eylul University, İzmir, TURKEY

               Background:  Flap  endonuclease  1  (FEN1)  involves  in  DNA  replication,  long-patch  excision  repair,  and
               telomere maintenance. FEN1 overexpression has been reported to be associated with the different types
               of cancers and it might be a predictive biomarker and therapeutic target in some cancers. But still there is
               no pan-cancer analysis available now. Materials and methods: Through analysis of 33 types of tumors based
               on the datasets of TCGA and GEO, we conduct the FEN1 gene expression analysis through TIMER2, then
               based on the CPTAC dataset, we analyzed the total protein expression level of FEN1 between normal tissue
               and primary tissue of breast cancer, ovarian cancer, colon cancer, clear cell RCC and UCEC. FEN1 genetic
               alteration evaluated by using cBioPortal web and survival status analyzed with GEPIA2. Results: Fen1 is
               highly expressed in most cancers (Fig.1,2). Highly expressed FEN1 was linked to poor prognosis of overall
               Survival  for  cancers  of  LIHC  (p=0.007),  KICH(p=0.039),  ACC(p=0.007),  PAAD(p=0.014),  MESO(p=0.002),
               LGG(p=0.019),  UVM(p=0.014)  and  LUAD(p=0.007),  while  low  expression  is  poor  prognosis  only  in
               THYM(p=0.04) within the TCGA (Fig.3).  The genetic alteration status of FEN1 in different tumor samples of
               the TCGA cohorts were observed. The highest alteration frequency of FEN1 (> 8%) appeared with primary
               Cholangiocarcinoma  with  “CNA  amplification”  and  nearly  5,26%  in  uterine  carcinosarcomas.  The
               “mutation”  type  was  the  primary  Uterine  Corpus  Endometrial  Carcinomas,  which  show  an  alteration
               frequency  of  ~3,51%  (Fig.4).  Conclusion:  It  seems  FEN1  play  a  common  molecular  pathway  in  the
               pathogenesis  of  different  tumors.  But  still  remains  to  be  answered.  Our  pan-cancer  study  provides  a
               relatively comprehensive understanding of the roles of FEN1 in different tumorigenesis.













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