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Gene Review

WT1-AS  -  WT1 antisense RNA

Homo sapiens

Synonyms: WIT-1, WIT1, WT1-AS1, WT1AS, Wilms tumor-associated antisense RNA
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Disease relevance of WIT1


High impact information on WIT1

  • Complementary DNA clones representing transcripts of 2.5 (WIT-1) and 3.5 kb (WIT-2) mapping to this region were isolated from a kidney complementary DNA library [6].
  • However, seven of eight (87.5%) diagnostic BM samples from primary refractory AML (chemosensitive) showed methylation of WIT-1 [2].
  • Sequence analysis showed that the spot represented a portion of the WIT-1 gene on human chromosome 11p13 [2].
  • Rp18 was missing in the relapse sample due to a distinct DNA methylation pattern of the WIT-1 gene [2].
  • Twenty-seven AML patients that entered CR after therapy (i.e., chemosensitive) were studied and only 10 (37%) of the diagnostic bone marrow (BM) samples showed methylation of WIT-1 [2].

Biological context of WIT1

  • The other transcript, WIT1, encodes a product of unknown function that is subject to alternate splicing in the region immediately 5' of the WT1 gene [7].
  • In one case this was coincident with reduction of WT1 and WIT1 gene expression, and in 3 other cases it occurred in addition to 11p LOH [8].
  • The cloning and molecular characterization of two putative tumor genes, WT1 and WIT1, from the chromosome 11p13 region has provided a means of evaluating their role in the generation of Wilms' tumor heterogeneity [1].
  • We conclude that SNPs in WT1 and WIT1 genes are significantly associated with FSGS, suggesting that variants in these genes may mediate pathogenesis by altering WT1 function [9].
  • Wit1 promoter activity was identified in a DNA fragment extending from 200 bp upstream of the putative Wit1 TATA box to 130 bp downstream [10].

Anatomical context of WIT1


Other interactions of WIT1


Analytical, diagnostic and therapeutic context of WIT1

  • In situ hybridization using antisense RNA probes showed that WT1 and WIT1 were concordantly expressed in normal fetal kidney and in the blastema of tumors [1].
  • A series of 29 tumors were analyzed for WT1 and WIT1 expression by Northern blot or RNase protection analyses, and results were compared with tumor histopathology [1].
  • To test whether genetic variations in WT1 and WIT1 (gene immediately 5' to WT1) associate with focal segmental glomerulosclerosis (FSGS), patients with biopsy-proven idiopathic and HIV-1-associated FSGS were enrolled in a multicenter study [9].


  1. Coordinate expression of Wilms' tumor genes correlates with Wilms' tumor phenotypes. Yeger, H., Cullinane, C., Flenniken, A., Chilton-MacNeil, S., Campbell, C., Huang, A., Bonetta, L., Coppes, M.J., Thorner, P., Williams, B.R. Cell Growth Differ. (1992) [Pubmed]
  2. Restriction landmark genome scanning for aberrant methylation in primary refractory and relapsed acute myeloid leukemia; involvement of the WIT-1 gene. Plass, C., Yu, F., Yu, L., Strout, M.P., El-Rifai, W., Elonen, E., Knuutila, S., Marcucci, G., Young, D.C., Held, W.A., Bloomfield, C.D., Caligiuri, M.A. Oncogene (1999) [Pubmed]
  3. Ectopic production of erythropoietin in Wilms tumor patients in relation to clinical stage and disease activity. Murphy, G.P., Mirand, E.A., Sinks, L.F., Allen, J.E., Staubitz, W.J. J. Urol. (1975) [Pubmed]
  4. Wilms tumor extending into the dilated renal pelvis as a mold. Chiba, T., Ohashi, E. J. Urol. (1980) [Pubmed]
  5. Sarcomatous Wilms tumor associated with consumption coagulopathy. Ogawa, Y., Yazaki, T., Kano, S., Takahashi, M., Ohkawa, H., Hanada, T., Yabuta, K., Ishikawa, S., Takahashi, S., Kitagawa, R., Kenmotsu, H., Sawaguchi, S., Takita, H. Urology (1983) [Pubmed]
  6. Tissue, developmental, and tumor-specific expression of divergent transcripts in Wilms tumor. Huang, A., Campbell, C.E., Bonetta, L., McAndrews-Hill, M.S., Chilton-MacNeill, S., Coppes, M.J., Law, D.J., Feinberg, A.P., Yeger, H., Williams, B.R. Science (1990) [Pubmed]
  7. Antisense transcripts and protein binding motifs within the Wilms tumour (WT1) locus. Campbell, C.E., Huang, A., Gurney, A.L., Kessler, P.M., Hewitt, J.A., Williams, B.R. Oncogene (1994) [Pubmed]
  8. Loss of heterozygosity mapping in Wilms tumor indicates the involvement of three distinct regions and a limited role for nondisjunction or mitotic recombination. Coppes, M.J., Bonetta, L., Huang, A., Hoban, P., Chilton-MacNeill, S., Campbell, C.E., Weksberg, R., Yeger, H., Reeve, A.E., Williams, B.R. Genes Chromosomes Cancer (1992) [Pubmed]
  9. Variants in the Wilms' tumor gene are associated with focal segmental glomerulosclerosis in the African American population. Orloff, M.S., Iyengar, S.K., Winkler, C.A., Goddard, K.A., Dart, R.A., Ahuja, T.S., Mokrzycki, M., Briggs, W.A., Korbet, S.M., Kimmel, P.L., Simon, E.E., Trachtman, H., Vlahov, D., Michel, D.M., Berns, J.S., Smith, M.C., Schelling, J.R., Sedor, J.R., Kopp, J.B. Physiol. Genomics (2005) [Pubmed]
  10. Characterization of the transcriptional regulatory region of the human WT1 gene. Hofmann, W., Royer, H.D., Drechsler, M., Schneider, S., Royer-Pokora, B. Oncogene (1993) [Pubmed]
  11. Transcriptomic and proteomic responses of human renal HEK293 cells to uranium toxicity. Prat, O., Berenguer, F., Malard, V., Tavan, E., Sage, N., Steinmetz, G., Quemeneur, E. Proteomics (2005) [Pubmed]
  12. Wilms tumor associated with elevated alpha-fetoprotein level. Erol, K., Vedat, K., Erkan, D., Mustafa, G., Duygu, H., Avni, A.A., Suzi, D. Pediatric blood & cancer. (2005) [Pubmed]
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