The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Gene Review

MDS1  -  myelodysplasia syndrome 1

Homo sapiens

This record was replaced with 2122.
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of MDS1


High impact information on MDS1


Biological context of MDS1

  • EVI-1 and its variant form, MDS1/EVI1, have been reported to act in an antagonistic manner and be differentially regulated in samples from patients with acute myeloid leukaemia and rearrangements of the long arm of chromosome 3 [7].
  • The resulting chimeric transcript consists of the first two exons of ETV6 fused to MDS1 sequences, which in turn is fused to the second exon of the EVI1 gene [2].
  • Furthermore, a comparison can be made with the formation of an AML1/MDS1/EVI1 fusion gene in translocations (3;21)(q26;q22) [2].
  • In this study, genes were searched near the breakpoints at 1p36.3, and a novel gene was isolated that encoded a zinc finger protein with a PR domain, which is highly homologous to the MDS1/EVI1 gene [8].
  • The novel gene, designated as MEL1 (MDS1/EVI1-like gene 1), with 1257 amino acid residues is 64% similar in nucleotide and 63% similar in amino acid sequences to MDS1/EVI1 with the same domain structure [8].

Anatomical context of MDS1


Associations of MDS1 with chemical compounds


Other interactions of MDS1

  • AME is obtained by in-frame fusion of the AML1 and MDS1/EVI1 genes [12].
  • In some of these samples, MDS1/EVI1 was also transcribed at elevated levels compared to those of healthy controls [13].
  • The two genes are EAP, which codes for the abundant ribosomal protein L22, and MDS1, which encodes a small polypeptide of unknown function [14].
  • We identified rare structural rearrangements in childhood acute myeloblastic leukemia, involving 3q21 and 3q26 loci around RPN1 and MDS1/EVI1 respectively [15].
  • For all protocols, the immunostained cells were visualized by the same alkaline-phosphatase (AP) detection system (APAAP) followed by detection of the cells by manual screening and by two different automated screening systems (ACIS from Chromavision and MDS1 from Applied Imaging) [16].

Analytical, diagnostic and therapeutic context of MDS1

  • In our analysis of 702 integration sites in rhesus macaques that underwent transplantation up to 7 years earlier with autologous CD34+ cells transduced with amphotropic murine leukemia virus (MLV)-derived retroviral vectors containing marker genes, we detected insertion into one locus, the Mds1/Evi1 region, a total of 14 times in 9 animals [10].
  • To discriminate between EVI1 and MDS1-EVI1 transcripts, distinct real-time quantitative polymerase chain reaction (PCR) assays were developed [17].


  1. Intergenic splicing of MDS1 and EVI1 occurs in normal tissues as well as in myeloid leukemia and produces a new member of the PR domain family. Fears, S., Mathieu, C., Zeleznik-Le, N., Huang, S., Rowley, J.D., Nucifora, G. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  2. Fusion of ETV6 to MDS1/EVI1 as a result of t(3;12)(q26;p13) in myeloproliferative disorders. Peeters, P., Wlodarska, I., Baens, M., Criel, A., Selleslag, D., Hagemeijer, A., Van den Berghe, H., Marynen, P. Cancer Res. (1997) [Pubmed]
  3. Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML. Cuenco, G.M., Nucifora, G., Ren, R. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  4. Targeted Degradation of the AML1/MDS1/EVI1 Oncoprotein by Arsenic Trioxide. Shackelford, D., Kenific, C., Blusztajn, A., Waxman, S., Ren, R. Cancer Res. (2006) [Pubmed]
  5. 16S rDNA sequence and phylogenetic position of an uncultivated spirochete from the hindgut of the termite Mastotermes darwiniensis Froggatt. Berchtold, M., Ludwig, W., König, H. FEMS Microbiol. Lett. (1994) [Pubmed]
  6. Correction of X-linked chronic granulomatous disease by gene therapy, augmented by insertional activation of MDS1-EVI1, PRDM16 or SETBP1. Ott, M.G., Schmidt, M., Schwarzwaelder, K., Stein, S., Siler, U., Koehl, U., Glimm, H., Kühlcke, K., Schilz, A., Kunkel, H., Naundorf, S., Brinkmann, A., Deichmann, A., Fischer, M., Ball, C., Pilz, I., Dunbar, C., Du, Y., Jenkins, N.A., Copeland, N.G., Lüthi, U., Hassan, M., Thrasher, A.J., Hoelzer, D., von Kalle, C., Seger, R., Grez, M. Nat. Med. (2006) [Pubmed]
  7. The leukaemia-associated transcription factors EVI-1 and MDS1/EVI1 repress transcription and interact with histone deacetylase. Vinatzer, U., Taplick, J., Seiser, C., Fonatsch, C., Wieser, R. Br. J. Haematol. (2001) [Pubmed]
  8. A novel gene, MEL1, mapped to 1p36.3 is highly homologous to the MDS1/EVI1 gene and is transcriptionally activated in t(1;3)(p36;q21)-positive leukemia cells. Mochizuki, N., Shimizu, S., Nagasawa, T., Tanaka, H., Taniwaki, M., Yokota, J., Morishita, K. Blood (2000) [Pubmed]
  9. Establishment of a novel human myeloid leukaemia cell line (HNT-34) with t(3;3)(q21;q26), t(9;22)(q34;q11) and the expression of EVI1 gene, P210 and P190 BCR/ABL chimaeric transcripts from a patient with AML after MDS with 3q21q26 syndrome. Hamaguchi, H., Suzukawa, K., Nagata, K., Yamamoto, K., Yagasaki, F., Morishita, K. Br. J. Haematol. (1997) [Pubmed]
  10. Recurrent retroviral vector integration at the Mds1/Evi1 locus in nonhuman primate hematopoietic cells. Calmels, B., Ferguson, C., Laukkanen, M.O., Adler, R., Faulhaber, M., Kim, H.J., Sellers, S., Hematti, P., Schmidt, M., von Kalle, C., Akagi, K., Donahue, R.E., Dunbar, C.E. Blood (2005) [Pubmed]
  11. Quantitative analysis of bone marrow CD34 cells in aplastic anemia and hypoplastic myelodysplastic syndromes. Matsui, W.H., Brodsky, R.A., Smith, B.D., Borowitz, M.J., Jones, R.J. Leukemia (2006) [Pubmed]
  12. The leukemia-associated transcription repressor AML1/MDS1/EVI1 requires CtBP to induce abnormal growth and differentiation of murine hematopoietic cells. Senyuk, V., Chakraborty, S., Mikhail, F.M., Zhao, R., Chi, Y., Nucifora, G. Oncogene (2002) [Pubmed]
  13. Quantitative comparison of the expression of EVI1 and its presumptive antagonist, MDS1/EVI1, in patients with myeloid leukemia. Vinatzer, U., Mannhalter, C., Mitterbauer, M., Gruener, H., Greinix, H., Schmidt, H.H., Fonatsch, C., Wieser, R. Genes Chromosomes Cancer (2003) [Pubmed]
  14. Rearrangement of the AML1/CBFA2 gene in myeloid leukemia with the 3;21 translocation: expression of co-existing multiple chimeric genes with similar functions as transcriptional repressors, but with opposite tumorigenic properties. Zent, C., Kim, N., Hiebert, S., Zhang, D.E., Tenen, D.G., Rowley, J.D., Nucifora, G. Curr. Top. Microbiol. Immunol. (1996) [Pubmed]
  15. Multipoint interphase FISH analysis of chromosome 3 abnormalities in 28 childhood AML patients. Haltrich, I., Kost-Alimova, M., Kovács, G., Klein, G., Fekete, G., Imreh, S. Eur. J. Haematol. (2006) [Pubmed]
  16. A European interlaboratory testing of three well-known procedures for immunocytochemical detection of epithelial cells in bone marrow. Results from analysis of normal bone marrow. Borgen, E., Pantel, K., Schlimok, G., M??ller, P., Otte, M., Renolen, A., Ehnle, S., Coith, C., Nesland, J.M., Naume, B. Cytometry. Part B, Clinical cytometry. (2006) [Pubmed]
  17. High EVI1 expression predicts poor survival in acute myeloid leukemia: a study of 319 de novo AML patients. Barjesteh van Waalwijk van Doorn-Khosrovani, S., Erpelinck, C., van Putten, W.L., Valk, P.J., van der Poel-van de Luytgaarde, S., Hack, R., Slater, R., Smit, E.M., Beverloo, H.B., Verhoef, G., Verdonck, L.F., Ossenkoppele, G.J., Sonneveld, P., de Greef, G.E., Löwenberg, B., Delwel, R. Blood (2003) [Pubmed]
WikiGenes - Universities