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Gene Review

MAGED4B  -  melanoma antigen family D, 4B

Homo sapiens

Synonyms: melanoma antigen family D4B
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Disease relevance of MAGED4


High impact information on MAGED4

  • A subset of highly homologous MAGE genes (group A; MAGE-A) belong to the chromosome X-clustered cancer/testis antigens [5].
  • We report here that these CpG are demethylated in the tumor cell lines that express MAGE-1, and are methylated in those that do not express the gene [6].
  • The two major MAGE-1 promoter elements have an Ets binding site, which contains a CpG dinucleotide [6].
  • Besides antigens known to elicit T-cell responses, such as MAGE-1 and tyrosinase, numerous additional antigens that were overexpressed or specifically expressed in tumors of the same type were identified [7].
  • MAGE-Xp is expressed only in testis and, unlike the Xq27-qter MAGE genes, it is not expressed in any of 12 different tumor tissues tested [8].

Chemical compound and disease context of MAGED4


Biological context of MAGED4

  • Three alternatively spliced variants (MAGE-E1a-c) were found, and deduced amino acid sequence showed that MAGE-E1a and -E1b shared the MAGE-conserved region, whereas -E1c did not [3].
  • Tissue distribution analysis showed that MAGE-E1 was distinct from other MAGEs [3].
  • Expressed sequence tags containing this tag were homologous to the melanoma-associated antigen gene (MAGE) family, and this new cDNA, named MAGE-E1, was cloned by the 5'-rapid amplification of cDNA ends technique [3].
  • The open reading frame encoding the MAGE-E1 peptides initiates in exon 2 and ends in exon 13 [11].
  • The MAGE-E1 gene is composed of 13 exons, and three of these (exon 2, exon 3 and exon 12) are alternatively spliced in each variant (E1a-c) [11].

Anatomical context of MAGED4

  • Real-time quantitative reverse transcription-PCR showed that MAGE-E1 expression was 2.6-15-fold enriched in glioblastoma relative to human astrocytes [3].
  • The four new MAGE genes are not expressed in normal tissues, except for testis, and are expressed in tumors of different histological origins [12].
  • The tumor origin of the cell lines was supported by the expression of the ErbB2 oncogene (seven of nine) and MAGE mRNA (eight of eight) [13].
  • The first human members of the MAGE gene family that have been described are expressed in tumor cells but silent in normal adult tissues except in the male germ line [14].
  • Analysis of primary prostate cancer revealed MAGE expression patterns considerably concordant with those found in the corresponding bone marrow aspirates [15].

Associations of MAGED4 with chemical compounds

  • Treatment with the DNA hypomethylating agent 5-aza-2'-deoxycytidine induced and up-regulated the mRNA expression of MAGE-1 and epitope presentation by autologous MHC [16].
  • The expression of cell cycle regulatory transcription factors E2F4 and the MAGE protein necdin were similarly altered in all subjects after rosiglitazone treatment [17].
  • The metabolic control of 11 brittle diabetic subjects, as assessed by the M value and the MAGE index (used as indexes of blood glucose control and of glycemic fluctuations, respectively), was compared during a 5-day period before and after a 24-h connection to the artificial pancreas [18].
  • In further analysis, we showed that treatment with brefeldin A or paraformaldehyde fixation of Epstein-Barr virus-transformed B cells prevented the presentation of the Mage 1 T cell epitope, which excluded extracellular processing of the antigen [19].
  • Subsequent to sodium bisulfite modification and MS-PCR analysis, the promoter hypomethylation of MAGE-A1 and MAGE-A3 was confirmed in both at 81% each [9].

Other interactions of MAGED4

  • These results suggest that MAGE-D and -E1 may be evolutionarily distant from other members of the MAGE family, and the two may be ancestral genes for the others [11].

Analytical, diagnostic and therapeutic context of MAGED4


  1. MAGED4-expression in renal cell carcinoma and identification of an HLA-A*25-restricted MHC class I ligand from solid tumor tissue. Krämer, B.F., Schoor, O., Krüger, T., Reichle, C., Müller, M., Weinschenk, T., Hennenlotter, J., Stenzl, A., Rammensee, H.G., Stevanovic, S. Cancer Biol. Ther. (2005) [Pubmed]
  2. Contrasting frequencies of antitumor and anti-vaccine T cells in metastases of a melanoma patient vaccinated with a MAGE tumor antigen. Lurquin, C., Lethé, B., De Plaen, E., Corbière, V., Théate, I., van Baren, N., Coulie, P.G., Boon, T. J. Exp. Med. (2005) [Pubmed]
  3. MAGE-E1, a new member of the melanoma-associated antigen gene family and its expression in human glioma. Sasaki, M., Nakahira, K., Kawano, Y., Katakura, H., Yoshimine, T., Shimizu, K., Kim, S.U., Ikenaka, K. Cancer Res. (2001) [Pubmed]
  4. CT10: a new cancer-testis (CT) antigen homologous to CT7 and the MAGE family, identified by representational-difference analysis. Güre, A.O., Stockert, E., Arden, K.C., Boyer, A.D., Viars, C.S., Scanlan, M.J., Old, L.J., Chen, Y.T. Int. J. Cancer (2000) [Pubmed]
  5. MAGE-A tumor antigens target p53 transactivation function through histone deacetylase recruitment and confer resistance to chemotherapeutic agents. Monte, M., Simonatto, M., Peche, L.Y., Bublik, D.R., Gobessi, S., Pierotti, M.A., Rodolfo, M., Schneider, C. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  6. The activation of human gene MAGE-1 in tumor cells is correlated with genome-wide demethylation. De Smet, C., De Backer, O., Faraoni, I., Lurquin, C., Brasseur, F., Boon, T. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  7. Human neoplasms elicit multiple specific immune responses in the autologous host. Sahin, U., Türeci, O., Schmitt, H., Cochlovius, B., Johannes, T., Schmits, R., Stenner, F., Luo, G., Schobert, I., Pfreundschuh, M. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  8. Isolation and characterization of a MAGE gene family in the Xp21.3 region. Muscatelli, F., Walker, A.P., De Plaen, E., Stafford, A.N., Monaco, A.P. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  9. Promoter hypomethylation and reactivation of MAGE-A1 and MAGE-A3 genes in colorectal cancer cell lines and cancer tissues. Kim, K.H., Choi, J.S., Kim, I.J., Ku, J.L., Park, J.G. World J. Gastroenterol. (2006) [Pubmed]
  10. The tumour-associated antigen MAGE-1 is detectable in formalin-fixed paraffin sections of malignant melanoma. Gudat, F., Zuber, M., Dürmüller, U., Kocher, T., Schaefer, C., Noppen, C., Spagnoli, G. Virchows Arch. (1996) [Pubmed]
  11. Structural characterization and chromosomal localization of the MAGE-E1 gene. Kawano, Y., Sasaki, M., Nakahira, K., Yoshimine, T., Shimizu, K., Wada, H., Ikenaka, K. Gene (2001) [Pubmed]
  12. MAGE-B5, MAGE-B6, MAGE-C2, and MAGE-C3: four new members of the MAGE family with tumor-specific expression. Lucas, S., De Plaen, E., Boon, T. Int. J. Cancer (2000) [Pubmed]
  13. Phenotypic characteristics of cell lines derived from disseminated cancer cells in bone marrow of patients with solid epithelial tumors: establishment of working models for human micrometastases. Putz, E., Witter, K., Offner, S., Stosiek, P., Zippelius, A., Johnson, J., Zahn, R., Riethmüller, G., Pantel, K. Cancer Res. (1999) [Pubmed]
  14. An overview of the MAGE gene family with the identification of all human members of the family. Chomez, P., De Backer, O., Bertrand, M., De Plaen, E., Boon, T., Lucas, S. Cancer Res. (2001) [Pubmed]
  15. Heterogeneous expression of MAGE-A genes in occult disseminated tumor cells: a novel multimarker reverse transcription-polymerase chain reaction for diagnosis of micrometastatic disease. Kufer, P., Zippelius, A., Lutterbüse, R., Mecklenburg, I., Enzmann, T., Montag, A., Weckermann, D., Passlick, B., Prang, N., Reichardt, P., Dugas, M., Köllermann, M.W., Pantel, K., Riethmüller, G. Cancer Res. (2002) [Pubmed]
  16. HER-2, gp100, and MAGE-1 are expressed in human glioblastoma and recognized by cytotoxic T cells. Liu, G., Ying, H., Zeng, G., Wheeler, C.J., Black, K.L., Yu, J.S. Cancer Res. (2004) [Pubmed]
  17. Necdin and E2F4 are modulated by rosiglitazone therapy in diabetic human adipose and muscle tissue. Goldfine, A.B., Crunkhorn, S., Costello, M., Gami, H., Landaker, E.J., Niinobe, M., Yoshikawa, K., Lo, D., Warren, A., Jimenez-Chillaron, J., Patti, M.E. Diabetes (2006) [Pubmed]
  18. Use of an artificial pancreas as a tool to determine subcutaneous insulin doses in juvenile diabetes. Lambert, A.E., Buysschaert, M., Lambotte, L. Diabetes Care (1979) [Pubmed]
  19. Major histocompatibility complex class I presentation of exogenous soluble tumor antigen fused to the B-fragment of Shiga toxin. Lee, R.S., Tartour, E., van der Bruggen, P., Vantomme, V., Joyeux, I., Goud, B., Fridman, W.H., Johannes, L. Eur. J. Immunol. (1998) [Pubmed]
  20. Expression of gene MAGE-A4 in Reed-Sternberg cells. Chambost, H., Van Baren, N., Brasseur, F., Godelaine, D., Xerri, L., Landi, S.J., Theate, I., Plumas, J., Spagnoli, G.C., Michel, G., Coulie, P.G., Olive, D. Blood (2000) [Pubmed]
  21. Frequent cytolytic T-cell responses to peptide MAGE-A10(254-262) in melanoma. Valmori, D., Dutoit, V., Rubio-Godoy, V., Chambaz, C., Liénard, D., Guillaume, P., Romero, P., Cerottini, J.C., Rimoldi, D. Cancer Res. (2001) [Pubmed]
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