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Gene Review

GML  -  glycosylphosphatidylinositol anchored...

Homo sapiens

Synonyms: Glycosyl-phosphatidylinositol-anchored molecule-like protein, LY6DL
 
 
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Disease relevance of GML

 

High impact information on GML

  • As the predicted amino acid sequence showed a high degree of homology to the family of glycosyl-phosphatidylinositol (GPI)-anchored membrane proteins, we termed this gene GML (GPI-anchored molecule-like protein) [1].
  • For Ly-6H, GML and G6C, no or very low expression was observed in keratinocytes and HNSCC [6].
  • GML gene expression was detected in 9 (30%) samples [3].
  • The GML gene (glycosylphosphatidylinositol-anchored molecule-like protein gene) is a novel gene specifically induced by wild-type p53, which may participate in cell cycle control or the cell apoptotic pathway [3].
  • HemT-3 cDNA has a major open reading frame related to a human glycosylphosphatidylinositol (GPI)-anchored protein, GML [7].
 

Chemical compound and disease context of GML

  • CONCLUSION: GML expression and p53 mutation in colorectal cancer may be useful predictive genetic markers for sensitivity to MMC and 5-FU, respectively [8].
 

Biological context of GML

  • A correlation between the presence of GML expression and the sensitivity of esophageal cancer cells to anti-cancer drugs implied that the gene product plays a significant role in the apoptotic pathway or cell-cycle regulation induced by p53 after DNA damage [1].
  • FISH analysis revealed that the GML gene is located on human chromosome 8q24 [9].
  • The GML gene consists of four exons; and the p53-binding sequence is present in the 5'-flanking region [9].
  • To characterize the GML gene further, we determined 35.8 kb of DNA sequence that included a consensus binding sequence for p53 and the entire GML gene [9].
  • Further investigation demonstrated that GML expression enhances G2/M arrest and apoptosis induced by gamma-irradiation [4].
 

Anatomical context of GML

  • We analyzed a randomly selected series of 130 gastric biopsies with histologically described lymphoid follicle formation and investigated these for the prevalence of B-cell clonality using different PCR-based methods to discuss its usefulness in the differential diagnosis of GML [10].
  • B-cell clonality, assessed by PCR for amplification of the VDJ region of the immunoglobulin heavy chain gene (IgH), is used to support the diagnosis of gastric mucosa-associated lymphoid tissue (MALT) lymphoma (GML) [10].
  • The introduction of GML cDNA to RPMI4788 (RPMI4788-GML) showed that the sensitivity of RPMI4788-GML to MMC was enhanced almost to the level of HCT116 cells [8].
  • In the woman the mammary gland was investigated in the little girl (GMF), in the adult nonpregnant woman (GMA), during the first trimester of pregnancy (GMG), during lactation (GML), during climacterium (GMM), in glandular carcinomas of the adult female (GMAC) and during menopause (GMMC) [11].
 

Associations of GML with chemical compounds

  • To investigate the function of GML further, we introduced the GML cDNA into various cancer cell lines under control of the tetracycline-regulated system [5].
  • For 5-FU treatment with 24-h exposure, HCT116 showed the highest sensitivity, and SW837, which had p53 mutations without expression of GML, showed the lowest sensitivity [8].
 

Analytical, diagnostic and therapeutic context of GML

References

  1. Isolation of a novel GPI-anchored gene specifically regulated by p53; correlation between its expression and anti-cancer drug sensitivity. Furuhata, T., Tokino, T., Urano, T., Nakamura, Y. Oncogene (1996) [Pubmed]
  2. Prognostic value of translocation t(11;18) in tumoral response of low-grade gastric lymphoma of mucosa-associated lymphoid tissue type to oral chemotherapy. Lévy, M., Copie-Bergman, C., Gameiro, C., Chaumette, M.T., Delfau-Larue, M.H., Haioun, C., Charachon, A., Hemery, F., Gaulard, P., Leroy, K., Delchier, J.C. J. Clin. Oncol. (2005) [Pubmed]
  3. p53-regulated GML gene expression in non-small cell lung cancer. a promising relationship to cisplatin chemosensitivity. Higashiyama, M., Miyoshi, Y., Kodama, K., Yokouchi, H., Takami, K., Nishijima, M., Nakayama, T., Kobayashi, H., Minamigawa, K., Nakamura, Y. Eur. J. Cancer (2000) [Pubmed]
  4. Overexpression of GML promotes radiation-induced cell cycle arrest and apoptosis. Kagawa, K., Inoue, T., Tokino, T., Nakamura, Y., Akiyama, T. Biochem. Biophys. Res. Commun. (1997) [Pubmed]
  5. Induction of apoptosis in T98G glioblastoma cells by transfection of GML, a p53 target gene. Ueda, K., Miyoshi, Y., Tokino, T., Watatani, M., Nakamura, Y. Oncol. Res. (1999) [Pubmed]
  6. Characterization of the human Ly-6 antigens, the newly annotated member Ly-6K included, as molecular markers for head-and-neck squamous cell carcinoma. de Nooij-van Dalen, A.G., van Dongen, G.A., Smeets, S.J., Nieuwenhuis, E.J., Stigter-van Walsum, M., Snow, G.B., Brakenhoff, R.H. Int. J. Cancer (2003) [Pubmed]
  7. HemT-3, an alternative transcript of mouse gene HemT specific to male germ cells. Xue, H., O'Neill, D., Wang, X., Wolgemuth, D.J., Bank, A. Gene (1999) [Pubmed]
  8. The potential clinical value of GML and the p53 gene as a predictor of chemosensitivity for colorectal cancer. Hashimoto, Y., Ueda, K., Minami, K., Watatani, M. Int. J. Clin. Oncol. (2001) [Pubmed]
  9. Genomic structure and chromosomal localization of GML (GPI-anchored molecule-like protein), a gene induced by p53. Kimura, Y., Furuhata, T., Urano, T., Hirata, K., Nakamura, Y., Tokino, T. Genomics (1997) [Pubmed]
  10. Clonality analyses in gastric MALT (mucosa-associated lymphoid tissue). Steiff, J.N., Neubauer, A., Stolte, M., Wündisch, T. Pathol. Res. Pract. (2006) [Pubmed]
  11. Relationships between specialized cells, capillaries and intermediary cyto-fibrillary stroma. Note 6. The capillary stereotype and the factors which influence it. Mârza, V.D., Bogdan, F., Bălan, R. Morphologie et embryologie. (1975) [Pubmed]
  12. GPI-anchored molecule-like protein (GML) expression in non-small cell lung cancer (NSCLC). Komiya, T., Hirashima, T., Kikui, M., Fukuoka, M., Ohno, A., Kawase, I. Anticancer Res. (1999) [Pubmed]
 
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