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Gene Review:

CTAG1B - cancer/testis antigen 1B

Homo sapiens

Synonyms: CT6.1, CTAG, CTAG1, ESO1, LAGE-2, ...

Jäger, E. et al., Hong, J.A. et al., Chen, Y.T. et al., Li, M. et al., Batchu, R.B. et al., et al.

Söling, Schurr, Berthold, Atanackovic, Arfsten, Cao, Gnjatic, Schnieders, Bartels, Schilling, Faltz, Wolschke, Dierlamm, Ritter, Eiermann, Hossfeld, Zander, Jungbluth, Old, Bokemeyer, Kröger, Gnjatic, Atanackovic, Jäger, Matsuo, Selvakumar, Altorki, Maki, Dupont, Ritter, Chen, Knuth, Old, van Rhee, Szmania, Zhan, Gupta, Pomtree, Lin, Batchu, Moreno, Spagnoli, Shaughnessy, Tricot, Zeng, Aldridge, Tian, Seiler, Zhang, Jin, Rao, Li, Chen, Langford, Duggan, Belldegrun, Dubinett, Chen, Boyer, Viars, Tsang, Old, Arden, Jäger, Jäger, Karbach, Chen, Ritter, Nagata, Gnjatic, Stockert, Arand, Old, Knuth,

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Disease relevance of CTAG1B

Lung cancers exhibit genome-wide demethylation associated with derepression of a specific class of genes encoding cancer-testis (CT) antigens such as NY-ESO-1 [1].
Cotransfection experiments using promoter-reporter constructs confirmed that BORIS modulates NY-ESO-1 expression in lung cancer cells [1].
NY-ESO-1 gene may serve as a marker for local metastasis and advanced disease [2].
Recombinant virus of pMV-NY-ESO-1 was generated with vesicular stomatitis virus G envelope protein (VSV-G) in the GP2-293 cell line for efficient transduction [3].
CTAG was initially cloned from an esophageal squamous cell carcinoma cDNA expression library by immunoscreening with autologous patient's serum [4].

High impact information on CTAG1B

To identify possible epitopes presented by distinct HLA class II alleles, overlapping 18-mer peptides derived from NY-ESO-1 were synthetized and tested for recognition by CD4(+) T lymphocytes in autologous settings [5].
NY-ESO-1 is a member of the cancer-testis family of tumor antigens that elicits strong humoral and cellular immune responses in patients with NY-ESO-1-expressing cancers [5].
We identified three NY-ESO-1-derived peptides presented by DRB4*0101-0103 and recognized by CD4(+) T lymphocytes of two melanoma patients sharing these HLA class II alleles [5].
Autologous monocyte-derived dendritic cells of cancer patients were incubated with recombinant NY-ESO-1 protein and used in enzyme-linked immunospot (ELISPOT) assays to detect NY-ESO-1-specific CD4(+) T lymphocyte responses [5].
Since CD4(+) T lymphocytes play a critical role in generating antigen-specific cytotoxic T lymphocyte and antibody responses, we searched for NY-ESO-1 epitopes presented by histocompatibility leukocyte antigen (HLA) class II molecules [5].

Chemical compound and disease context of CTAG1B

Quantitative reverse transcription-PCR analysis revealed robust, coincident induction of BORIS and NY-ESO-1 expression in lung cancer cells, but not normal human bronchial epithelial cells following 5-aza-2'-deoxycytidine (5-azadC), Depsipeptide FK228 (DP), or sequential 5-azadC/DP exposure under clinically relevant conditions [1].

Biological context of CTAG1B

We present evidence that the DC phenotype is unaltered after transduction and that more than 85% of DCs express NY-ESO-1, which secrete approximately 40 ng of GM-CSF per 10(6) DCs [3].
Serological and biochemical analyses identified a de novo expression of NY-ESO-1 protein and a concomitant and persistent upregulation of HLA class I antigens and of HLA-A1 and -A2 alleles [6].
Genomic cloning and localization of CTAG, a gene encoding an autoimmunogenic cancer-testis antigen NY-ESO-1, to human chromosome Xq28 [4].
In this paper, we report on a melanoma patient with a high-titer antibody response against the "cancer-testis" antigen NY-ESO-1 [7].
Simultaneous humoral and cellular immune response against cancer-testis antigen NY-ESO-1: definition of human histocompatibility leukocyte antigen (HLA)-A2-binding peptide epitopes [7].

Anatomical context of CTAG1B

High-level expression of cancer/testis antigen NY-ESO-1 and human granulocyte-macrophage colony-stimulating factor in dendritic cells with a bicistronic retroviral vector [3].
In our study, NY-ESO-1 mRNA was found to express in 9.9% of the samples, and also correlated significantly with stages (P = 0.041) and local lymph node metastasis (P = 0.002) [2].
CTAG mRNA is expressed in a proportion of human cancers in a lineage-nonspecific fashion, whereas its expression in normal tissues is restricted to testis and ovary only [4].
Concurrently, a strong MHC class I-restricted CTL reactivity against the autologous NY-ESO-1-positive tumor cell line was found [7].
None of the 18 patients that tested seronegative for NY-ESO-1 had detectable CD4+ T cell responses [8].

Associations of CTAG1B with chemical compounds

NY-ESO-1 gene expression was associated with age older than one year (p = 0.017), more differentiated tumor histology (p = 0.044), elevated urinary vanillylmandelic acid (VMA, p = 0.018) and normal serum ferritin levels (p = 0.023) [9].
A consensus 5' splice sequence reads /GTAGAGT while the 3' splice sequence is pyrimidine rich and contains CTAG/ at the splice junction [10].
The fine specificity of interaction between peptide NY-ESO-1 C165A, HLA-A*0201, and T-cell receptor was analyzed at the molecular level using a series of variant peptides containing single alanine substitutions [11].
In vitro stimulation of CD8 and CD4 T cells by dendritic cells loaded with a complex of cholesterol-bearing hydrophobized pullulan and NY-ESO-1 protein: Identification of a new HLA-DR15-binding CD4 T-cell epitope [12].
The site selectivity of TOTO for the CTAG-CTAG site is explained by its ability to adapt to the base pair propeller twist of dsDNA to optimize stacking and the hydrophobic interaction between the thymidine methyl group and the benzothiazole ring [13].

Physical interactions of CTAG1B

In contrast, CD34-derived DCs were unable to process either soluble or immune complexed NY-ESO-1, although they efficiently presented preprocessed NY-ESO-1 peptides [14].
Both were specific for NY-ESO-1 because neither bound to homologous LAGE-1 peptides despite 84% overall amino acid homology [15].

Regulatory relationships of CTAG1B

CTp11 tended to be expressed by primary melanomas and NY-ESO-1 by metastatic samples (P < 0.02) [16].
T cells specific to these epitopes not only recognized autologous dendritic cells loaded with NY-ESO-1 but also NY-ESO-1-expressing tumor cell lines treated with IFN-gamma [17].
Calreticulin Abs blocked NY-ESO-1 binding on immature DC and its cross-presentation to CD8(+) T cells in vitro [18].

Other interactions of CTAG1B

CONCLUSIONS: These results suggested that CT genes, especially NY-ESO-1 and LAGE-1, do express in CRC [2].
Analyzing patients with MM (n = 66) for antibody responses against MAGEA3, SSX2, and NY-ESO-1, we found strong antibody responses against CT antigens preferentially in patients who had received allogeneic stem cell transplantation (alloSCT) [19].
MAGE-A, BAGE and NY-ESO-1/LAGE-1 mRNAs were the most frequently detected, respectively in 5677%, 212% and 89% of superficial and in 6461%, 4139% and 276% of invasive tumours [20].
The favorable prognostic effect of intraepithelial CD8+ TILs did not correlate with concurrent expression of NY-ESO-1 or MAGE antigens [21].
We compared the abilities of human monocyte-derived DCs and DCs derived in vitro from CD34-positive stem cells to present NY-ESO-1 epitopes to MHC class I-restricted cytotoxic T cells [14].

Analytical, diagnostic and therapeutic context of CTAG1B

To confirm the protein expression, immunohistochemistry was done for detecting the NY-ESO-1 antigen in mRNA-positive CRC tissues [2].
The presence of autologous antibodies against NY-ESO-1 was examined in serum samples by ELISA [2].
This expression pattern suggests that the CTAG product (NY-ESO-1) is an aberrantly activated tumor antigen and can potentially be an antigenic target for tumor vaccination [4].
NY-ESO-1 should therefore be an ideal tumor target antigen for immunotherapy of patients with poor-prognosis MM [22].
Expression of NY-ESO-1 in EOC was demonstrated by RT-PCR and/or IHC in 82 of 190 (43%) specimens [23].

References

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Expression profile of cancer-testis genes in 121 human colorectal cancer tissue and adjacent normal tissue. Li, M., Yuan, Y.H., Han, Y., Liu, Y.X., Yan, L., Wang, Y., Gu, J. Clin. Cancer Res. (2005) [Pubmed]
High-level expression of cancer/testis antigen NY-ESO-1 and human granulocyte-macrophage colony-stimulating factor in dendritic cells with a bicistronic retroviral vector. Batchu, R.B., Moreno, A.M., Szmania, S., Gupta, S.K., Zhan, F., Rosen, N., Kozlowski, M., Spencer, T., Spagnoli, G.C., Shaughnessy, J., Barlogie, B., Tricot, G., van Rhee, F. Hum. Gene Ther. (2003) [Pubmed]
Genomic cloning and localization of CTAG, a gene encoding an autoimmunogenic cancer-testis antigen NY-ESO-1, to human chromosome Xq28. Chen, Y.T., Boyer, A.D., Viars, C.S., Tsang, S., Old, L.J., Arden, K.C. Cytogenet. Cell Genet. (1997) [Pubmed]
Identification of NY-ESO-1 epitopes presented by human histocompatibility antigen (HLA)-DRB4*0101-0103 and recognized by CD4(+) T lymphocytes of patients with NY-ESO-1-expressing melanoma. Jäger, E., Jäger, D., Karbach, J., Chen, Y.T., Ritter, G., Nagata, Y., Gnjatic, S., Stockert, E., Arand, M., Old, L.J., Knuth, A. J. Exp. Med. (2000) [Pubmed]
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