MAGE-A3/4 and NY-ESO-1 antigens expression in metastatic esophageal squamous cell carcinoma

Bujas, Tatjana; Marušić, Zlatko; Balja, Melita Perić; Mijić, August; Krušlin, Božo; Tomas, Davor

doi:10.4081/ejh.2011.e7

Cited by 32 publications

(28 citation statements)

References 25 publications

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“…comparable to those reported previously [11,12,[21][22][23][24][25][26][27]. Among the 585 tumour samples, 214 oesophageal cancer samples were evaluable for the expression of all 3 CT antigens.…”

Section: Eso-1 And/or Sage Expression the Mage-a Ny-eso-1 And Sagesupporting

confidence: 84%

“…We identified 5 reports about the co-expression of CT antigens in oesophageal cancer in international journals. Among these 5 reports, 4 assessed CT antigen expression by immunohistochemistry (IHC) [21,22,24,25] and 1 assessed it by PCR [23]. IHC can be performed on formalin-fixed, paraffinembedded samples, enabling us to study a large number of samples retrospectively.…”

Section: Eso-1 And/or Sage Expression the Mage-a Ny-eso-1 And Sagementioning

confidence: 99%

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MAGE-A4, NY-ESO-1 and SAGE expression rates and co-expression relationships in solid tumours

Ishihara

Kageyama

Miyahara

et al. 2020

Preprint

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Abstract Background Cancer testis (CT) antigens are promising targets for cancer immunotherapies such as cancer vaccines and genetically modified adoptive T cell therapy. In this study, we evaluated the expression of three CT antigens, melanoma-associated antigen A4 (MAGE-A4), New York oesophageal squamous cell carcinoma 1 (NY-ESO-1) and sarcoma antigen gene (SAGE). Methods MAGE-A4, NY-ESO-1 and/or SAGE antigen expression in tumour samples was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). Informed consent was obtained from individuals prior to study enrolment. Results In total, 585 samples in 21 tumour types were evaluated between June 2009 and March 2018. The positive expression rates of these CT antigens were as follows: MAGE-A4, 34.6% (range, 30.7-38.7); NY-ESO-1, 21.0% (range, 17.2-25.1); and SAGE, 21.8% (range, 18.5-25.4). The MAGE-A4 antigen was expressed in 54.9% of oesophageal cancers, 37.5% of head and neck cancers, 35.0% of gastric cancers and 34.2% of ovarian cancers; the NY-ESO-1 antigen was expressed in 28.6% of lung cancers, 25.3% of oesophageal cancers and 22.6% of ovarian cancers; and the SAGE antigen was expressed in 35.3% of prostate cancers, 32.9% of oesophageal cancers and 26.3% of ovarian cancers. The most common tumour type was oesophageal cancer in this study. MAGE-A4, NY-ESO-1 and SAGE antigen expression were assessed in 214 oesophageal cancer samples, among which 24 (11.2%) were triple-positive, 58 (27.1%) were positive for any two, 59 (27.6%) were positive for any one, and 73 (34.1%) were triple-negative. Conclusions Oesophageal cancer exhibited a relatively high rate of CT antigen positivity. Our data indicate that oesophageal cancer is a promising candidate tumour for CT antigen-targeting immunotherapy and immune monitoring.

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Section: Eso-1 And/or Sage Expression the Mage-a Ny-eso-1 And Sagesupporting

confidence: 84%

Section: Eso-1 And/or Sage Expression the Mage-a Ny-eso-1 And Sagementioning

confidence: 99%

MAGE-A4, NY-ESO-1 and SAGE expression rates and co-expression relationships in solid tumours

Ishihara

Kageyama

Miyahara

et al. 2020

Preprint

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“…Desmoplastic melanoma 3/32 (9%)/IHC/E978 [56] Primary tumor 45%/IHC/E978 [35] Metastatic tumor 45%/IHC/E978 50/120 (42%)/qRT-PCR 48/120 (40%)/IHC/E978 [143] Stage I and stage II primary cutaneous melanoma 120/321(37%)/IHC/E978 [73] 12/38 (38%)/TMA (IHC) [114] Metastatic tumor 14/63 (23%)/RT-PCR [145] 10/23 (44%)/RT-PCR [146] 143/202 (71%)/RT-PCR [147] Melanoma Metastatic Humoral response in 12/127 (9.4%)/ELISA [94] Humoral response in 3/44 (7%)/ SEREX [148] 2/9 (2%)/RT-PCR Humoral response in 2/9 (2%)/ ELISA CD8 + T-cell responses/ ELISPOT [149] Humoral response in 17/148 (11%)/ELISA HLA-DP4 in 16/17 (94%) of seropositive patients CD4 + T cells specific for the NY-ESO-1 epitopes were generated from 5 of 6 melanoma patients with NY-ESO-1 Ab [150] Humoral response in 13/31 (42%)/ELISA CD4 + T cell 11/13 (85%) of seropositive patients/ ELISPOT [151] 22/39 (56%)/IHC/E978 [152] Primary tumor 8/61 (13%)/IHC/E978 [54] Metastatic Metastatic 53/55 (96%)/IHC/D8.38 [154] Squamous cell carcinoma 32/109 (29%)/TMA [155] 6/9 (67%)of mRNA positive samples/IHC/ ES121 [114] Humoral response in 4/20 (20%)/SEREX and ELISA [161] 9/23 (39%)/RT-PCR Humoral response in 12/23 (52%) patients and in 5/9 (55%) of NY-ESO-1 expressing tumors/ ELISA [162] 78/92 (85%)/IHC/D8.38 [127] 3/20 (15%)/IHC/D8.38…”

Section: Metastaticmentioning

confidence: 99%

New York Esophageal Squamous Cell Carcinoma-1 and Cancer Immunotherapy

Esfandiary

Ghafouri‐Fard

2015

Immunotherapy

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New York esophageal squamous cell carcinoma 1 (NY-ESO-1) is a known cancer testis gene with exceptional immunogenicity and prevalent expression in many cancer types. These characteristics have made it an appropriate vaccine candidate with the potential application against various malignancies. This article reviews recent knowledge about the NY-ESO-1 biology, function, immunogenicity and expression in cancers as well as and the results of clinical trials with this antigen.

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“…However, observations support exploring immunotherapeutic modalities in GI malignancies: tumor associated antigens (TAA) associated with tumor-specific immune responses in esophageal (MAGE-A3/4 and NYESO-1), gastric (Her-2/neu), pancreatic (MUC1 and mesothelin), hepatocellular (AFP, GPC3, NY-ESO-1, SSX-2, MAGE-A and TERT) and colorectal (CEA) malignancies [1]- [12]; tumor-specific cytotoxic T-cells higher levels of which correlate with improved prognosis [13] [14]; and T-cell inhibitory factors [CD4+ Foxp3+ regulatory T-cells (Tregs) and myeloid-derived suppressor cells (MDSCs)] higher levels of which correlate with poorer prognosis [15] [16]. In this article, we broadly delineate the various immunotherapeutic options that have been or are explored in GI malignancies.…”

Section: Introductionmentioning

confidence: 99%

Immunotherapy for Gastrointestinal Malignancies

Davar¹,

Sun²

2014

JCT

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Gastrointestinal (GI) malignancies (esophageal, gastric, pancreatic, intra-and extra-biliary ductal, hepatocellular, and colorectal cancers) are an important cause of cancer incidence and mortality in the US and globally. GI cancers account for 15.4% and 23.8% of incident cancers and cancerrelated deaths respectively in the US alone. Although earlier diagnosis and treatment advances have improved outcomes for some GI malignancies, the need for improved therapies in all disease phases (adjuvant, neoadjuvant and advanced) is paramount. Utilization of monoclonal antibodies targeting against vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR) has shown the success in selected colorectal carcinoma patients. More investigations of immunotherapy are on going in the treatment of GI malignances with different mechanisms and methods. In this article, we review data for established and evolving immunotherapy-related treatment options in GI malignancies. * Corresponding author. cess determines the eventual phenotype [19].Cetuximab (a mouse/human chimeric, IgG1) and panitumumab (a full human, IgG2) are anti-EGFR monoclonal antibodies (MoAb) that competitively inhibit ligand-receptor binding and GTP phosphorylating, effectively disrupting downstream signaling. Additionally, given IgG1 isotype, cetuximab may activate complement pathway and mediate antibody-dependent cellular cytotoxicity (ADCC). Early phase studies of EGFR inhibition in CRC yielded positive results and prompted phase III studies [20]- [40]. Given KRAS' role in mediating EGFR signaling, it was postulated that gain of function mutations would result in constitutively activated KRAS and consequent loss of sensitivity to EGFR inhibition in colorectal carcinoma. Proof of concept was initially provided by retrospective analysis of the NCIC CTG/AGITG CO17 phase III trial. KRAS mutation status was determined in 68.9% of the original cohort, and was fortuitously well-balanced in both arms. Authors reported KRAS mutant patients did not benefit from cetuximab, while KRAS wild type (WT) patients had significantly improved PFS/OS [20] [21]. This observation was buttressed by analyses of the CRYSTAL and OPUS studies [26]. Other published data supports a lower rate of response to EGFR inhibition in patients with BRAF/ NRAS/HRAS mutations or activating mutations of PIK3CA pathway [41]. The FDA and EMA recommend that EGFR inhibitors be utilized only in KRAS WT patients, and NCCN guideline recommends further that EGFR inhibitorsshould only be considered in mCRC patients with KRAS and NRAS WT [42].Cetuximab was the first EGFR inhibitor to be approved by the Food and Drug Administration (FDA) and European Medicine Agency (EMA) both as a single agent in relapsed/refractory colorectal carcinomaand together with combination chemotherapy in the 1st line setting on the basis of several randomized phase III studies. Similar results have been observed with panitumumab subsequently. These results are discussed below and depicted in Table 2.Since agents ta...

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MAGE-A3/4 and NY-ESO-1 antigens expression in metastatic esophageal squamous cell carcinoma

Cited by 32 publications

References 25 publications

MAGE-A4, NY-ESO-1 and SAGE expression rates and co-expression relationships in solid tumours

MAGE-A4, NY-ESO-1 and SAGE expression rates and co-expression relationships in solid tumours

New York Esophageal Squamous Cell Carcinoma-1 and Cancer Immunotherapy

Immunotherapy for Gastrointestinal Malignancies

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