Relevant bibliographies by topics / Melanoma Antigen Genes (MAGE)

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Academic literature on the topic 'Melanoma Antigen Genes (MAGE)'

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Published: 14 March 2023

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Journal articles on the topic "Melanoma Antigen Genes (MAGE)"

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Van den Eynde, B., O. Peeters, O. De Backer, B. Gaugler, S. Lucas, and T. Boon. "A new family of genes coding for an antigen recognized by autologous cytolytic T lymphocytes on a human melanoma." Journal of Experimental Medicine 182, no. 3 (September 1, 1995): 689–98. http://dx.doi.org/10.1084/jem.182.3.689.

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Human melanoma MZ2-MEL expresses several distinct antigens that are recognized by autologous cytolytic T lymphocytes (CTL). Some of these antigens are encoded by genes MAGE-1, MAGE-3, and BAGE, which are expressed in a large fraction of tumors of various histological types but are silent in normal adult tissues with the exception of testis. We report here the identification of the gene coding for MZ2-F, another antigen recognized by autologous CTL on MZ2-MEL cells. This gene, which was named GAGE-1, is not related to any presently known gene. It belongs to a family of genes that are expressed in a variety of tumors but not in normal tissues, except for the testis. Antigenic peptide YRPRPRRY, which is encoded by GAGE-1, is recognized by anti-MZ2-F CTL on class I molecule HLA-Cw6. The two genes of the GAGE family that code for this peptide, namely GAGE-1 and GAGE-2, are expressed in a significant proportion of melanomas (24%), sarcomas (25%), non-small cell lung cancers (19%), head and neck tumors (19%), and bladder tumors (12%). About 50% of melanoma patients carry on their tumor at least one of the presently defined antigens encoded by the MAGE, BAGE, and GAGE genes.
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Ulloa-Montoya, Fernando, Jamila Louahed, Benjamin Dizier, Olivier Gruselle, Bart Spiessens, Frédéric F. Lehmann, Stefan Suciu, et al. "Predictive Gene Signature in MAGE-A3 Antigen-Specific Cancer Immunotherapy." Journal of Clinical Oncology 31, no. 19 (July 1, 2013): 2388–95. http://dx.doi.org/10.1200/jco.2012.44.3762.

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Purpose To detect a pretreatment gene expression signature (GS) predictive of response to MAGE-A3 immunotherapeutic in patients with metastatic melanoma and to investigate its applicability in a different cancer setting (adjuvant therapy of resected early-stage non–small-cell lung cancer [NSCLC]). Patients and Methods Patients were participants in two phase II studies of the recombinant MAGE-A3 antigen combined with an immunostimulant (AS15 or AS02B). mRNA from melanoma biopsies was analyzed by microarray analysis and quantitative polymerase chain reaction. These results were used to identify and cross-validate the GS, which was then applied to the NSCLC data. Results In the patients with melanoma, 84 genes were identified whose expression was potentially associated with clinical benefit. This effect was strongest when the immunostimulant AS15 was included in the immunotherapy (hazard ratio [HR] for overall survival, 0.37; 95% CI, 0.13 to 1.05; P = .06) and was less strong with the other immunostimulant AS02B (HR, 0.84; 95% CI, 0.36 to 1.97; P = .70). The same GS was then used to predict the outcome for patients with resected NSCLC treated with MAGE-A3 plus AS02B; actively treated GS-positive patients showed a favorable disease-free interval compared with placebo-treated GS-positive patients (HR, 0.42; 95% CI, 0.17 to 1.03; P = .06), whereas among GS-negative patients, no such difference was found (HR, 1.17; 95% CI, 0.59 to 2.31; P = .65). The genes identified were mainly immune related, involving interferon gamma pathways and specific chemokines, suggesting that their pretreatment expression influences the tumor's immune microenvironment and the patient's clinical response. Conclusion An 84-gene GS associated with clinical response for MAGE-A3 immunotherapeutic was identified in metastatic melanoma and confirmed in resected NSCLC.
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Huang, Lan-Qing, Francis Brasseur, Alfonso Serrano, Etienne De Plaen, Pierre van der Bruggen, Thierry Boon, and Aline Van Pel. "Cytolytic T Lymphocytes Recognize an Antigen Encoded by MAGE-A10 on a Human Melanoma." Journal of Immunology 162, no. 11 (June 1, 1999): 6849–54. http://dx.doi.org/10.4049/jimmunol.162.11.6849.

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Abstract From melanoma patient LB1751, cytolytic T lymphocytes (CTL) were generated that lysed specifically autologous tumor cells. To establish whether these CTL recognized one of the Ags that had previously been defined, a CTL clone was stimulated with cells expressing various MAGE genes. It produced TNF upon stimulation with target cells expressing MAGE-A10. The Ag was found to be nonapeptide GLYDGMEHL (codons 254–262), which is presented by HLA-A2.1. This is the first report on the generation of anti-MAGE CTL by autologous mixed lymphocyte-tumor cell culture (MLTC) from a melanoma patient other than patient MZ2, from whom the first MAGE gene was identified. MAGE genes are expressed in many tumors but not by normal tissues except male germline cells and placenta, which do not express HLA molecules. Therefore, the identification of an antigenic peptide derived from MAGE-A10 adds to the repertoire of tumor-specific shared Ags available for anti-tumoral vaccination trials.
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Miyashiro, Isao, Christine Kuo, Kelly Huynh, Aritoshi Iida, Donald Morton, Anton Bilchik, Armando Giuliano, and Dave S. B. Hoon. "Molecular Strategy for Detecting Metastatic Cancers with Use of Multiple Tumor-specific MAGE-A Genes." Clinical Chemistry 47, no. 3 (March 1, 2001): 505–12. http://dx.doi.org/10.1093/clinchem/47.3.505.

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Abstract Background: The human melanoma-associated antigen family A (MAGE-A) has high specificity and expression in various malignancies, but individual family members are expressed at low frequency in any one particular type of cancer. We therefore developed a method to detect mRNAs from multiple MAGE-A genes in a single reaction. Methods: Universal MAGE-A (uMAGE-A) primers and probe were designed to reverse-transcribe, amplify, and detect by electrochemiluminescence (ECL) MAGE-A mRNAs on the Origen Analyzer. The assay was performed on total RNA of melanoma (n = 9 cell lines and 24 tumors), breast cancer (n = 7 and 26), and colorectal cancer (CRC; n = 5 and 12). We also evaluated blood from melanoma (n = 50), breast cancer (n = 16), and CRC (n = 21) patients. Results: The uMAGE-A mRNA was detectable in 0.01–1 ng of cell line RNA. The identity of the uMAGE-A cDNA products was confirmed by sequencing and polyacrylamide gel electrophoresis. The uMAGE-A assay increased detection of melanoma, breast cancer, and CRC tumor by 13%, 31%, and 25%, respectively, compared with a MAGE-A1 assay, and by 17%, 19%, and 25%, respectively, compared with a MAGE-A3 assay. The uMAGE-A assay detected circulating tumor cells in the blood of melanoma (24%), breast cancer (25%), and CRC (29%) patients. Conclusions: The uMAGE-A reverse transcription-PCR/ECL assay provides a practical and sensitive approach for detection of various metastatic cancers in tissues and blood.
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Baurain, J., M. Stas, B. Neyns, G. Schuler, T. Velu, K. Thielemans, N. Van Baren, T. Dorval, M. Marchand, and P. Coulie. "Comparing immunogenicities of tumor-specific antigens administered as therapeutic vaccines in metastatic melanoma patients." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 3003. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.3003.

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3003 Background: Therapeutic vaccination of metastatic melanoma patients with detectable disease is followed by some tumor regression in only about 10% of the patients, with no clear difference observed between studies carried out with various tumor-specific antigens and vaccination modalities. For antigenic peptide MAGE-A3168–176, presented by HLA-A1 molecules and administered as peptide alone or recombinant ALVAC poxvirus, anti-vaccine T lymphocyte (CTL) responses have been observed in no progressor patient and in only half of the regressors, suggesting a poor immunogenicity of these vaccines. Methods and Results: We compiled anti-vaccine CTL responses measured in the blood of 202 metastatic melanoma patients vaccinated with various associations of 10 different tumor antigens administered as peptides, alone or with adjuvant, recombinant ALVAC poxvirus, or peptide-pulsed dendritic cells. Blood lymphocytes collected before and after vaccination were all analyzed with the same method involving in vitro restimulation in limiting dilution condition followed by labeling with tetramers for each antigen. A CTL response was deemed to have occurred if the CTL frequency increased by at least 10 times, and if the pre-vaccination frequency was lower than 2 x 10-6 of the CD8 cells. No responses were detected against peptides MAGE- A4230–239 (0/26) and MAGE-C2336–344 (0/22). Some were observed against MAGE-A3168–176 (11/81), MAGE-A1278–286 (2/22), MAGE-A3112–120 (2/55), and MAGE-A10254–262 (2/35). Responses were frequently found against NY-ESO-1157–165 (10/19), GnTVVLPDVFIRC (18/73), gp100209–217 (21/33), or Tyrosinase369–377 (11/59). For the latter four antigens, there was no correlation between the occurrence of CTL responses and that of tumor regressions. Neither did we find a correlation between the CTL responses and the expression of the antigen-encoding genes in pre- vaccination tumor samples. Conclusions: These results suggest that some of the antigenic peptides that are commonly used in melanoma vaccines are more immunogenic than others but do not induce more tumor regressions. Therefore, inducing strong CTL responses against these immunogenic peptides is probably not the most appropriate endpoint of future vaccine trials. No significant financial relationships to disclose.
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Florke Gee, Rebecca R., Helen Chen, Anna K. Lee, Christina A. Daly, Benjamin A. Wilander, Klementina Fon Tacer, and Patrick Ryan Potts. "Emerging roles of the MAGE protein family in stress response pathways." Journal of Biological Chemistry 295, no. 47 (September 13, 2020): 16121–55. http://dx.doi.org/10.1074/jbc.rev120.008029.

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The melanoma antigen (MAGE) proteins all contain a MAGE homology domain. MAGE genes are conserved in all eukaryotes and have expanded from a single gene in lower eukaryotes to ∼40 genes in humans and mice. Whereas some MAGEs are ubiquitously expressed in tissues, others are expressed in only germ cells with aberrant reactivation in multiple cancers. Much of the initial research on MAGEs focused on exploiting their antigenicity and restricted expression pattern to target them with cancer immunotherapy. Beyond their potential clinical application and role in tumorigenesis, recent studies have shown that MAGE proteins regulate diverse cellular and developmental pathways, implicating them in many diseases besides cancer, including lung, renal, and neurodevelopmental disorders. At the molecular level, many MAGEs bind to E3 RING ubiquitin ligases and, thus, regulate their substrate specificity, ligase activity, and subcellular localization. On a broader scale, the MAGE genes likely expanded in eutherian mammals to protect the germline from environmental stress and aid in stress adaptation, and this stress tolerance may explain why many cancers aberrantly express MAGEs. Here, we present an updated, comprehensive review on the MAGE family that highlights general characteristics, emphasizes recent comparative studies in mice, and describes the diverse functions exerted by individual MAGEs.
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Park, Myeng Sun, Jong Wook Park, Chang Ho Jeon, Kang Dae Lee, and Hee Kyung Chang. "Expression of Melanoma Antigen-Encoding Genes (MAGE) by Common Primers for MAGE-A1 to -A6 in Colorectal Carcinomas Among Koreans." Journal of Korean Medical Science 17, no. 4 (2002): 497. http://dx.doi.org/10.3346/jkms.2002.17.4.497.

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Lin, Yuquan, Ti Wen, Xianyi Meng, Zhenzhou Wu, Liqing Zhao, Puyue Wang, Zhangyong Hong, and Zhinan Yin. "The mouse Mageb18 gene encodes a ubiquitously expressed type I MAGE protein and regulates cell proliferation and apoptosis in melanoma B16-F0 cells." Biochemical Journal 443, no. 3 (April 16, 2012): 779–88. http://dx.doi.org/10.1042/bj20112054.

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Although many cancer vaccines have been developed against type I MAGE (melanoma antigen) genes owing to their shared tumour-specific expression properties, studies about their expression and functions are relatively limited. In the present study, we first identify a non-testis-specific type I MAGE gene, Mageb18 (melanoma antigen family B 18). Mouse Mageb18 is also expressed in digestion- and immune-related tissues as well as testis, and its expression in testis is age-dependent. Mageb18 is expressed in many mouse-derived cell lines, and DNA demethylation and histone acetylation mediate the reactivation of Mageb18 in Mageb18-negtive H22 and C6 cells. We also show that mouse Mageb18 encodes a 46 kDa protein which is predominantly localized in the cytoplasm. In testis, the endogenous MAGEB18 protein is mainly expressed in proliferative spermatogonia and primary and secondary spermatocytes, but less so in spermatids. Finally, we demonstrate that knockdown of MAGEB18 inhibits the growth of B16-F0 cells and induces apoptosis, which correlates with increased levels of TP53 (tumour protein 53), p21, Bax and caspase 3. The results of the present study thus uncover an important phenomenon that the expression of certain type I MAGE genes, at least for Mageb18, is non-testis-specific. Although they can regulate various malignant phenotypes of cancer cells, it is necessary to study further their expression pattern in normal tissues before using them to develop more effective and safer cancer vaccines.
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Ries, Jutta, Nur Mollaoglu, Takeshi Toyoshima, Eleftherios Vairaktaris, Friedrich W. Neukam, Sabine Ponader, and Emeka Nkenke. "A novel Multiple-Marker Method for the Early Diagnosis of Oral Squamous Cell Carcinoma." Disease Markers 27, no. 2 (2009): 75–84. http://dx.doi.org/10.1155/2009/510124.

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Objective: Melanoma associated antigens-A (MAGE-A) expression is highly specific to cancer cells. Thus, they can be the most suitable targets for the diagnosis of malignancy. The aim of this study was to evaluate the sensitivity of multiple MAGE-A expression analysis for the diagnosis of oral squamous cell carcinoma (OSCC).Methods: Total of 70 OSSC and 20 normal oral mucosal (NOM) samples of otherwise healthy volunteers were examined for the expression of 10 different single antigens out of 12 different MAGE-A subtypes by highly sensitive reverse transcriptase polymerase chain reaction (RT-PCR) methods. The results were correlated to clinicopathological parameters of tumor samples.Results: Expression of MAGE-A was restricted to OSCC. The expression frequency of single antigen was between 10% and 55%. However, expression rate was increased up to 93% by the elevated number of genes examined. A significant correlation was found between the expression of MAGE-A and malignancy (p = 0.0001). In addition, multiple MAGE-A detection has also correlated to the incidence of lymph node metastasis, grading and advanced clinical stages.Conclusions: Analysis of multiple MAGE-A expression is more sensitive than the analysis of a single MAGE-A for the diagnostic evaluation of OSCC. Multiple MAGE-A expression analysis may be a very sensitive method to be used for the diagnosis even in the early stage of OSCC.
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Fon Tacer, Klementina, Marhiah C. Montoya, Melissa J. Oatley, Tessa Lord, Jon M. Oatley, Jonathon Klein, Ramya Ravichandran, et al. "MAGE cancer-testis antigens protect the mammalian germline under environmental stress." Science Advances 5, no. 5 (May 2019): eaav4832. http://dx.doi.org/10.1126/sciadv.aav4832.

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Ensuring robust gamete production even in the face of environmental stress is of utmost importance for species survival, especially in mammals that have low reproductive rates. Here, we describe a family of genes called melanoma antigens (MAGEs) that evolved in eutherian mammals and are normally restricted to expression in the testis (http://MAGE.stjude.org) but are often aberrantly activated in cancer. Depletion of Mage-a genes disrupts spermatogonial stem cell maintenance and impairs repopulation efficiency in vivo. Exposure of Mage-a knockout mice to genotoxic stress or long-term starvation that mimics famine in nature causes defects in spermatogenesis, decreased testis weights, diminished sperm production, and reduced fertility. Last, human MAGE-As are activated in many cancers where they promote fuel switching and growth of cells. These results suggest that mammalian-specific MAGE genes have evolved to protect the male germline against environmental stress, ensure reproductive success under non-optimal conditions, and are hijacked by cancer cells.
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Dissertations / Theses on the topic "Melanoma Antigen Genes (MAGE)"

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Peche, Leticia Yamila. "Evidence of functional specificity within the MAGE-I family of tumor expressed proteins." Doctoral thesis, SISSA, 2008. http://hdl.handle.net/20.500.11767/4674.

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The Melanoma Antigen Genes (MAGE) belong to a large family of highly conserved genes, sharing an elevated degree of sequence homology. The characteristic feature of MAGE proteins is a C-terminal domain present in all the members of the family, termed the MAGE homology domain (MHD). Based on their expression pattern MAGE genes are classified in MAGE-I and MAGE-II genes. MAGE-I genes expression is restricted to tumor and male germ cells, and for this reason they form part of a growing group of genes named Cancer Testis Antigens (CTA). Expression of MAGE-I genes seems to be an early event during gametogenesis and tumorigenesis, and correlates with genomewide hypomethylation, an important event frequently observed in carcinogenesis. Since their discovery in 1991, MAGE-I genes were mostly studied for their potential use in immunotherapy against cancer or as prognostic markers in tumors. The biological roles that these proteins play in tumor development and progression were poorly investigated. Moreover, due to their sequence homology, MAGE-I proteins are still considered functionally redundant proteins. In the present work, we functionally characterized different MAGE-I genes, in particular MageA2 and MageB2 genes, demonstrating their functional specificity. We show that MageA2 protein confers wild-type p53 tumor suppressor-sensitive resistance to chemotherapeutic drugs, such as etoposide, by recruitment of HDAC3 to p53/MageA2 complex, thus repressing p53 transactivation function. The mechanism responsible for the repressive effect of MageA2, relies on an impaired acetylation of both p53 and histones surrounding p53 binding sites by MageA2/HDAC3 complexes. The correlation between MAGE-A expression and resistance to apoptosis has been analyzed in short-term melanoma cell lines, where combined treatment with etoposide and trichostatin A (an inhibitor of histone deacetylases) restores the p53 response and reverts chemoresistance in cells expressing high levels of MAGE-A. We also present evidence that MageA2 is able to repress PML3-induced p53 activity in a specific manner, by affecting PML3 mediated p53 acetylation at the PML3 nuclear bodies (PML3-NBs). The relevance of MageA2 expression on PML3 activity has been analyzed in a normal cellular context, in which PML3 induces premature senescence, an important barrier against cell transformation. In this regard, we demonstrate that MageA2 impairs the senescence response associated to PML3 expression in normal human fibroblast. A possible mechanism for the inhibitory effect of MageA2 on PML3 is that MageA2 could interfere with PML3 sumoylation. The specificity of MageA2 functions is demonstrated by the fact that, despite high level of homology, MageA4 is not recruited to the NBs, it does not affect p53 activity nor is able to interfere with PML3 induced senescence. Finally, we have preliminarily characterized the MageB2 protein, showing that it specifically localizes to the nucleolus where it is able to interact with many nucleolar proteins. Nucleolar stress induces MageB2 relocalization to the nucleoplasm, a characteristic behavior of nucleolar proteins that regulate processes such as rRNA metabolism or RNA processing. Moreover, since we observed that MageB2 induces pRb relocalization to the nucleoli and increases E2F1 transactivation function, including E2F1-induced rRNA transcription, we hypothesize that it could play a positive role in the regulation of cell proliferation. Altogether the work presented here consistently supports the notion that, despite the high level of sequence homology, there is a clear degree of functional specificity within members of the MAGE-I family. Hence, we can hypothesize that different MAGE-I proteins, for instance MageA2 and MageB2, could act within different pathways in the regulation of complex processes such as apoptosis, proliferation, and senescence. By targeting different signal transduction pathways their final outcome could be related to the establishment and progression of the tumors where they are expressed. In this Thesis, we give a comprehensive view on the functional differences among MAGE-I members, focusing on Mage-A and Mage-B members. Implementation of our investigation could be the first step leading to understanding of how expression of specific MAGE-I members could impact cancer cell behaviour thus prompting the use of MAGE-I genes as novel cancer specific targets for the development of new drug-based therapies.
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Book chapters on the topic "Melanoma Antigen Genes (MAGE)"

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Wilson, Elizabeth M. "Primate-Specific Multi-Functional Androgen Receptor Coregulator and Proto-Oncogene Melanoma Antigen-A11 (MAGE-A11)." In Nuclear Receptors: From Structure to the Clinic, 137–54. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18729-7_8.

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Juretic, Antonio, Rajko Kavalar, Guilio C. Spagnoli, Bozena Sarcevic, and Luigi Terracciano. "Immunohistochemical Detection of Melanoma Antigen E (MAGE) Expression in Breast Carcinoma." In Handbook of Immunohistochemistry and in Situ Hybridization of Human Carcinomas, 471–76. Elsevier, 2002. http://dx.doi.org/10.1016/s1874-5784(04)80057-6.

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Liu, Wei, Alice Guo, Sylvia Asa, and Shereen Ezzat. "The Melanoma Associated Antigen A (MAGE-A3) Engages Multiple Tumorigenic Pathways To Promote Breast Cancer Progression." In Posters I, P2–46—P2–46. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part2.p1.p2-46.

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Conference papers on the topic "Melanoma Antigen Genes (MAGE)"

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Neubert, Natalie J., Laure Tillé, David Barras, Charlotte Soneson, Petra Baumgaertner, Donata Rimoldi, Mauro Delorenzi, Silvia A. Fuertes Marraco, and Daniel E. Speiser. "Abstract B34: Melanoma cells respond to CD8+ T cell attack by upregulation of genes associated with antigen processing and presentation." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-b34.

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Strekalova, Elena, Dmitry Malin, David Good, and Vincent Cryns. "Abstract A265: L-methionine restriction sensitizes triple-negative breast cancer cells to a TRAIL receptor-2 agonist by reducing the expression of the melanoma-associated antigen MAGE-D2." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a265.

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Zekri, Abdel-Rahman N., and Abeer Bahnassy. "Abstract 3540: Evaluation of Alpha-fetoprotein (AFP), telomerase, melanoma associated antigen (MAGE1 and MAGE 3), cancer stem cell markers cytokeratin (CK) and (CD133,) as potential biomarkers for hepatocellular carcinoma (HCC)." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3540.

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