Induction of MAGE-3 expression in lung and esophageal cancer cells

Weiser, Todd S.; Ohnmacht, Galen A.; Guo, Zong Sheng; Fischette, Maria R.; Chen, Gustavio A; Hong, Julie A.; Nguyen, Dao M.; Schrump, David S.

doi:10.1016/s0003-4975(00)02421-8

Cited by 76 publications

(42 citation statements)

References 28 publications

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“…As HDACs regulate a wide variety of processes involved in carcinogenesis, multiple mechanisms may explain the clinical activity of HDAC inhibitors [249,250], including altered gene expression of cell-cycle and apoptotic regulatory proteins [251][252][253][254][255], acetylation of nonhistone proteins regulating cell growth and survival [256][257][258][259], angiogenesis [260,261], aggresome formation [262], and DNA repair [263]. In addition, HDAC inhibitors may have important effects on the tumor microenvironment via reactive oxygen species [264,265], enhanced antigen presentation [266] and downregulation of immunomodulatory cytokines, like IL-10 [267].…”

Section: Hdac Inhibitorsmentioning

confidence: 99%

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Wilcox

2011

American J Hematol

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Disease overview: Cutaneous T‐cell lymphomas are a heterogenous group of T‐cell lymphoproliferative disorders involving the skin, the majority of which may be classified as Mycosis fungoides (MF) or Sézary syndrome (SS).Diagnosis: The diagnosis of MF or SS requires the integration of clinical and histopathologic data.Risk‐adapted therapy: Tumor, node, metastasis, and blood (TNMB) staging remains the most important prognostic factor in MF/SS and forms the basis for a “risk‐adapted,” multidisciplinary approach to treatment. For patients with disease limited to the skin, expectant management or skin‐directed therapies is preferred, as both disease‐specific and overall survival for these patients is favorable. In contrast, patients with advanced‐stage disease with significant nodal, visceral, or blood involvement are generally approached with biologic‐response modifiers, denileukin diftitox, and histone deacetylase inhibitors before escalating therapy to include systemic, single‐agent chemotherapy. Multiagent chemotherapy may be used for those patients with extensive visceral involvement requiring rapid disease control. In highly‐selected patients with disease refractory to standard treatments, allogeneic stem‐cell transplantation may be considered. Am. J. Hematol., 2011. © 2011 Wiley‐Liss, Inc.

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Section: Hdac Inhibitorsmentioning

confidence: 99%

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Wilcox

2011

American J Hematol

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“…Conceivably, innovative treatment regimens that enhance CTA expression in primary malignancies may facilitate the development of efficacious immunotherapy protocols with broad applicability in cancer patients (22). Our group has shown previously that NY-ESO-1 and MAGE-3 can be induced in vitro in thoracic cancer cell lines by 5-aza-2'-deoxycytidine (5-azadC) alone or in combination with the histone deacetylase inhibitor depsipeptide (23)(24)(25). Others have also shown that MAGE antigens and LAGE-1 can be induced by 5-azadC in certain cancer cell lines in vitro (26,27).…”

Section: Introductionmentioning

confidence: 99%

De novoInduction of a Cancer/Testis Antigen by 5-Aza-2′-Deoxycytidine Augments Adoptive Immunotherapy in a Murine Tumor Model

Hong²,

et al. 2006

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Recent studies suggest that immunotherapy targeting specific tumor-associated antigens (TAAs) may be beneficial in cancer patients. However, most of these TAAs are tumor type specific and heterogeneous among patients, thus limiting their applications. Here, we describe the de novo induction of a cancer/testis antigen (CTA) for immunotherapy of tumors of various histologies. The murine CTA P1A, normally expressed only in a few tumor lines, could be induced de novo in all P1A-negative cancer lines of eight histologic origins in vitro and in various murine xenografts by systemic administration of 5-aza-2V -deoxycytidine. The induction of P1A expression correlated strongly with demethylation of the CpG island in the promoter region of this gene. The induced antigen was processed and presented properly for recognition by H-2L drestricted P1A-specific CTLs. The combination of a demethylating agent and adoptive transfer of P1A-specific CTL effectively treated lung metastases in syngeneic mice challenged with P1A-negative 4T1 mammary carcinoma cells. These data show a novel strategy of combined chemoimmunotherapy of cancer targeting a CTA induced de novo in a broad range of tumor histologies, and support further evaluation of chromatin-remodeling agents for human cancer therapy. (Cancer Res 2006; 66(2): 1105-13)

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“…Another study used low-dose DAC treatment followed by the HDAC inhibitor desipeptide in lung and esophageal cancer-cell lines and found induction of MAGE-3 and NY-ESO-1 cancer testes antigens that augment the immunogenicity of cancer cells [Weiser et al 2001a[Weiser et al , 2001b. Taking another combination approach, studies have combined HDAC inhibitors with adenovirus or coxsackievirus-mediated p53 gene therapy in esophageal squamous cell carcinoma cell lines and found improved transduction efficacy of the virusto-cancer cells with improved antitumor activity [Hoshino et al 2008;Ma et al 2012].…”

Section: Epigenetic Therapy In Noncolorectal Gastrointestinal Cancersmentioning

confidence: 99%

Epigenetic therapy in gastrointestinal cancer: the right combination

Abdelfatah

Kerner

Nanda

et al. 2016

Therap Adv Gastroenterol

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Abstract:Epigenetics is a relatively recent field of molecular biology that has arisen over the past 25 years. Cancer is now understood to be a disease of widespread epigenetic dysregulation that interacts extensively with underlying genetic mutations. The development of drugs targeting these processes has rapidly progressed; with several drugs already FDA approved as first-line therapy in hematological malignancies. Gastrointestinal (GI) cancers possess high degrees of epigenetic dysregulation, exemplified by subtypes such as CpG island methylator phenotype (CIMP), and the potential benefit of epigenetic therapy in these cancers is evident. The application of epigenetic drugs in solid tumors, including GI cancers, is just emerging, with increased understanding of the cancer epigenome. In this review, we provide a brief overview of cancer epigenetics and the epigenetic targets of therapy including deoxyribonucleic acid (DNA) methylation, histone modifications, and chromatin remodeling. We discuss the epigenetic drugs currently in use, with a focus on DNA methyltransferase (DNMT) and histone deacetylase (HDAC) inhibitors, and explain the pharmacokinetic and mechanistic challenges in their application. We present the strategies employed in incorporating these drugs into the treatment of GI cancers, and explain the concept of the cancer stem cell in epigenetic reprogramming and reversal of chemo resistance. We discuss the most promising combination strategies in GI cancers including: (1) epigenetic sensitization to radiotherapy, (2) epigenetic sensitization to cytotoxic chemotherapy, and (3) epigenetic immune modulation and priming for immune therapy. Finally, we present preclinical and clinical trial data employing these strategies thus far in various GI cancers including colorectal, esophageal, gastric, and pancreatic cancer.

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Induction of MAGE-3 expression in lung and esophageal cancer cells

Cited by 76 publications

References 28 publications

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

De novoInduction of a Cancer/Testis Antigen by 5-Aza-2′-Deoxycytidine Augments Adoptive Immunotherapy in a Murine Tumor Model

Epigenetic therapy in gastrointestinal cancer: the right combination

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