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  1. Article ; Online: The Role of EBV-Induced Hypermethylation in Gastric Cancer Tumorigenesis.

    Stanland, Lyla J / Luftig, Micah A

    Viruses

    2020  Volume 12, Issue 11

    Abstract: Epstein-Barr-virus-associated Gastric Cancer (EBVaGC) comprises approximately 10% of global gastric cancers and is known to be the most hypermethylated of all tumor types. EBV infection has been shown to directly induce the hypermethylation of both the ... ...

    Abstract Epstein-Barr-virus-associated Gastric Cancer (EBVaGC) comprises approximately 10% of global gastric cancers and is known to be the most hypermethylated of all tumor types. EBV infection has been shown to directly induce the hypermethylation of both the host and viral genome following initial infection of gastric epithelial cells. Many studies have been completed in an attempt to identify genes that frequently become hypermethylated and therefore significant pathways that become silenced to promote tumorigenesis. It is clear that EBV-induced hypermethylation silences key tumor suppressor genes, cell cycle genes and cellular differentiation factors to promote a highly proliferative and poorly differentiated cell population. EBV infection has been shown to induce methylation in additional malignancies including Nasopharyngeal Carcinoma and Burkitt's Lymphoma though not to the same level as in EBVaGC. Lastly, some genes silenced in EBVaGC are common to other heavily methylated tumors such as colorectal and breast tumors; however, some genes are unique to EBVaGC and can provide insights into the major pathways involved in tumorigenesis.
    MeSH term(s) Carcinogenesis/genetics ; CpG Islands ; DNA Methylation/genetics ; Epstein-Barr Virus Infections/complications ; Gene Expression Regulation, Neoplastic ; Genome ; Herpesvirus 4, Human/pathogenicity ; Humans ; Stomach Neoplasms/genetics ; Stomach Neoplasms/physiopathology ; Tumor Suppressor Proteins/genetics
    Chemical Substances Tumor Suppressor Proteins
    Language English
    Publishing date 2020-10-28
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v12111222
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: The Role of EBV-Induced Hypermethylation in Gastric Cancer Tumorigenesis

    Stanland, Lyla J / Luftig, Micah A

    Viruses. 2020 Oct. 28, v. 12, no. 11

    2020  

    Abstract: Epstein–Barr-virus-associated Gastric Cancer (EBVaGC) comprises approximately 10% of global gastric cancers and is known to be the most hypermethylated of all tumor types. EBV infection has been shown to directly induce the hypermethylation of both the ... ...

    Abstract Epstein–Barr-virus-associated Gastric Cancer (EBVaGC) comprises approximately 10% of global gastric cancers and is known to be the most hypermethylated of all tumor types. EBV infection has been shown to directly induce the hypermethylation of both the host and viral genome following initial infection of gastric epithelial cells. Many studies have been completed in an attempt to identify genes that frequently become hypermethylated and therefore significant pathways that become silenced to promote tumorigenesis. It is clear that EBV-induced hypermethylation silences key tumor suppressor genes, cell cycle genes and cellular differentiation factors to promote a highly proliferative and poorly differentiated cell population. EBV infection has been shown to induce methylation in additional malignancies including Nasopharyngeal Carcinoma and Burkitt’s Lymphoma though not to the same level as in EBVaGC. Lastly, some genes silenced in EBVaGC are common to other heavily methylated tumors such as colorectal and breast tumors; however, some genes are unique to EBVaGC and can provide insights into the major pathways involved in tumorigenesis.
    Keywords breast neoplasms ; carcinogenesis ; carcinoma ; cell cycle ; cell differentiation ; epithelial cells ; gastric mucosa ; lymphoma ; methylation ; stomach neoplasms ; tumor suppressor genes
    Language English
    Dates of publication 2020-1028
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2516098-9
    ISSN 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v12111222
    Database NAL-Catalogue (AGRICOLA)

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  3. Article: Molecular features and translational outlook for Epstein-Barr virus-associated gastric cancer.

    Stanland, Lyla J / Luftig, Micah A

    Future virology

    2018  Volume 13, Issue 11, Page(s) 803–818

    Abstract: Epstein-Barr Virus (EBV) was the first discovered human tumor virus and is the etiological agent of B cell lymphomas and also epithelial cancers. Indeed, nearly 10% of gastric cancers worldwide are EBV-positive and display unique molecular, epigenetic, ... ...

    Abstract Epstein-Barr Virus (EBV) was the first discovered human tumor virus and is the etiological agent of B cell lymphomas and also epithelial cancers. Indeed, nearly 10% of gastric cancers worldwide are EBV-positive and display unique molecular, epigenetic, and clinicopathological features. EBV-positive gastric cancers display the highest rate of host genome methylation of all tumor types studied and harbor recurrent mutations activating PI3Kα, silencing ARID1A, and amplifying PD-L1. While EBV infection of B cells can be studied efficiently,
    Language English
    Publishing date 2018-10-24
    Publishing country England
    Document type Journal Article
    ZDB-ID 2254606-6
    ISSN 1746-0808 ; 1746-0794
    ISSN (online) 1746-0808
    ISSN 1746-0794
    DOI 10.2217/fvl-2018-0071
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: CBF-Beta Mitigates PI3K-Alpha-Specific Inhibitor Killing through PIM1 in PIK3CA-Mutant Gastric Cancer.

    Stanland, Lyla J / Ang, Hazel X / Hoj, Jacob P / Chu, Yunqiang / Tan, Patrick / Wood, Kris C / Luftig, Micah A

    Molecular cancer research : MCR

    2023  Volume 21, Issue 11, Page(s) 1148–1162

    Abstract: PIK3CA is the second most mutated gene in cancer leading to aberrant PI3K/AKT/mTOR signaling and increased translation, proliferation, and survival. Some 4%-25% of gastric cancers display activating PIK3CA mutations, including 80% of Epstein-Barr virus- ... ...

    Abstract PIK3CA is the second most mutated gene in cancer leading to aberrant PI3K/AKT/mTOR signaling and increased translation, proliferation, and survival. Some 4%-25% of gastric cancers display activating PIK3CA mutations, including 80% of Epstein-Barr virus-associated GCs. Small molecules, including pan-PI3K and dual PI3K/mTOR inhibitors, have shown moderate success clinically, due to broad on-target/off-tissue effects. Thus, isoform-specific and mutant selective inhibitors have been of significant interest. However, drug resistance is a problem and has affected success of new drugs. There has been a concerted effort to define mechanisms of resistance and identify potent combinations in many tumor types, though gastric cancer is comparatively understudied. In this study, we identified modulators of the response to the PI3Kα-specific inhibitor, BYL719, in PIK3CA-mutant GCs. We found that loss of NEDD9 or inhibition of BCL-XL conferred hypersensitivity to BYL719, through increased cell-cycle arrest and cell death, respectively. In addition, we discovered that loss of CBFB conferred resistance to BYL719. CBFB loss led to upregulation of the protein kinase PIM1, which can phosphorylate and activate several overlapping downstream substrates as AKT thereby maintaining pathway activity in the presence of PI3Kα inhibition. The addition of a pan-PIM inhibitor re-sensitized resistant cells to BYL719. Our data provide clear mechanistic insights into PI3Kα inhibitor response in PIK3CA-mutant gastric tumors and can inform future work as mutant-selective inhibitors are in development for diverse tumor types.
    Implications: Loss of either NEDD9 or BCL-XL confers hypersensitivity to PI3K-alpha inhibition whereas loss of CBFB confers resistance through a CBFB/PIM1 signaling axis.
    MeSH term(s) Humans ; Stomach Neoplasms/drug therapy ; Stomach Neoplasms/genetics ; Protein Kinase Inhibitors/pharmacology ; Phosphatidylinositol 3-Kinases/genetics ; Proto-Oncogene Proteins c-akt/genetics ; Epstein-Barr Virus Infections ; Cell Line, Tumor ; Herpesvirus 4, Human ; Phosphoinositide-3 Kinase Inhibitors ; Class I Phosphatidylinositol 3-Kinases/genetics ; Mutation ; Adaptor Proteins, Signal Transducing/genetics
    Chemical Substances Alpelisib (08W5N2C97Q) ; Protein Kinase Inhibitors ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Phosphoinositide-3 Kinase Inhibitors ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; NEDD9 protein, human ; Adaptor Proteins, Signal Transducing ; PIK3CA protein, human (EC 2.7.1.137) ; PIM1 protein, human (EC 2.7.11.1)
    Language English
    Publishing date 2023-09-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-23-0034
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Identification of Host Biomarkers of Epstein-Barr Virus Latency IIb and Latency III.

    Messinger, Joshua E / Dai, Joanne / Stanland, Lyla J / Price, Alexander M / Luftig, Micah A

    mBio

    2019  Volume 10, Issue 4

    Abstract: Deciphering the molecular pathogenesis of virally induced cancers is challenging due, in part, to the heterogeneity of both viral gene expression and host gene expression. Epstein-Barr virus (EBV) is a ubiquitous herpesvirus prevalent in B-cell lymphomas ...

    Abstract Deciphering the molecular pathogenesis of virally induced cancers is challenging due, in part, to the heterogeneity of both viral gene expression and host gene expression. Epstein-Barr virus (EBV) is a ubiquitous herpesvirus prevalent in B-cell lymphomas of immune-suppressed individuals. EBV infection of primary human B cells leads to their immortalization into lymphoblastoid cell lines (LCLs), serving as a model of these lymphomas. In previous studies, reports from our laboratory have described a temporal model for immortalization with an initial phase characterized by expression of Epstein-Barr nuclear antigens (EBNAs), high levels of c-Myc activity, and hyperproliferation in the absence of the latent membrane proteins (LMPs), called latency IIb. This is followed by the long-term outgrowth of LCLs expressing the EBNAs along with the LMPs, particularly NFκB-activating LMP1, defining latency III. However, LCLs express a broad distribution of LMP1 such that a subset of these cells express LMP1 at levels similar to those seen in latency IIb, making it difficult to distinguish these two latency states. In this study, we performed mRNA sequencing (mRNA-Seq) on early EBV-infected latency IIb cells and latency III LCLs sorted by NFκB activity. We found that latency IIb transcriptomes clustered independently from latency III independently of NFκB. We identified and validated mRNAs defining these latency states. Indeed, we were able to distinguish latency IIb cells from LCLs expressing low levels of LMP1 using multiplex RNA-fluorescence
    MeSH term(s) Biomarkers/analysis ; Cells, Cultured ; Epstein-Barr Virus Infections/virology ; Gene Expression Profiling ; Herpesvirus 4, Human/growth & development ; Host-Pathogen Interactions ; Humans ; In Situ Hybridization, Fluorescence ; Lymphocytes/virology ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Sequence Analysis, RNA ; Virus Latency
    Chemical Substances Biomarkers ; RNA, Messenger
    Language English
    Publishing date 2019-07-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2557172-2
    ISSN 2150-7511 ; 2161-2129
    ISSN (online) 2150-7511
    ISSN 2161-2129
    DOI 10.1128/mBio.01006-19
    Database MEDical Literature Analysis and Retrieval System OnLINE

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