Current Immune-Related Molecular Approach in Combating Nasopharyngeal Cancer

Soehartati  Argadikoesoema; Marlinda Adham; Henry Kodrat; Demak Lumban Tobing; I. Made Haryoga; Agustinus Gatot Dwiyono; Yoseph Adi Kristian

doi:10.14740/wjon1214

Current Immune-Related Molecular Approach in Combating Nasopharyngeal Cancer

Soehartati Argadikoesoema, Marlinda Adham, Henry Kodrat, Demak Lumban Tobing, I. Made Haryoga, Agustinus Gatot Dwiyono, Yoseph Adi Kristian

Research output: Contribution to journal › Article › peer-review

Abstract

Nasopharyngeal cancer is a cancer closely related to Epstein-Barr virus (EBV) infection. EBV protein has been shown to be related to various oncogenic development. Suppression of tumor suppressor genes, upregulating molecules to prevent immune attack, downregulating pro-apoptotic proteins, and stimulating local immune suppressive environment are among some roles that EBV proteins can exert on host cells. All those factors combined together with underlying genetic susceptibility of host cells further increase the chance of nasopharyngeal cancer development. Approach targeting those carcinogenesis pathways has been tested with marginal benefit. A newer approach boosting immune cells to increase recognition of tumor antigen and promoting cytotoxic T cell attack has shown promising clinical benefit. Further combination of those immunotherapies with other modality, in particular radiotherapy, has resulted in amplification of cancer killing.

Original language	English
Pages (from-to)	157-161
Journal	World Journal of Oncology
Volume	10
Issue number	4-5
DOIs	https://doi.org/10.14740/wjon1214
Publication status	Published - 1 Jan 2019

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World Journal of Oncology

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title = "Current Immune-Related Molecular Approach in Combating Nasopharyngeal Cancer",

abstract = "Nasopharyngeal cancer is a cancer closely related to Epstein-Barr virus (EBV) infection. EBV protein has been shown to be related to various oncogenic development. Suppression of tumor suppressor genes, upregulating molecules to prevent immune attack, downregulating pro-apoptotic proteins, and stimulating local immune suppressive environment are among some roles that EBV proteins can exert on host cells. All those factors combined together with underlying genetic susceptibility of host cells further increase the chance of nasopharyngeal cancer development. Approach targeting those carcinogenesis pathways has been tested with marginal benefit. A newer approach boosting immune cells to increase recognition of tumor antigen and promoting cytotoxic T cell attack has shown promising clinical benefit. Further combination of those immunotherapies with other modality, in particular radiotherapy, has resulted in amplification of cancer killing.",

author = "Soehartati Argadikoesoema and Marlinda Adham and Henry Kodrat and Tobing, {Demak Lumban} and Haryoga, {I. Made} and Dwiyono, {Agustinus Gatot} and Kristian, {Yoseph Adi}",

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AU - Argadikoesoema, Soehartati

AU - Adham, Marlinda

AU - Kodrat, Henry

AU - Tobing, Demak Lumban

AU - Haryoga, I. Made

AU - Dwiyono, Agustinus Gatot

AU - Kristian, Yoseph Adi

PY - 2019/1/1

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AB - Nasopharyngeal cancer is a cancer closely related to Epstein-Barr virus (EBV) infection. EBV protein has been shown to be related to various oncogenic development. Suppression of tumor suppressor genes, upregulating molecules to prevent immune attack, downregulating pro-apoptotic proteins, and stimulating local immune suppressive environment are among some roles that EBV proteins can exert on host cells. All those factors combined together with underlying genetic susceptibility of host cells further increase the chance of nasopharyngeal cancer development. Approach targeting those carcinogenesis pathways has been tested with marginal benefit. A newer approach boosting immune cells to increase recognition of tumor antigen and promoting cytotoxic T cell attack has shown promising clinical benefit. Further combination of those immunotherapies with other modality, in particular radiotherapy, has resulted in amplification of cancer killing.

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