Byong Chul Yoo

National Cancer Center Korea, Kōyō, Gyeonggi Province, South Korea

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Publications (59)192.64 Total impact

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    ABSTRACT: At present, a radical shift in cancer treatment is occurring in terms of predictive, preventive and personalised medicine (PPPM). Individual patients will participate in more aspects of their health care. During the development of PPPM, many rapid, specific, and sensitive new methods for earlier detection of cancer will result in more efficient management of the patient, and hence a better quality of life. Coordination of the various activities among different healthcare professionals in primary, secondary, and tertiary care requires well-defined competencies, implementation of training and educational programs, sharing of data, and harmonized guidelines. In this position paper the current knowledge to understand cancer pre-disposition and risk factors, the cellular biology of cancer, predictive markers and treatment outcome, the improvement in technologies to screen, diagnose and provision of better drug development solutions, are discussed in the context of a better implementation of personalised medicine. Recognition of the major risk factors for cancer initiation is the key for preventive strategies [1]. Of interest, cancer predisposing syndromes in particular the monogenic subtypes that lead to cancer progression are well defined and one should focus on implementation strategies to identify individuals at risk to allow preventive measures and early screening/diagnosis. Implementation of such measures are disturbed by improper use of the data, with breach of data protection as one of the risks to be heavily controlled. Population screening requires in depth cost-benefit analysis to justify health care costs and the parameters screened should provide information that allow an actionable deliverable, for better health care provision. http://www.epmajournal.com/content/pdf/s13167-015-0030-6.pdf
    EPMA Journal, The 04/2015; 6:9. DOI:10.1186/s13167-015-0030-6
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    ABSTRACT: Gouania leptostachya DC. var. tonkinensis Pitard. Rhamnaceae is a traditional medicinal plant used in Thailand for treating various inflammatory symptoms. However, no systematic studies have been performed concerning the anti-inflammatory effects or molecular mechanisms of this plant. The immunopharmacological activities of a methanol extract from the leaves and twigs of G. leptostachya (Gl-ME) were elucidated based on the gastritis symptoms of mice treated with HCl/EtOH and the inflammatory responses, such as nitric oxide (NO) release and prostaglandin E2 (PGE2 ) production, from RAW264.7 cells and peritoneal macrophages. Moreover, inhibitory target molecules were also assessed. Gl-ME dose-dependently diminished the secretion of NO and PGE2 from LPS-stimulated RAW264.7 cells and peritoneal macrophages. The gastritis lesions of HCl/EtOH-treated mice were also attenuated after Gl-ME treatment. The extract (50 and 300 µg/mL) clearly reduced mRNA expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2, nuclear translocation of p65/nuclear factor (NF)-κB, phosphorylation of p65-activating upstream enzymes, such as protein kinase B (AKT), inhibitor of κBα kinase (IKK), and inhibitor of κB (IκBα), and the enzymatic activity of Src. By HPLC analysis, one of the major components in the extract was revealed as resveratrol with NO and Src inhibitory activities. Moreover, this compound suppressed NO production and HCl/EtOH-induced gastric symptoms. Therefore, these results suggest that Gl-ME might be useful as an herbal anti-inflammatory medicine through the inhibition of Src and NF-κB activation pathways. The efficacy data of G. leptostachya also implies that this plant could be further tested to see whether it can be developed as potential anti-inflammatory preparation. Copyright © 2014 John Wiley & Sons, Ltd. Copyright © 2014 John Wiley & Sons, Ltd.
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    ABSTRACT: To perform chemoradiotherapy (CRT) effectively, it is clinically beneficial to identify predictors of tumor response after CRT. This study examined the association between plasma fibrinogen level before preoperative CRT and tumor response in advanced rectal cancer. This was a retrospective study of 947 patients who received preoperative CRT followed by curative surgery for primary rectal cancer. We analyzed clinical factors that could be associated with pathologic tumor response in terms of downstaging (ypStage 0-I), primary tumor regression (ypT0-1), and complete response (ypT0N0). Downstaging was observed in 366 patients (38.6%), primary tumor regression in 187 patients (19.7%) and complete response in 138 patients (14.6%). Multivariate analysis found that pre-CRT carcinoembryonic antigen (CEA) level, fibrinogen level, hemoglobin level, clinical T and N classification, distance from anal verge, and histologic grade were significant predictive factors for downstaging; CEA level, fibrinogen level, and N classification predicted primary tumor regression; CEA level, and fibrinogen level were predictive for complete response. This study demonstrated that fibrinogen level was a significant predictor of pathologic tumor response after preoperative CRT.
    Annals of Surgical Oncology 11/2014; 22(1). DOI:10.1245/s10434-014-3962-5 · 3.94 Impact Factor
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    Mi-Yeon Kim, Byong Chul Yoo, Jae Youl Cho
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    ABSTRACT: Background Ginsenoside Rp1 (G-Rp1) is a novel ginsenoside derived from ginsenoside Rk1. This compound was reported to have anti-cancer, anti-platelet, and anti-inflammatory activities. In this study, we examined the molecular target of G-Rp1’s anti-proliferative and pro-apoptotic activities. Methods To examine the effects of G-Rp1, cell proliferation assays, propidium iodine staining, proteomic analysis by two-dimensional gel electrophoresis, immunoblotting analysis, and a knockdown strategy were employed. Results G-Rp1 dose-dependently suppressed the proliferation of colorectal cancer LoVo cells and also increased the apoptosis of these cells. Interestingly, G-Rp1 remarkably up-regulated the protein level of apolipoprotein (Apo)-A1 in LoVo, SNU-407, DLD-1, SNU-638, AGS, KPL-4, and SK-BR-3 cells. The knockdown of Apo-A1 by its siRNA increased the levels of cleaved poly(ADP-ribose) polymerase (c-PARP) and p53 and diminished the proliferation of LoVo cells. Conclusion These results suggest that G-Rp1 may act as an anti-cancer agent by strongly inhibiting cell proliferation and enhancing cell apoptosis through the up-regulation of Apo-A1.
    Journal of ginseng research 10/2014; DOI:10.1016/j.jgr.2014.06.003 · 2.30 Impact Factor
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    ABSTRACT: Current fecal screening tools for colorectal cancer (CRC), such as fecal occult blood tests (FOBT), are limited by their low sensitivity. Calgranulin B (CALB) was previously reported as a candidate fecal marker for CRC. This study investigated whether a combination of the FOBT and fecal CALB has increased sensitivity and specificity for a diagnosis of CRC.
    PLoS ONE 09/2014; 9(9):e106182. DOI:10.1371/journal.pone.0106182 · 3.53 Impact Factor
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    Kun Kim, Seung-Gu Yeo, Byong Chul Yoo
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    ABSTRACT: Patients show variable responses to chemoradiotherapy (CRT), which is generally administered before surgery for locally advanced rectal cancer (LARC). The aim of this study was to identify molecular markers predictive of CRT responses by analysis of low-mass ions (LMIs) in serum of LARC patients.
    Cancer Research and Treatment 08/2014; 47(1). DOI:10.4143/crt.2013.127 · 2.98 Impact Factor
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    ABSTRACT: Introduction The purpose of this study was the development of 68Ga-labeled neolactosylated human serum albumin (LSA) for imaging asialoglycoprotein receptors in the liver by using positron emission tomography (PET), which would enable functional imaging with higher resolution than single-photon emission computed tomography (SPECT). Methods LSA was synthesized by conjugating α-lactose to human serum albumin (HSA) by reductive amination. LSA was conjugated with 2-(p-isothiocyanatobenzyl)-1,4,7-triazacyclononane-1,4,7-triacetic acid (SCN-NOTA) and the resultant NOTA-LSA was labeled with 68Ga at room temperature. The labeling efficiency of NOTA-LSA was evaluated as a function of pH and time. The stability of 68Ga-NOTA-LSA in phosphate buffered saline (PBS) and human serum at 37 °C was determined. Biodistribution and PET studies of 68Ga-NOTA-LSA were performed in mice following tail vein injection of radiotracer. Results The numbers of lactose and NOTA units per HSA were determined to be 31.7 and 4.6, respectively. When the reaction was done at room temperature, the labeling efficiency of NOTA-LSA was higher than 99% at pH 4.8 and 96% at pH 6. More than 95% of the detected radioactivity was associated with the intact molecule for at least the 4 h following synthesis when incubated in PBS or human serum at 37 °C. Biodistribution and animal PET studies showed specific retention of 68Ga-NOTA-LSA in liver following intravenous administration. Conclusion 68Ga-NOTA-LSA was successfully developed for imaging asialoglycoprotein receptors in the liver with a simple labeling method, high labeling efficiency, and high stability.
    Nuclear Medicine and Biology 08/2014; DOI:10.1016/j.nucmedbio.2014.08.009 · 2.41 Impact Factor
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    ABSTRACT: Ovarian cancer (OVC) is one of the most difficult types of cancer to detect in the early stages of its development. There have been numerous attempts to identify a biomarker for OVC; however, an accurate diagnostic marker has yet to be identified. The present study profiled OVC candidate metabolites from the serum to identify potential diagnostic markers for OVC. Data regarding low-mass ions (LMIs) in the serum were obtained using matrix-assisted laser desorption/ionization (MALDI)-time-of-flight analysis. MALDI-mass spectrometry (MS) analysis of each serum sample was repeated six times in order to reduce the likelihood of experimental errors. The intensity of the LMI mass peaks were normalized using total peak area sums. The normalized intensity of LMI was used in principal component analysis-discriminant analysis to differentiate between 142 patients with OVC and 100 healthy control participants. Liquid chromatography-MS/MS was used to identify the selected LMIs. Extracted ion chromatogram analysis was used to measure the relative quantity of candidate metabolites from the LMI mass peak areas. The concentration of common metabolites in the serum was determined using ELISA. The top 20 LMI mass peaks with a weigh factor over 0.05 were selected to distinguish between the patients with OVC and the controls. Among the LMIs, two with 184.05 and 496.30 m/z were identified as L-homocysteic acid (HCA) and lysophosphatidylcholine (LPC) (16:0), respectively. The relative quantity of LPC (16:0) was found to be decreased in the OVC serum (P=0.05), while the quantity of HCA was observed to be significantly higher in the OVC serum (P<0.001). HCA was not detected in 59 cases out of the 63 control participants; however, the majority of the cases of OVC (16/25) exhibited significantly higher quantities of HCA. When the cutoff was 10 nmol/ml, the sensitivity and specificity of HCA were 64.0 and 96.9%, respectively. The level of LPC (16:0) was significantly correlated with tumor grade (P=0.045). HCA and LPC (16:0) showed correlation with stage and tumor histology, but the limited sample size resulted in a lack of statistical significance. The findings of the present study suggest that HCA may have potential to be a biomarker for OVC. The stratified screening including LPC (16:0) did not significantly increase the power for OVC screening; however, the present study showed that profiling LMIs in serum may be useful for identifying candidate metabolites for OVC screening.
    Oncology letters 08/2014; 8(2):566-574. DOI:10.3892/ol.2014.2214 · 0.99 Impact Factor
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    ABSTRACT: Activating transcription factor 2 (ATF2) is a member of the leucine zipper family of DNA-binding proteins and is widely distributed in tissues including the liver, lung, spleen, and kidney. Like c-Jun and c-Fos, ATF2 responds to stress-related stimuli and may thereby influence cell proliferation, inflammation, apoptosis, oncogenesis, neurological development and function, and skeletal remodeling. Recent studies clarify the regulatory role of ATF2 in inflammation and describe potential inhibitors of this protein. In this paper, we summarize the properties and functions of ATF2 and explore potential applications of ATF2 inhibitors as tools for research and for the development of immunosuppressive and anti-inflammatory drugs.
    Mediators of Inflammation 06/2014; 2014:950472. DOI:10.1155/2014/950472 · 2.42 Impact Factor
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    ABSTRACT: Blood metabolites can be detected as low-mass ions (LMIs) by mass spectrometry (MS). These LMIs may reflect the pathological changes in metabolism that occur as part of a disease state, such as cancer. We constructed a LMI discriminant equation (LOME) to investigate whether systematic LMI profiling might be applied to cancer screening. LMI information including m/z and mass peak intensity was obtained by five independent MALDI-MS analyses, using 1,127 sera collected from healthy individuals and cancer patients with colorectal cancer (CRC), breast cancer (BRC), gastric cancer (GC) and other types of cancer. Using a two-stage principal component analysis to determine weighting factors for individual LMIs and a two-stage LMI selection procedure, we selected a total of 104 and 23 major LMIs by the LOME algorithms for separating CRC from control and rest of cancer samples, respectively. CRC LOME demonstrated excellent discriminating power in a validation set (sensitivity/specificity; 93.21%/96.47%). Furthermore, in a fecal occult blood test (FOBT) of available validation samples, the discriminating power of CRC LOME was much stronger (sensitivity/specificity; 94.79%/97.96%) than that of the FOBT (sensitivity/specificity; 50.00%/100.0%), which is the standard CRC screening tool. The robust discriminating power of the LOME scheme was reconfirmed in screens for BRC (sensitivity/specificity; 92.45%/96.57%) and GC (sensitivity/specificity; 93.18%/98.85%). The present study demonstrates that LOMEs might be powerful non-invasive diagnostic tools with high sensitivity/specificity in cancer screening. The use of LOMEs could potentially enable screening for multiple diseases (including different types of cancer) from a single sampling of LMI information. © 2013 Wiley Periodicals, Inc.
    International Journal of Cancer 04/2014; 134(8). DOI:10.1002/ijc.28517 · 5.01 Impact Factor
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    Un Young Yu, Byong Chul Yoo, Jung-Hyuck Ahn
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    ABSTRACT: Overexpression of amyloid precursor protein with the Swedish mutation causes abnormal hyperphosphorylation of the microtubule-associated protein tau. Hyperphosphorylated isoforms of tau are major components of neurofibrillary tangles, which are histopathological hallmarks of Alzheimer's disease. Protein phosphatase 2A (PP2A), a major tau protein phosphatase, consists of a structural A subunit, catalytic C subunit, and a variety of regulatory B subunits. The B subunits have been reported to modulate function of the PP2A holoenzyme by regulating substrate binding, enzyme activity, and subcellular localization. In the current study, we characterized regulatory B subunit-specific regulation of tau protein phosphorylation. We showed that the PP2A B subunit PPP2R2A mediated dephosphorylation of tau protein at Ser-199, Ser-202/Thr-205, Thr-231, Ser-262, and Ser-422. Down-regulation of PPP2R5D expression decreased tau phosphorylation at Ser-202/Thr-205, Thr-231, and Ser-422, which indicates activation of the tau kinase glycogen synthase kinase 3 beta (GSK3β) by PP2A with PPP2R5D subunit. The level of activating phosphorylation of the GSK3β kinase Akt at Thr-308 and Ser-473 were both increased by PPP2R5D knockdown. We also characterized B subunit-specific phosphorylation sites in tau using mass spectrometric analysis. Liquid chromatography-mass spectrometry revealed that the phosphorylation status of the tau protein may be affected by PP2A, depending on the specific B subunits. These studies further our understanding of the function of various B subunits in mediating site-specific regulation of tau protein phosphorylation.
    Korean Journal of Physiology and Pharmacology 04/2014; 18(2):155-61. DOI:10.4196/kjpp.2014.18.2.155 · 1.26 Impact Factor
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    ABSTRACT: Resistance to 5-fluorouracil (5-FU) in patients with colorectal cancer prevents effective treatment and leads to unnecessary and burdensome chemotherapy. Therefore, prediction of 5-FU resistance is imperative. To identify the proteins linked to 5-FU resistance, two-dimensional gel electrophoresis-based proteomics was performed using the human colon cancer cell line SNU-C4R with induced 5-FU resistance. Proteins showing altered expression in SNU-C4R were identified by matrix-associated laser desorption/ionization-time-of-flight analysis, and their roles in susceptibility to 5-FU or radiation were evaluated in various cell lines by transfection of specific siRNA or creation of overexpression constructs. Changes in cellular signaling and expression of mitochondrial apoptotic factors were investigated by Western Blot analysis. A mitochondrial membrane potential probe (JC-1 dye) and a flow cytometry system were employed to determine the mitochondrial membrane potential. Finally, protein levels were determined by Western Blot analysis in tissues from 122 patients with rectal cancer to clarify whether each identified protein is a useful predictor of a chemoradiation response. We identified mitochondrial phosphoenolpyruvate carboxykinase (mPEPCK) as a candidate predictor of 5-FU resistance. PEPCK was downregulated in SNU-C4R compared with its parent cell line SNU-C4. Overexpression of mPEPCK did not significantly alter the susceptibility to either 5-FU or radiation. Suppression of mPEPCK led to a decrease in both the cellular level of phosphoenolpyruvate and the susceptibility to 5-FU and radiation. Furthermore, the cellular levels of phosphoenolpyruvate (an end product of PEPCK and a substrate of pyruvate kinase), phosphorylated AKT, and phosphorylated 4EBP1 were decreased significantly secondary to the mPEPCK suppression in SNU-C4. However, mPEPCK siRNA transfection induced changes in neither the mitochondrial membrane potential nor the expression levels of mitochondrial apoptotic factors such as Bax, Bcl-2, and Bad. Downregulation of total PEPCK was observed in tissues from patients with rectal cancer who displayed poor responses to preoperative 5-FU-based radiation therapy. Our overall results demonstrate that mPEPCK is a useful predictor of a response to chemoradiotherapy in patients with rectal cancer.
    BMC Cancer 03/2014; 14(1):160. DOI:10.1186/1471-2407-14-160 · 3.32 Impact Factor
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    ABSTRACT: The aim of this study was to investigate whether profiling metabolic compounds in human colon cancer cells with induced 5-florouracil resistance enables identification of predictive biomarkers for 5-florouracil resistance.
    Hepato-gastroenterology 03/2014; 61(130):343-8. · 0.91 Impact Factor
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    ABSTRACT: Numerous derivatives of kojic acid have been synthesised to expand its immunopharmacological uses. Kojic acid is known to have anti-cancer, anti-inflammatory, and anti-melanogenesis effects. We found that (5-hydroxy-4-oxo-4H-pyran-2-yl)methyl 6-hydroxynaphthalene-2-carboxylate (MHNC) strongly suppressed the production of nitric oxide (NO) in an initial screening experiment. In this study, we explored the in vitro and in vivo anti-inflammatory activity of MHNC and its inhibitory mechanisms using lipopolysaccharide (LPS)-treated RAW264.7 cells and HCl/EtOH-treated ICR mice. MHNC dose-dependently diminished the secretion of nitric oxide (NO) and prostaglandin (PG)E2 in LPS-treated RAW264.7 cells. This compound also suppressed the upregulation of mRNA levels for the inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 genes. Additionally, the transcriptional activation of these genes was inhibited by MHNC through the suppression of the nuclear translocation of nuclear factor (NF)-κB subunits (p65 and p50), as determined by a luciferase reporter assay. Interestingly, MHNC treatment was found to suppress a series of upstream signalling cascades consisting of IκBα, AKT, PDK1, Src, and Syk for NF-κB activation. Furthermore, a direct enzyme assay with purified Src and Syk and luciferase assays using Src and Syk overexpression indicated that these enzymes were directly inhibited by MHNC. Finally, MHNC (20mg/kg) prevented inflammatory symptoms of the stomach in mice treated with HCl/EtOH by reducing phospho-IκBα levels. Taken together, our data suggest that MHNC may negatively modulate in vitro and in vivo inflammatory responses via the direct suppression of Syk/Src and NF-κB.
    International immunopharmacology 02/2014; DOI:10.1016/j.intimp.2014.02.019 · 2.71 Impact Factor
  • EPMA Journal, The 02/2014; 5(Suppl 1):A47. DOI:10.1186/1878-5085-5-S1-A47
  • 02/2014; 5(Suppl 1):A46-A46. DOI:10.1186/1878-5085-5-S1-A46
  • EPMA Journal, The 02/2014; 5(Suppl 1):A45. DOI:10.1186/1878-5085-5-S1-A45
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    ABSTRACT: Cancer stem cells (CSCs) are known to be resistant to conventional chemotherapy and radiotherapy. Specific CSC targeting and eradication is therefore a therapeutically important challenge. CD133 is a colorectal CSC marker with unknown function(s). Assessing proteomic changes induced by CD133 may provide clues not only to new CD133 functions but also to the chemotherapy and radiation susceptibility of colon cancer cells. To identify the proteins affected by CD133, CD133-positive (CD133+), and CD133-negative (CD133-) human colon cancer cells were obtained by cell sorting. Whole proteomes were profiled from SW620/CD133+ and SW620/CD133- cells and analyzed by 2D-based proteome analysis. Nucleophosmin (NPM1) was identified as a protein regulated by CD133. CD133 protein level was not affected by NPM1, and an interaction between the two proteins was not observed. CD133 and NPM1 protein levels were positively correlated in 11 human colon cancer cell lines. The CD133+ subpopulation percentage or its value normalized against CD133 protein level was only linked to intrinsic susceptibility of human colon cancer cells to 5-fluorouracil (5-FU). However, either suppression of CD133 or NPM1 significantly increased 5-FU susceptibility of SW620. The present study suggests that CD133-regulated NPM1 protein level may provide a clue to novel CD133 function(s) linked to human colon cancer cell susceptibility to chemotherapy.
    Electrophoresis 02/2014; 35(4). DOI:10.1002/elps.201300364 · 3.16 Impact Factor
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    ABSTRACT: Pancreatic cancer is the fourth leading cause of cancer-related deaths. Therefore, in order to improve survival rates, the development of biomarkers for early diagnosis is crucial. Recently, diabetes has been associated with an increased risk of pancreatic cancer. The aims of this study were to search for novel serum biomarkers that could be used for early diagnosis of pancreatic cancer and to identify whether diabetes was a risk factor for this disease. Blood samples were collected from 25 patients with diabetes (control) and 93 patients with pancreatic cancer (including 53 patients with diabetes), and analyzed using matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF/MS). We performed preprocessing, and various classification methods with imputation were used to replace the missing values. To validate the selection of biomarkers identified in pancreatic cancer patients, we measured biomarker intensity in pancreatic cancer patients with diabetes following surgical resection and compared our results with those from control (diabetes-only) patients. By using various classification methods, we identified the commonly splitting protein peaks as m/z 1,465, 1,206, and 1,020. In the follow-up study, in which we assessed biomarkers in pancreatic cancer patients with diabetes after surgical resection, we found that the intensities of m/z at 1,465, 1,206, and 1,020 became comparable with those of diabetes-only patients.
    Cancer informatics 01/2014; 13(Suppl 7):45-53. DOI:10.4137/CIN.S16341
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    ABSTRACT: Inflammation is a natural host defensive process that is largely regulated by macrophages during the innate immune response. Mitogen-activated protein kinases (MAPKs) are proline-directed serine and threonine protein kinases that regulate many physiological and pathophysiological cell responses. p38 MAPKs are key MAPKs involved in the production of inflammatory mediators, including tumor necrosis factor- α (TNF- α ) and cyclooxygenase-2 (COX-2). p38 MAPK signaling plays an essential role in regulating cellular processes, especially inflammation. In this paper, we summarize the characteristics of p38 signaling in macrophage-mediated inflammation. In addition, we discuss the potential of using inhibitors targeting p38 expression in macrophages to treat inflammatory diseases.
    Mediators of Inflammation 01/2014; 2014:352371. DOI:10.1155/2014/352371 · 2.42 Impact Factor

Publication Stats

729 Citations
192.64 Total Impact Points

Institutions

  • 2004–2014
    • National Cancer Center Korea
      • Colorectal Cancer Branch
      Kōyō, Gyeonggi Province, South Korea
    • Seoul National University
      • Cancer Research Institute
      Seoul, Seoul, South Korea
  • 2013
    • National Cancer Institute (USA)
      베서스다, Maryland, United States
    • Sungkyunkwan University
      • Department of Genetic Engineering
      Seoul, Seoul, South Korea
  • 2011
    • Kangwon National University
      Shunsen, Gangwon, South Korea