• Journal of the Society of Cosmetic Scientists of Korea
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• 제35권1호
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• pp.73-78
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• 2009

In order to investigate the potential of a Dayflower (Commelina communis L.) extract as an active in gredient for whitening cosmetics, we prepared aqueous Commelina communis L. extract We measured its mushroom tyrosinase inhibitory activity, cellular tyrosinase activity, and melanin synthesis inhibitory activity in B16 melanoma cells. It did not show inhibitory activity against mushroom tyrosinase but showed melanin synthesis inhibitory activity. In a melanin synthesis inhibition assay using mouse B16-F10 melanoma cell, it suppressed melanin production up to 32% at a concentration of $1,000{\mu}/mL$ without cytotoxicity, and also reduced cellular tyrosinase activity to above 50 % above the concentration of $250{\mu}g/mL$. In study on the melanogenic protein expressions, it had especially influence on expression of tyrosinase protein, which is a well-known key protein on melanogenesis, and tyrosinase expression was gradually decreased in a dose-dependent. Dayflower also blocked N-glycosylation of TRP-2, but affected on the expression of TRP-1 rather than on blocking of N-glycosylation processing. Therefore, this result suggests that aqueous Commelina communis L. extract could be used as an active ingredient for whitening cosmetics.

• Journal of the Society of Cosmetic Scientists of Korea
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• 제30권2호
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• pp.247-251
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• 2004

UV radiation exerts various influences in the skin, including photoaging and inflammation (1). The MMPs (Matrix metalloproteinases), which are induced by UV irradiation, can degrade matrix proteins, and these results in a collagen deficiency in photodamaged skin that leads to skin wrinkling. It has been known that the production of PGE$_2$ stimulates MMPs expression, and inhibits procollagen (2). Thus, it is possible that the induction of MMPs and the inhibition of matrix protein synthesis by UV -induced PGE$_2$ may play some role in UV-induced collagen deficiency in photoaged skin. Fructose-1,6-diphosphate (FDP), a glycolytic metabolite, is reported to have cytoprotective effects against ischemia and postischemic reperfusion injury of brain and heart, presumably by augmenting anaerobic carbohydrate metabolism (3). And also, FDP significantly prevent skin aging by decreasing facial winkle compared with vehicle alone after 6 months of use. We studied the mechanism of anti-aging effect of FDP on UVB-irradiated HaCaT keratinocyte model. FDP has protective role in UVB injured keratinocyte by attenuating prostaglandin E$_2$ (PGE$_2$) production and COX-2 expression. And FDP also suppressed UVB-induced MMP-2 expression. Further, to delineate the inhibition of UVB-induced COX-2 and MMPs expression with cell signaling pathways, treatment of FDP to HaCaT keratinocytes resulted in marked inhibition of UVB-induced phosphorylation of ERK1/2, JNK. It also prevents UV induced NFB translocation, which are activated by cellular inflammatory signal. Our results indicate that FDP has protecting effects in UV-injured skin aging by decreasing UVB-induced COX-2 and MMPs expression, which are possibly through blocking UVB-induced signal cascades.

• Journal of Life Science
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• 제15권6호
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• pp.895-903
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• 2005

Thrombospondin-1 (TSP-1), a negative regulator in tumor growth and angiogenesis, is cell-type specifically regulated under pathological conditions or by extracellular stimuli, and the regulation of TSP-1 gene expression is important for developing new approaches in tumor therapy. Mistletoe is a parasitir plant that have been used for immunomodulation and antitumor therapy. Helixor A is an aqueous part of mistletoes extract. Here we showed that TSP-1 expression was significantly induced at both mRNA and protein levels in the Hepatocarcinorna cell line (Hep3B) and primary bovine endothelial cell line (BAE) exposed to Helixor A. Our promoter analysis confirmed that the expression of TSP-1 gene was regulated by Helixor A at the transcriptional level. In cell invasion assay, the conditioned media obtained from treatment of these cells significantly reduced the number of invasive cells and also inhibited capillary-like tube formation of BAE cells on Matrigel. Moreover, the inhibitory efforts of the conditioned media on cell invasion and tube formation were reversed by blocking with anti-TSP-1 neutralizing antibodies, suggesting that TSP-1 is involved in Helixor A-indured antiangiogenic effect. Taken together, our results suggest that Helixor A have an antiangiogenic effects through upregulation of TSP-1.

• Archives of Pharmacal Research
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• 제29권7호
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• pp.591-597
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• 2006

Aerial parts of Artemisia asiatica (Compositae) have been traditionally used as an oriental medicine for the treatment of inflammatory and ulcerogenic diseases. In the present study, artemisolide was isolated as a nuclear factor $(NF)-{\kappa}B$ inhibitor from A. asiatica by activity-guided fractionation. Artemisolide inhibited $NF-{\kappa}B$ transcriptional activity in lipopolysaccharide (LPS)-stimulated macrophages RAW 264.7 with an $IC_{50}$ value of $5.8\;{\mu}M$. The compound was also effective in blocking $NF-{\kappa}B$ transcriptional activities elicited by the expression vector encoding the $NF-{\kappa}B$ p65 or p50 subunits bypassing the inhibitory kB degradation signaling $NF-{\kappa}B$ activation. The macrophages markedly increased their $PGE_2$ and NO production upon exposure to LPS alone. Artemisolide inhibited LPS-induced $PGE_2$ and NO production with $IC_{50}$ values of $8.7\;{\mu}M$ and $6.4\;{\mu}M$, respectively, but also suppressed LPS-induced synthesis of cyclooxygenase (COX)-2 or inducible NO synthase (iNOS). Taken together, artemisolide is a $NF-{\kappa}B$ inhibitor that attenuates LPS-induced production of $PGE_2$ or NO via down-regulation of COX-2 or iNOS expression in macrophages RAW 264.7. Therefore, artemisolide could represent and provide the anti-inflammatory principle associated with the traditional medicine, A. asiatica.

• The Korea Journal of Herbology
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• 제32권2호
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• pp.107-114
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• 2017

Objectives : Tribulus terrestris $Linn{\acute{e}}$ (Tribuli Fructus; TF) has been used to treat hypochondrium, agalactia, nebula, itching and vitiligo in traditional Korean medicine. In this study, we investigated the effects of TF 30% ethanol extract on inflammatory responses in IgE-stimulated RBL-2H3 mast cells. Methods : TF extract was prepared by 30% ethanol. RBL-2H3 cells, a rat mast cell line, were treated with TF extract at different concentrations for 1 hr and then stimulated with DNP-IgE/HSA for indicated times. Cell viability was measured by WST-1 assay. The expression of inflammatory cytokines (IL-4, IL-13 and $IFN-{\gamma}$) mRNA was determined by reverse transcriptase-PCR, and the phosphorylation of ERK1/2, p38 and JNK MAP kinases (MAPKs) was determined by Western blot. The nuclear expression of $NF-{\kappa}B$ p65 in the cells was detected by Western blot and immunocytochemistry, respectively. Results : The treatment of TF extract at 0.1 and $0.2mg/m{\ell}$ significantly decreased the expression of IL-4 and IL-13 mRNA in IgE-stimulated RBL-2H3 mast cells, while significantly increased the expression of $IFN-{\gamma}$ mRNA. TF extract treatment was also inhibited the phosphorylation of ERK1/2, p38 and JNK MAPKs in IgE-stimulated RBL-2H3 mast cells in a dose-dependent manner. In addition, TF extract significantly blocked the translocation of $NF-{\kappa}B$ p65 into the nuclear of cells after IgE stimulation. Conclusions : These results indicate that TF extract inhibits inflammatory response in IgE-stimulated mast cells through blocking MAPKs/$NF-{\kappa}B$ pathway. This suggests that TF extract has an anti-inflammatory activity in mast cell activation.

• Journal of Life Science
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• 제19권4호
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• pp.423-428
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• 2009

Selenium was investigated using human origin preadipocytes to see whether it possesses preventive or therapeutic effects for obesity. Unveiling the potential of selenium in the reduction of adipogenesis can help predict the therapeutic capabilities of selenium in obesity. In the present study, the molecular mechanism of the inhibition of adipogenesis by selenium was explored to unravel the involvement of the AMP-activated protein kinase. There is emerging evidence that AMPK, a sensor of cellular energy status, is a possible molecular target of controlling adipocyte differentiation on the basis of discovery that AMPK is responsible for the major metabolic responses to exercise, and integration of nutritional and hormonal signals to modulate feeding behavior or energy expenditure in the hypothalamus. Treatment of selenium resulted in inhibition of the adipocyte differentiation process and induction of mature apoptosis in 3T3-L1 adipocytes. We hypothesized that selenium may exert anti-adipogenic potential though modulating AMPK. We have found that selenium significantly activated AMPK and phosphorylated its substrate acetyl-CoA carboxylase ($ACC-serine^{79}$) during the inhibitory process of adipocytes. Also, the inhibition process of adipocyte differentiation by selenium was comparable to either reveratrol or a synthetic AMPK activator, AICAR (5-aminoimidazole-4-carboxamide-1-${\beta}$-D-ribofuranoside). To evaluate the involvement of AMPK in anti-lipogensis, we applied AICAR and Compound C, an AMPK inhibitor, to 3T3-L1-adipocytes and found that AMPK is required for the adipocyte differentiation blocking process. These results suggest that selenium has a potential to control adipogenesis and that this effect is mediated by AMPK, an essential kinase for both inhibition of adipocyte differentiation and apoptosis of mature adipocytes.

• Journal of Life Science
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• 제20권12호
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• pp.1772-1776
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• 2010

Transcription factors Nrf2 and NF-${\kappa}B$ are important regulators of the innate immune response, and their cross-talks in inflammation have been reported. Previously, we demonstrated that gold(I)-compound auranofin, an inhibitor of NF-${\kappa}B$ signal, induced Nrf2 activation in human synovial cells and monocytic cells. To investigate whether the Nrf2 activation is involved in the mechanism of the auranofin-attenuated NF-${\kappa}B$ signaling, we examined the effects of Nrf2 knockdown on NF-${\kappa}B$ activation using rheumatic synovial cells. When the cells were transfected with a specific siRNA for Nrf2, the gene expression was perfectly blocked. However, the Nrf2 knockdown did not cancel the suppressive effect of auranofin on TNF-$\alpha$-induced $I{\kappa}B-{\alpha}$ degradation. Treatment with a specific siRNA for HO-1, which is a target of Nrf2 and plays a role in anti-inflammation, also did not affect the blocking activity of auranofin on $I{\kappa}B-{\alpha}$ degradation. In addition, auranofin-inhibited ICAM-1 expression was not restored by Nrf2 knockdown. These findings indicate that the activated Nrf2 and HO-1 are not associated with the suppressive action of auranofin on the pro-inflammatory cytokines-stimulated NF-${\kappa}B$ activation. This suggests that Nrf2/HO-1 and NF-${\kappa}B$ signals, which are regulated by auranofin, participate in the anti-inflammatory action of auranofin via independent pathways in rheumatic synovial cells.

• Tuberculosis and Respiratory Diseases
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• 제57권5호
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• pp.449-460
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• 2004

Background : PS-341 is a novel, highly selective and potent proteasome inhibitor, which showed cytotoxicity against some tumor cells. Its anti-tumor activity has been suggested to be associated with modulation of the expression of apoptosis-associated proteins, such as p53, $p21^{WAF/CIP1}$, $p27^{KIP1}$, NF-${\kappa}B$, Bax and Bcl-2. c-Jun N-terminal kinase (JNK) and glycogen synthase kinase-$3{\beta}$ (GSK-$3{\beta}$) are important modulators of apoptosis. However, their role in PS-341-induced apoptosis is unclear. This study was undertaken to elucidate the role of JNK and GSK-$3{\beta}$ in the PS-341-induced apoptosis in lung cancer cells. Method : NCI-H157 and A549 cells were used in the experiments. The cell viability was assayed using the MTT assay and apoptosis was evaluated by proteolysis of PARP. The JNK activity was measured by an in vitro immuno complex kinase assay and by phosphorylation of endogenous c-Jun. The protein expression was evaluated by Western blot analysis. Dominant negative JNK1 (DN-JNK1) and GSK-$3{\beta}$ were overexpressed using plasmid and adenovirus vectors, respectively. Result : PS-341 reduced the cell viability via apoptosis, activated JNK and increased the c-Jun expression. Blocking of the JNK activation by overexpression of DN-JNK1, or pretreatment with SP600125, suppressed the apoptosis induced by PS-341. The activation of caspase 3 was mediated by JNK activation. Blocking of the caspase 3 activation suppressed PS-341-induced apoptosis. PS-341 activated the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, but its blockade enhanced the PS-341-induced cell death via apoptosis. GSK-$3{\beta}$ was inactivated by PS-341 via the PI3K/Akt pathway. Overexpression of constitutively active GSK-$3{\beta}$ enhanced PS-341-induced apoptosis; in contrast, this was suppressed by dominant negative GSK-$3{\beta}$ (DN-GSK-$3{\beta}$). Inactivation of GSK-$3{\beta}$ by pretreatment with lithium chloride or the overexpression of DN-GSK-$3{\beta}$ suppressed both the JNK activation and c-Jun up-regulation induced by PS-341. Conclusion : The JNK/caspase pathway is involved in PS-341-induced apoptosis, which is negatively regulated by the PI3K/Akt-mediated inactivation of GSK-$3{\beta}$ in lung cancer cells.

• Journal of Haehwa Medicine
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• 제9권1호
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• pp.513-545
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• 2000

I. Introduction Bi(痺) means blocking. It can reach at the joints or muscles or whole body and make pains. Numbness and movement disorders. BiJeung can be devided into SilBi and HeoBi. In SilBi there are PungHanSeupBi, YeolBi and WanBi. In HeoBi, there are GiHyeolHeoBi, EumHeoBi and YangHeoBi. The common principle for the treatment of BiJeung is devision of the chronic stage and the acute stage. In the acute stage, BiJeung is usually cured easily but in the chronic stage, it is difficult. In the terminal stage, BiJeung can reach at the internal organs. BiJeung is one kind of symptoms making muscles, bones and jonts feel pain, numbness or edema. For example it can be gout or SLE etc. Many famous doctors studied medical science by their fathers or teachers. So the history of medical science is long. So I studied ${\ll}Bijeungjujip{\gg}$. II. Final Decision 1. BanSuMun(斑秀文) thought that BiJeung can be cured by blocking of blood stream. So he insisted that the important thing to cure BiJeung is to improve the blood stream. He usually used DangGuiSaYeokTang(當歸四逆湯), DangGuiJakYakSanHapORyeongSan, DoHong-SaMulTang(桃紅四物湯), SaMyoSanHapHeuiDongTang and HwangGiGyeJiOMulTang. 2. JangGeonBu(張健夫) focused on soothing muscles and improving blood seam. So he used many herbs like WiRyeongSeon(威靈仙), GangHwal(羌活), DokHwal(獨活), WooSeul(牛膝), etc. Especially he pasted wastes of the boiled herbs. 3. OSeongNong(吳聖農) introduced four rules to treat arthritis. So he usually used SeoGak-SanGaGam(犀角散加減), BoYanHwanOTang(補陽還五湯), ODuTang(烏頭湯), HwangGiGyeJiOMulTang. 4. GongJiSin thought disk hernia as one kind of BiJeung. And he said that Pung can hurt upper limbs and Seup can hurt lower limbs. He used to use GyeJiJakYakJiMoTang(桂枝芍藥知母湯). 5. LoJiJeong(路志正) introduced four principles to treat BiJeung. He used BangPungTang(防風湯), DaeJinGuTang) for PungBi(風痺), OPaeTang(烏貝湯) for HanBi(寒痺), YukGunJaTang(六君子湯) for SeupBi(濕痺) and SaMyoTang(四妙湯), SeonBiTang(宣痺湯), BaekHoGaGyeTang(白虎加桂湯) for YeolBi(熱痺). 6. GangChunHwa(姜春華) discussed herbs. He said SaengJiHwang(生地黃) is effective for PungSeupBi and WiRyungSun(威靈仙) is effective for the joints pain. He usually used SipJeonDaeBoTang(十全大補湯), DangGuiDaeBoTang(當歸大補湯), YoukGunJaTang(六君子湯) and YukMiJiHwanTang(六味地黃湯). 7. DongGeonHwa(董建華) said that the most important thing to treat BiJeung is how to use herbs. He usually used CheonO(川烏), MaHwang(麻黃) for HanBi, SeoGak(犀角) for YeolBi, BiHae) or JamSa(蠶沙) for SeupBi, SukJiHwang(熟地黃) or Vertebrae of Pigs for improving the function of kidney and liver, deer horn or DuChung(杜沖) for improving strength of body and HwangGi(黃?) or OGaPi(五加皮) for improving the function of heart. 8. YiSuSan(李壽山) devided BiJeung into two types(PungHanSeupBi, PungYeolSeupBi). And he used GyeJiJakYakJiMoTang(桂枝芍藥知母湯) for the treatment of gout. And he liked to use HwanGiGyeJiOMulTangHapSinGiHwan 枝五物湯合腎氣丸) for the treat ment of WanBi(頑痺). 9. AnDukHyeong(顔德馨) made YongMaJeongTongDan(龍馬定痛丹)-(MaJeonJa(馬錢子) 30g, JiJaChung 3g, JiRyong(地龍) 3g, JeonGal(全蝎) 3g, JuSa(朱砂) 0.3g) 10. JangBaekYou(張伯臾) devided BiJeung into YeolBi and HanBi. And he focused on improving blood stream. 11. JinMuO(陳茂梧) introduced anti-wind and dampness prescription(HoJangGeun(虎杖根) 15g, CheonChoGeun 15g, SangGiSaeng(桑寄生) 15g, JamSa(蠶絲) 15g, JeMaJeonJa(制馬錢子) 3g). 12. YiChongBo(李總甫) explained basic prescriptions to treat BiJeung. He used SinJeongChuBiEum(新定推痺陰) for HaengBi(行痺), SinJeongHwaBiSan(新定化痺散) for TongBi(痛痺), SinJeongGaeBiTang(新定開痺湯) for ChakBi(着痺), SinJeongCheongBiEum(新定淸痺飮) for SeupYeolBi(濕熱痺), SinRyeokTang(腎瀝湯) for PoBi(胞痺), ORyeongSan for BuBi(腑痺), OBiTang(五痺湯) for JangBi(臟痺), SinChakTang(腎着湯) for SingChakByeong(腎着病). 13. HwangJeonGeuk(黃傳克) used SaMu1SaDeungHapJe(四物四藤合制) for the treatment of a acute arthritis, PalJinHpPalDeungTang(八珍合八藤湯) or BuGyeJiHwangTangHapTaDeungTang(附桂地黃湯合四藤湯) for the chronic stage and ByeolGapJeungAekTongRakEum(鱉甲增液通絡飮) for EumHeo(陰虛) 14. GaYeo(柯與參) used HwalRakJiTongTang(活絡止痛湯) for shoulder ache, SoJongJinTongHwalRakTank(消腫鎭痛活絡湯) for YeolBi(熱痺), LiGwanJeolTang(利關節湯) for ChakBi(着痺), SinBiTang(腎痺湯) for SinBi(腎痺) and SamGyoBoSinHwan(三膠補腎丸) for back ache. 15. JangGilJin(蔣길塵) liked to use hot-character herbs and insects. And he used SeoGeunLipAnTang(舒筋立安湯) as basic prescription. 16. RyuJangGeol(留章杰) used GuMiGangHwalTang(九味羌活湯) and BangPungTang(防風湯) at the acute stage, ODuTang(烏頭湯) or GyeJiJakYakJiMoTang(桂枝芍藥知母湯) for HanBi of internal organs, YangHwaHaeEungTang(陽和解凝湯) for HanBi, DokHwalGiSaengTang(獨活寄生湯), EuiYiInTang(薏苡仁湯) for SeupBi, YukGunJaTang(六君子湯) for GiHeoBi(氣虛痺) and SeongYouTang(聖兪湯) for HyeolHeoBi(血虛痺). 17. YangYuHak(楊有鶴) liked to use SoGyeongHwalHyelTang(疏經活血湯) and he would rather use DoIn(桃仁), HongHwa(紅花), DangGui(當歸), CheonGung(川芎) than insects. 18. SaHongDo(史鴻濤) made RyuPungSeupTang(類風濕湯)-((HwangGi 200g, JinGu 20g, BangGi(防己) 15g, HongHwa(紅花) 15g, DoIn(桃仁) 15g, CheongPungDeung(靑風藤) 20g, JiRyong(地龍) 15g, GyeJi(桂枝) 15g, WoSeul(牛膝) 15g, CheonSanGap(穿山甲) 15g, BaekJi(白芷) 15g, BaekSeonPi(白鮮皮) 15g, GamCho(甘草) 15g).

• Tuberculosis and Respiratory Diseases
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• 제58권4호
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• pp.359-366
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• 2005

Background : IGFBP-3 inhibits the mitogenic and anti-apoptotic activity of IGF by blocking the binding of IGF to its receptor. However, under certain circumstances, IGFBP-3 can enhance the activity of IGF by protecting IGF from its degradation. More than half of the interindividual variations in IGFBP-3 levels are known to be genetically determined by the polymorphism at -202 locus of IGFBP-3 gene. Method : We attempted to ascertain whether A-202C polymorphic variation of IGFBP-3 gene constitutes a risk factor for non-small cell lung cancer (NSCLC), using PCR-restriction fragment length polymorphism (RFLP). Our study included 104 NSCLC patients and 104 age-, gender-, and smoking status-matched control subjects. Result : In the 104 NSCLC subjects, the genotypic frequencies at the -202 site were as follows: AA = 67 (64.4%), AC = 35 (33.7%), and CC = 2 (1.9%). We did detect significant differences in the genotypic distribution between the NSCLC and the control subjects (p<0.05), and the NSCLC risk correlated significantly with AA genotype at the -202 locus (AA>AC>CC). Using CC genotype as a reference, the odds ratio (OR) for the subjects with AC genotype was 2.60 (95% CI: 0.89 - 8.60), and the OR associated with AA genotype was 5.89 (95% CI: 1.92 - 21.16). Conclusion : These results indicate that the dysregulation of IGF axis should now be considered as another important risk factor for NSCLC, and a potential target for novel antineoplastic therapies and/or preventative strategies in high-risk groups.