• Journal of Korean Biological Nursing Science
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• v.8 no.2
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• pp.5-12
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• 2006

목적 : 본 연구는 암환자 및 암의 유형에 따라 중요한 종양억제 조절인자로 알려져 있는 모노카인을 flowcytometry를 이용하여 분석, 비교하고자 하였다. 방법 : 연구대상은 고형종양(solid tumor)으로 진단받은 33세에서 76세 사이의 암환자 30명(유방암, 난소암, 폐암, 위암)을 대상으로 말초혈액 단구의 intracellular monokine 중 $TNF{\alpha}$, MIG, MIP를 분석한 유사실험설계 연구이다. 연구결과 : 암환자 군에서의 $TNF{\alpha}$, MIG, MIP 수치는 대조 군인 정상 군에 비해서 유의하게 증가되었으며 특히, 유방암과 난소암 환자 군에서의 $TNF{\alpha}$ 수치는 폐암과 위암의 대상자에 비해 의미 있는 차이를 보여주었다. 논의 : 본 연구에서 제시된 암환자 군에서의 모노카인 수치는 선행연구의 결과와 통일하게 종양 대상자의 면역에 중요한 역할을 하는 것으로 규명 되었으나, $TNF{\alpha}$는 고형종양 중에서도 여성생식기계 암환자 군에서 더 증가하였다. 이에 따라 종양 유형에 따른 모노카인의 역할과 호르몬과의 상호작용기전 규명에 대한 추후 연구가 필요하다.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.9
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• pp.3851-3864
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• 2014

Cytokine research is currently at the forefront in cancer research. Deciphering the functions of these multiple small molecules, discovered within the cell and in intercellular spaces, with their abundance and pleotrophism, was initially a great challenge. Advances in analytical chemistry and molecular biology have made it possible to unravel the pathophysiological functions of these polypeptides/proteins which are called interleukins, chemokines, monokines, lymphokines and growth factors. With more than 5 million women contracting cervical cancer every year this cancer is a major cause of mortality and morbidity the world over, particularly in the developing countries. In more than 95% of cases it is associated with human papilloma virus (HPV) infection which is persistent, particularly in those with a defective immune system. Although preventable, the mere magnitude of prevalence of HPV in the world population makes it a dominating current health hazard. The discovery of cytokine dysregulation in cervical cancer has spurted investigation into the possibility of using them as biomarkers in the early diagnosis of cases at high risk of developing cancer. Their critical role in carcinogenesis and progression of cervical cancer is now being revealed to a great extent. From diagnostics to prognosis, and now with a possible role in therapeutics and prevention of cervical cancer, the cytokines are being evaluated in all anticancer approaches. This review endeavours to capture the essence of the astonishing journey of cytokine research in cervical neoplasia.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.513-520
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• 1994

Background: The pathogenesis of silicosis has been focused on the interaction between alveolar macrophages and silica particle. Although fibrosis in silicosis has been studied extensively, the mechanism is still not fully understood. There is increasing evidence that monokines and arachidonic acid metabolites macrophage are involved in pathogenesis of silicosis. Recently, it was reported that prostaglandin E2 produced from macrophage counteracts the stimulatory effects of other monokines on fibroblast proliferation or collagen production. Until now, it was remained uncertain by which mechanism silica particle may activate alveolar macrophage to an enhanced release of prostaglandin E2. Methods: In order to investigate the relationship between the activity of alveolar macrophage and the production of $PGE_2$ from activated alveolar macrophage, the authors measured hydrogen peroxide and $PGE_2$ from alveolar macrophages activated by silica in vitro and from alveolar macrophages in the silicotic nodules from rat. Experimental silicosis was induced by intratracheal infusion of silica($SiO_2$) suspended in saline(50 mg/ml) in Sprague-Dawley rats. Results: produced by 1) The silicotic nodules with fibrosis were seen from the sections of rat lung at 60 days after intratracheal injection with 50 mg aqueous suspension of silica(Fig. 1). 2) In vitro, silica caused the dose dependent increase of hydrogen peroxide(p<0.05, Fig. 2A) and $PGE_2$(p>0.05, Fig. 2B) release from alveolar macrophages. Alveolar macrophages from rat with silicotic nodules released more hydrogen peroxide and $PGE_2$ than those of control group(p<0.05, Fig. 3). Conclusion: These results suggest that silica particle could activate macrophage directly and enhanced the release of $PGE_2$ and hydrogen peroxide from the alveolar macrophage.