• Title/Summary/Keyword: 폐암(肺癌)

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Promoter -202 A/C Polymorphism of Insulin-like Growth Factor Binding Protein-3 Gene and Non-small Cell Lung Cancer Risk (인슐린양 성장 인자 결합 단백-3 유전자 -202 좌위의 다형성에 따른 비소세포폐암의 위험도)

  • Moon, Jin Wook;Chang, Yoon Soo;Han, Chang Hoon;Kang, Shin Myung;Park, Moo Suk;Byun, Min Kwang;Chung, Wou Young;Park, Jae Jun;Yoo, Kyeong Nam;Shin, Ju Hye;Kim, Young Sam;Chang, Joon;Kim, Sung Kyu;Kim, Hee Jung;Kim, Se Kyu
    • Tuberculosis and Respiratory Diseases
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    • v.58 no.4
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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.

Microsatellite Alterations of Plasma DNA in Non Small Cell Lung Cancer (비소세포폐암 환자의 혈장 DNA를 이용한 Microsatellite 분석)

  • Kim, Kyu-Sik;Kim, Eun-Jung;Kim, Soo-Ock;Oh, In-Jae;Park, Chang-Min;Jeong, Ju-Yeon;Kim, Yu-Il;Lim, Sung-Chul;Park, Jong-Tae;Kim, Young-Chul
    • Tuberculosis and Respiratory Diseases
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    • v.58 no.4
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    • pp.352-358
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    • 2005
  • Microsatellites are short tandem repeated nucleotide sequences that are present throughout the human genome. Variations in the repeat number or a loss of heterozygosity around the microsatellites have been termed a microsatellite alteration (MA). A MA reflects the genetic instability caused by an impairment in the DNA mismatch repair system and is suggested to be a novel tumorigenic mechanism. A number of studies have reported that MA in the DNA extracted from the plasma occurs at varying frequencies among patients with a non-small cell lung carcinoma (NSCLC). The genomic DNA from 9 subjects with a non-small cell lung cancer (squamous cell cancer 6, adenocarcinoma 2, non-small cell lung cancer1) and 9 age matched non-cancer control subjects (AMC: tuberculosis 3, other inflammatory lung disease 6) and 12 normal control subjects (NC) were extracted from the peripheral blood leukocytes and plasma. Three microsatellite loci were amplified with the primers targeting the Gene Bank sequence D21S1245, D3S1300, and D3S1234. MA in the form of an allelic loss or a band shift was examined with 6% polyacrylamide gel electrophoresis and silver staining. None (0/12) of the NC subjects less than 40 years of age showed a MA in any of the three markers, while 88.9%(8/9) of the AMC above 40 showed a MA in at least one of the three markers (p<0.05). Sixty percent(6/10) of the control subjects with a smoking history showed a MA in one of the three markers, while 9.1%(1/11) of the control subjects without smoking history showed a MA (p<0.05). However, not only did 66.7%(6/9) of lung cancer patients show a MA in at least one of the three markers but so did 88.9%(8/21) of the AMC patients (p>0.05). In conclusion, a MA in the D21S1245, D3S1300, and D3S1234 loci using DNA extracted from the plasma was detected in 66.7% of lung cancer while no MA was found in the young non-smoking control subjects. However, many of the non-cancer control subjects (aged smokers) also showed a MA, which compromised the specificity of the MA analysis as a screening test. Therefore, a further study with a larger sample size will be needed.

Radiation Therapy for Superior Vena Cava Syndrome (상대정맥증후군의 방사선치료)

  • Kim, Jin-Hee
    • Radiation Oncology Journal
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    • v.23 no.2
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    • pp.78-84
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    • 2005
  • Purpose: The studied the effect of such variables as the symptom improvement rate, survival and prognostic factors on the treatment results of radiation therapy for Superior Vena Cava Syndrome (SVCS). Materials and Methods: From 1988 to 2003, seventy two patients with SVCS were treated with radiation therapy at the Department of Radiation Oncology, Keimyung University Dongsan Medical Center. The patients' ages ranged from 10 to 83 years old with the median age being 61, and sixty four patients were male. For the causes of the SVCS, 64 patients had lung cancer, four had metastatic lung cancer, two had malignant lymphoma and two had thymoma. The radiotherapy was delivered with 6-MV X-rays and all patients received above 900 cGy up to 6,600 cGy, with the median dose being 4,000 cGy The follow-up periods were from 1 to 180 months with a median of 5.6 months. Results: The main clinical manifestations were dyspnea ($84.7\%$), facial edema ($81.9\%$), arm edema ($22.2\%$), neck vein distension ($25\%$), hoarseness ($12.5\%$) and facial plethora ($5.6\%$). Eighty percent of patients achieved excellent to good symptom improvement and $19.4\%$ experienced minimal improvement. The median survival period was 5.1 months, and overall survival rates were $17.7\%$ at 2 years (2YOS) and $14.8\%$ at five years (5YOS) for all the patients. The median survival period, the two and five year disease free survival rates were 4.3 months, $16.7\%$ and $13.4\%$ for the lung cancer patients, respectively. The total tumor dose was a statistically significant survival factor on the univariate analysis for the patients with lung cancer (2YSR; > 30 Gy, $25.6\%$, $\leq$ 30 Gy $6.7\%$, p<0.01). On the multivariated analysis, a higher total tumor dose (p<0.01) and younger age (p<0.05) were statistically significant factors of survival for the lung cancer patients. Patients with NSCLC showed better survival than did the patients with SCLC, but this was not statistically significant (p > 0.05), Conclusion: Radiation therapy for the patients with SVCS due to malignancy could be an effective treatment. We considered that radiation therapy above 30 Gy of the total tumor dose may improve survival for SVCS due to lung cancer.

Curcumin-induced Cell Death of Human Lung Cancer Cells (Curcumin에 의해 유도되는 인간 폐암 세포주의 세포사멸)

  • Hwasin Lee;Bobae Park;Sun-Nyoung Yu;Ho-Yeon Jeon;Bu Kyung Kim;Ae-Li Kim;Dong Hyun Sohn;Ye-Rin Kim;Sang-Yull Lee;Dong-Seob Kim;Soon-Cheol Ahn
    • Journal of Life Science
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    • v.33 no.9
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    • pp.713-723
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    • 2023
  • Lung cancer is a type of cancer that has the highest mortality rate. It is mainly classified into small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC). Chemotherapy is used to treat lung cancer, but long-term treatment causes side effects and drug resistances. Curcumin is a bright yellow polyphenol extracted from the root of turmeric. It has biological activities, such as anti-oxidant, anti-cancer, and anti-inflammatory effects. In this study, we observed differential cell death in human lung cancer cells. Based on the results, curcumin at 10, 30, and 50 μM exhibited a dose-dependent inhibition on the cell survival of several lung cancer cells, with minor differential phenotypes. In addition, apoptosis, autophagy, and reactive oxygen species (ROS) regeneration were observed through flow cytometry. Curcumin dose-dependently increased these phenotypes in A549 (NSCLC) and DMS53 (SCLC), which were restored by corresponding inhibitors. Western blotting was performed to measure the level of expression of apoptosis- and autophagy-related proteins. The results indicate that Bax, PARP, pro-caspase-3, and Bcl-2 were dose-dependently regulated by curcumin, with seemingly higher Bax/Bcl-2 ratios in DMS53. In addition, autophagic proteins, p-AKT, p62, and LC3B, were dose-dependently regulated by curcumin. ROS inhibition by diphenyleneiodonium reduced the induction of apoptosis and autophagy generated by curcumin. Taken together, it is suggested that curcumin induces apoptosis and autophagy via ROS generation, leading to cell death, with minor differences between human lung cancer cells.

폐암

  • 대한결핵협회 편집부
    • 보건세계
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    • v.38 no.3 s.415
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    • pp.17-21
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    • 1991
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폐암

  • 대한결핵협회 편집부
    • 보건세계
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    • v.38 no.4 s.416
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    • pp.26-29
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    • 1991
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폐암

  • 김성규
    • The Monthly Diabetes
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    • s.45
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    • pp.32-38
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    • 1993
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Adjuvant Chemotherapy after Surgical Resection for Small-Cell Carcinoma of Lung (소세포폐암에서 수술 후 복합화학요법의 성적)

  • Kim, Hak-Ryul;Jung, Jong-Hoon;Kim, Hwi-Jung;Yang, Sei-Hoon;Jeong, Eun-Taik
    • Tuberculosis and Respiratory Diseases
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    • v.57 no.5
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    • pp.443-448
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    • 2004
  • Background : Small-cell carcinomas of lung have a tendency for rapid growth and early wide metastasis. Despite the high response rates of combination chemotherapy alone or with radiotherapy, the overall long-term survival rate is very disappointing. According to autopsy findings, the common cause of failure is local recurrence in the primary cancer site. Therefore, surgical resection with combined chemotherapy has recently been attempted for very early stage small-cell carcinomas of the lung. Methods : 10 patients (TNM I & II: 5 cases each) undergoing surgical resection for small-cell carcinomas of the lung were treated with adjuvant chemotherapy in an attempt to prolong survival. Of these, 9 patients received chemotherapy, and a retrospective study for survival undertaken (Kaplan-Meier analysis). Results : The median survival time was 26 months, and the 2- and 5-year survival rates were 68.6 and 46.7%, respectively. If the 1 patient not having undergone chemotherapy was excluded, the 2-, 5-year survival rates were 76.2 and 50.8%, respectively? No difference in the survival rate was seen between patients with TNM stages I and II. Conclusion : Adjuvant chemotherapy after surgical resection results in prolonged survival for patients with TNM stages I and II small-cell carcinomas of the lung.