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Risk factors associated with EGFR mutated advanced lung cancer
( Won-il Choi ),( Jihyeon Jeong ),( Choong Won Lee ) 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.-
Background: Epidermal growth factor receptor (EGFR) mutation is the most frequently encountered oncogenic driver in lung cancer. Risk factors for EGFR mutation may help prevention, surveillance, and diagnosis strategies of EGFR mutated lung cancer. Methods: A nationwide, retrospective, longitudinal, cohort study was performed between January 2002 and December 2015. Patient data were collected from the Korean National Health Insurance Database. The lung cancer group included EGFR tyrosine kinase inhibitor (TKI) treated patients. Controls were randomly selected from people without a history of lung cancer and determined to be four times the number of patients with EGFR mutated advanced lung cancer. The risk model of developing EGFR mutated lung cancer was constructed by multiple logistic regression analysis with age, sex, smoking status, body mass index, comorbidities, residential area, and income. Results: Among the 2010 new cases of lung cancer treated in 2010-2015, 214 cases were classified as EGFR mutated advanced lung cancer. The risk of developing EGFR mutated advanced lung cancer was higher in patients in their 50s (odds ratio [OR]: 3.42; 95% confidence interval [CI]: 1.68-6.93), 60s (OR: 7.04; 95% CI: 3.35-14.77), 70s (OR: 10.27; 95% CI: 4.73-22.30), and >80 years (OR: 5.98; 95% CI: 2.25-15.92) compared to those in their 40s. The risk of developing EGFR mutated lung cancer was also higher in hospitalized patients with a history of pneumonia (OR: 5.22; 95% CI: 1.88-14.46) and those with gastroesophageal reflux disease (OR: 2.02; 95% CI: 1.32-3.07). The risk was not associated with cigarette smoking, sex, and body mass index. Conclusions: In this observational study of patients with EGFR mutated advanced lung cancer, compared with those who did not have lung cancer, it was associated with age, history of being hospitalized for pneumonia, and gastroesophageal reflux disease.
Choi, Won-Il,Kim, Min-Young,Jeon, Bu-Nam,Koh, Dong-In,Yun, Chae-Ok,Li, Yan,Lee, Choong-Eun,Oh, Jiyoung,Kim, Kunhong,Hur, Man-Wook American Society for Biochemistry and Molecular Bi 2014 The Journal of biological chemistry Vol.289 No.27
<P>Promyelocytic leukemia zinc finger (PLZF) is a transcription repressor that was initially isolated as a fusion protein with retinoic acid receptor α. PLZF is aberrantly overexpressed in various human solid tumors, such as clear cell renal carcinoma, glioblastoma, and seminoma. PLZF causes cellular transformation of NIH3T3 cells and increases cell proliferation in several cell types. PLZF also increases tumor growth in the mouse xenograft tumor model. PLZF may stimulate cell proliferation by controlling expression of the genes of the p53 pathway (<I>ARF</I>, <I>TP53</I>, and <I>CDKN1A</I>). We found that PLZF can directly repress transcription of <I>CDKN1A</I> encoding p21, a negative regulator of cell cycle progression. PLZF binds to the proximal Sp1-binding GC-box 5/6 and the distal p53-responsive elements of the <I>CDKN1A</I> promoter to repress transcription. Interestingly, PLZF interacts with Sp1 or p53 and competes with Sp1 or p53. PLZF interacts with corepressors, such as mSin3A, NCoR, and SMRT, thereby deacetylates Ac-H3 and Ac-H4 histones at the <I>CDKN1A</I> promoter, which indicated the involvement of the corepressor·HDACs complex in transcription repression by PLZF. Also, PLZF represses transcription of <I>TP53</I> and also decreases p53 protein stability by ubiquitination. PLZF may act as a potential proto-oncoprotein in various cell types.</P>
Choong Won Lee,Han Dong Sung,Byong Moon Choi,Chun Wook Kim,Su Jin Jun,Sang Jo Min 대한내과학회 2003 The Korean Journal of Internal Medicine Vol.18 No.2
A case of Mycobacterium avium arthritis in a 39-year-old female patient with mixed connective tissue disease (MCTD) was reported. An extra-articular abscess had formed outside the knee joint and extended down the calf. A culture was taken of the abscess a
Use of Antacid and the Incidence of Interstitial Lung Disease
( Won-il Choi ),( Jihyeon Jeong ),( Dong Yoon Lee ),( Choong Won Lee ) 대한결핵 및 호흡기학회 2020 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.128 No.-
Purpose To investigate whether Antacid (proton pump inhibitor and/or histamine-2 receptor antagonist) as a preventive measure to reduce the development of interstitial lung disease (ILD) in a real-world Methods This nationwide, retrospective, cohort study used data from the Korean National Health Insurance Database, NHIS-NSC 2002-2015. Eligible participants (n = 497,262) were people aged above 40 years who had treated with either PPI +/- H-2 blocker or H-2 blocker only between 2011 and 2015 and had no history of ILD between 2002 and 2010. The duration of antacid administration between January 2006 and December 2010 was calculated for each participant. Exposure to antacid medications was defined as administration of either proton pump inhibitors or histamine H2 receptor antagonists for more than 14 days, whereas no exposure or underexposure was defined as antacid treatment administered for less than 14 days. Newly developed ILDs were counted during the 5-year observation period (1 January 2011 to 31 December 2015). Results A total of 510 (0.14%) antacid-exposed patients (n = 345,904) developed ILD. Among patients with no antacid exposure or underexposure (n = 151,358), 162 (0.10%) developed ILD. In multivariable analysis, antacid exposure before the diagnosis of ILD cancer was independently associated with reduced incidence of ILD (hazard ratio [HR], 0.57; 95% confidence interval [CI], 0.45 to 0.71; P <0.001). Conclusions Antacid use might be independently associated with a decreased risk of ILD development.
Choi, Keun Hee,Shin, Choong Ho,Yang, Sei Won,Cheong, Hae Il The Korean Pediatric Society 2015 Clinical and Experimental Pediatrics (CEP) Vol.58 No.4
The calcium sensing receptor (CaSR) plays an important role in calcium homeostasis. Activating mutations of CaSR cause autosomal dominant hypocalcemia by affecting parathyroid hormone secretion in parathyroid gland and calcium resorption in kidney. They can also cause a type 5 Bartter syndrome by inhibiting the apical potassium channel in the thick ascending limb of the loop of Henle in the kidney. This study presents a patient who had autosomal dominant hypocalcemia with Bartter syndrome due to an activating mutation Y829C in the transmembrane domain of the CaSR. Symptoms of hypocalcemia occurred 12 days after birth and medication was started immediately. Medullary nephrocalcinosis and basal ganglia calcification were found at 7 years old and at 17 years old. Three hypercalcemic episodes occurred, one at 14 years old and two at 17 years old. The Bartter syndrome was not severe while the serum calcium concentration was controlled, but during hypercalcemic periods, the symptoms of Bartter syndrome were aggravated.
Reduction of Calbindin D-28k-Immunoreactive Neurons in the Dog Dentate Gyrus
CHOI, Jung Hoon,HWANG, In Koo,YOO, Ki-Yeon,YI, Sun Shin,PARK, Ok Kyu,LEE, Choong Hyun,YOON, Yeo Sung,WON, Moo-Ho Japanese Society of Veterinary Science 2009 The Journal of veterinary medical science Vol.71 No.8
<P>The calcium binding protein calbindin D-28k (CB) plays an important role in modulating the activity of neurons in the dentate gyrus. We observed CB immunoreactivity in the dentate gyrus of dogs of various ages (German shepherds). In the 1-year-old group, CB immunoreactivity was detected in almost all of granule cells with poor processes. In the 8-year-old group, the number of CB-immunoreactive <SUP>(+)</SUP> neurons in the granule cell layer was significantly reduced (73.2% vs. 1-year-old group), while CB<SUP>+</SUP> cell bodies and fibers were well developed. In the 10-year-old group, the number of CB<SUP>+</SUP> neurons was further reduced by 31.3% when compared to that in the 1-year-old group. This finding demonstrates that the number of CB<SUP>+</SUP> neurons decreases in the aged dog brain and this may be associated with reduction of function in the dentate gyrus.</P>