• 대한핵의학회:학술대회논문집
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• 대한핵의학회 1998년도 제37차 추계학술대회
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• pp.47.2-47.2
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• 1998

• Asian Pacific Journal of Cancer Prevention
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• 제14권1호
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• pp.373-379
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• 2013

Background: Although caregiving to patients with terminal illness is known to be a stressful burden to family members, little attention has been focused on work-related problems. We aimed to investigate employment status and work-related difficulties of family caregivers of terminal cancer patients, comparing with the general population. Methods: Using structured questionnaires, we assessed family caregivers of 481 cancer patients determined by physicians to be terminally ill, from 11 university hospitals and the National Cancer Center in Korea. Results: Among 381 family caregivers of terminal cancer patients (response rate, 87.6%), 169 (43.9%) were not working before cancer diagnosis, but currently 233 (63.7%) were not working. Compared with the general population (36.5%), the percentage of not working among the family caregivers was higher (OR=2.39; 95%CI=1.73-3.29). A major reason for not working was to provide assistance to the patients (71.6%). 40.6% of those who continued working and 32.3% of those who not working family members reported extreme fatigue. Caregivers of old age, those who were female, those with a lower household income, and those caring for patients with a low performance status were not working at a more significant rate. Conclusion: Family caregivers of terminal cancer patients suffer job loss and severe work-related difficulties, probably due to caregiving itself and to fatigue. We need to develop supportive programs to overcome the burden of caregivers of the terminally ill.

• Asian Pacific Journal of Cancer Prevention
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• 제14권8호
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• pp.4501-4507
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• 2013

Caveolin-1 is a scaffold protein on the cell membrane. As the main component of caveolae, caveolin-1 is involved in many biological processes that include substance uptake and transmembrane signaling. Many of these processes and thus caveolin-1 contribute to cell transformation, tumorigenesis, and metastasis. Of particular interest are the dual rolesof tumor suppressor and oncogene that caveolin-1 appear to play in different malignancies, including pancreatic cancer. Therefore, analyzing caveolin-1 regulators and understanding their mechanisms of actionis key to identifying novel diagnostic and therapeutic tools for pancreatic cancer. This review details the mechanisms of action of caveolin-1 regulators and the potential significance for pancreatic cancer treatment.

• 대한예방의학회:학술대회논문집
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• 대한예방의학회 2002년도 제54차 추계 학술대회 연제집
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• pp.398-398
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• 2002

• Asian Pacific Journal of Cancer Prevention
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• 제15권21호
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• pp.9093-9099
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• 2014

A growing body of evidence suggests that the peroxisome proliferator-activated receptor-gamma ($PPAR{\gamma}$) gene may harbor targets for the chemoprevention of breast cancer. However, it is unclear whether polymorphisms in the $PPAR{\gamma}$ gene are associated with the susceptibility of breast cancer. We performed a candidate gene association study between $PPAR{\gamma}$ polymorphisms and breast cancer and a meta-analysis on the association of breast cancer with selected $PPAR{\gamma}$ variants. Six single nucleotide polymorphisms (SNPs) in the $PPAR{\gamma}$ gene were analyzed among 456 breast cancer patients and 461 controls from the National Cancer Center in Korea. Association between the polymorphisms and breast cancer risk were assessed using the Cochrane-Armitage test for trend and a multivariate logistic regression model. Two SNPs, rs3856806 and rs1801282, had been previously analyzed, thus enabling us to perform pooled analyses on their associations with breast cancer susceptibility. Our findings from the candidate gene association study showed no association between the $PPAR{\gamma}$ gene polymorphisms and breast cancer risk. A meta-analysis combining existing studies and our current study also refuted an association of the $PPAR{\gamma}$ gene with breast cancer. Our findings suggest that the $PPAR{\gamma}$ gene may not harbor variants that alter breast cancer susceptibility, although a moderate sample size might have precluded a decisive conclusion.

• Asian Pacific Journal of Cancer Prevention
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• 제13권3호
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• pp.979-983
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• 2012

Background : Previous studies have suggested a lack of complete cross-resistance between steroidal (exemestane) and non-steroidal aromatase inhibitors (nSAI). Methods : Eighty-eight metastatic breast cancer (MBC) patients who received 25 mg of exemestane orally once a day at the National Cancer Center, Korea, between 2003 and 2009, were reviewed retrospectively. All patients had received nSAI for metastatic disease prior to exemestane therapy. Results : The median age was 52 years (range, 33-79), and 13 (14.8%) patients were premenopausal who concomitantly received GnRH agonist. Exemestane was given as a second- (80.7%) or third-line (19.3%) hormone therapy. The clinical benefit (CB) rate (complete response + partial response + stable disease ${\geq}$ 24 weeks) was 30.7%, with a median CB duration of 10.0 months (range, 6.3-78.7). The median progression-free survival (PFS) was 3.0 months (95% confidence interval [CI], 1.99-4.01) and the overall survival (OS) 21.5 months (95% CI, 17.96-25.04), with a median followup of 50.3 months. Patients who achieved CB had longer OS than those patients who did not (29.6 vs 17.9 months; P=0.002). On univariate analysis of predictive factors, patients who had achieved CB from previous nSAI tended to show lower CB rate (24.6% vs 44.4%, respectively; P=0.063) and shorter PFS (2.8 vs 4.8 months, respectively; p=0.233) than patients who had not. Achieving CB from previous nSAI became independent predictive factor for CBR to exemestane on multivariable analysis (Odds ratio = 2.852, P = 0.040). Conclusions : Exemestane after nSAI failure was effective in prolonging CB duration. The drug's efficacy seemed to be inferior in patients who had benefit from previous nSAI use.

• Asian Pacific Journal of Cancer Prevention
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• 제17권2호
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• pp.539-543
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• 2016

Background: It is well known that peritoneal carcinomatosis (PC) from colorectal cancer (CRC) is associated with a poor prognosis. However, data on the prognostic significance of modern chemotherapy containing bevacizumab, cetuximab or panitumumab are not available. Materials and Methods: This retrospective review concerned 526 patients with metastatic CRC who were classified into two groups according to the presence or absence of PC, and were treated with systemic chemotherapy, with or without bevacizumab or anti-EGFR antibodies. The genetic background, in particular KRAS, BRAF, and PIK3CA gene mutations, and overall survival (OS) were compared between the two groups. Results: The median OS values were 23.3 and 29.1 months for PC and non-PC patients, respectively (hazard ratio [HR]=1.20; p=0.17). Among all patients, tumor location, number of metastatic sites and BRAF mutation status were significant prognostic factors, whereas the presence of PC was not. In the PC group, chemotherapy with bevacizumab resulted in a significantly longer OS than forchemotherapy without bevacizumab (HR=0.38, p<0.01), but this was not the case in the non-PC group (HR=0.80, p=0.10). Furthermore, the incidence of the BRAF V600E mutation was significantly higher in PC than in non-PC patients (27.7% versus 7.3%, p<0.01). BRAF mutations displayed a strong correlation with shorter OS in non-PC (HR=2.26), but not PC patients (HR=1.04). Conclusions: Systemic chemotherapy, especially when combined with bevacizumab, improved survival in patients with PC from CRC as well as non-PC patients. While BRAF mutation demonstrated a high frequency in PC patients, but it was not associated with prognosis.

• 대한한의학회지
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• 제25권4호
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• pp.161-170
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• 2004

Objective : The purpose of this study was to investigate the effects of Armillaria mellea extract (AME) on immune modulation focused on anti-cancer activity. Methods : To prove the effects of AME, we performed NO assay, NK cytotoxicity assay and RT-PCR of cytokine related with macrophage and NK cell activity. Results : AME increased NO production produced by macrophages in part. AME also enhanced the NK cell activities in destroying target cells (YAC-1 cells). AME up-regulated gene expression of IL-l, iNOS, TNF-a in RAW 264.7 cells and IL-l, IL-2, IFN-(equation omitted), TNF-a in splenocytes, respectively. Conclusion : From the above results, we assumed that AME is a potential drug for anti-cancer by activation of the macrophages and NK cells.

• Journal of Korean Neurosurgical Society
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• 제63권5호
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• pp.566-578
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• 2020

Objective : Radiation is known to induce autophagy in malignant glioma cells whether it is cytocidal or cytoprotective. Dexamethasone is frequently used to reduce tumor-associated brain edema, especially during radiation therapy. The purpose of the study was to determine whether and how dexamethasone affects autophagy in irradiated malignant glioma cells and to identify possible intervening molecular pathways. Methods : We prepared p53 mutant U373 and LN229 glioma cell lines, which varied by phosphatase and tensin homolog (PTEN) mutational status and were used to make U373 stable transfected cells expressing GFP-LC3 protein. After performing cell survival assay after irradiation, the IC₅₀ radiation dose was determined. Dexamethasone dose (10 μM) was determined from the literature and added to the glioma cells 24 hours before the irradiation. The effect of adding dexamethasone was evaluated by cell survival assay or clonogenic assay and cell cycle analysis. Measurement of autophagy was visualized by western blot of LC3-I/LC3-II and quantified by the GFP-LC3 punctuated pattern under fluorescence microscopy and acridine orange staining for acidic vesicle organelles by flow cytometry. Results : Dexamethasone increased cell survival in both U373 and LN229 cells after irradiation. It interfered with autophagy after irradiation differently depending on the PTEN mutational status : the autophagy decreased in U373 (PTEN-mutated) cells but increased in LN229 (PTEN wild-type) cells. Inhibition of protein kinase B (AKT) phosphorylation after irradiation by LY294002 reversed the dexamethasone-induced decrease of autophagy and cell death in U373 cells but provoked no effect on both autophagy and cell survival in LN229 cells. After ATG5 knockdown, radiation-induced autophagy decreased and the effect of dexamethasone also diminished in both cell lines. The diminished autophagy resulted in a partial reversal of dexamethasone protection from cell death after irradiation in U373 cells; however, no significant change was observed in surviving fraction LN229 cells. Conclusion : Dexamethasone increased cell survival in p53 mutated malignant glioma cells and increased autophagy in PTEN-mutant malignant glioma cell but not in PTEN-wildtype cell. The difference of autophagy response could be mediated though the phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin signaling pathway.

• Tuberculosis and Respiratory Diseases
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• 제67권6호
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• pp.574-576
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• 2009

An intramedullary spinal cord metastasis (ISCM) rarely develops in systemic cancer but is indicative of a poor prognosis. A 56-year-old man was admitted due to weakness of the lower extremities. He had received radiotherapy 3 months prior for a brain metastasis that had developed 1 year after achieving a complete response from chemotherapy for extended stage small cell lung cancer. Although the brain lesion had improved partially, ISCM from the cervical to lumbar-sacral spinal cords, which was accompanied by a leptomeningeal dissemination, was diagnosed based on magnetic resonance imaging of the spine and cerebrospinal fluid cytology. Finally, he died of sudden cardiac arrest during treatment. This is the first case of ISCM involving the whole spinal segments. Physicians should be aware of the subsequent development of ISCM in lung cancer patients with a previously known brain metastasis who present with new neurological symptoms.