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Im, Chong Kun,Rha, Sun Young,Jeung, Hei-Cheul,Ahn, Joong Bae,Shin, Sang Joon,Noh, Sung Hoon,Roh, Jae Kyung,Chung, Hyun Cheol Lippincott Williams Wilkins, Inc. 2010 American journal of clinical oncology: cancer clin Vol.33 No.1
BACKGROUND:: There is no universally confirmed standard chemotherapeutic regimen for advanced gastric cancer (AGC). The aim of this study was to investigate the efficacy and safety of combined biweekly irinotecan and monthly cisplatin treatments of patients with AGC. The primary end point was progression-free survival. MATERIAL AND METHODS:: AGC patients with or without measurable lesions received 70 mg/m irinotecan on days 1 and 15, and 80 mg/m cisplatin on day 1 every 4 weeks. RESULTS:: Of 40 enrolled patients, 21 patients had measurable disease. With a median follow-up duration of 35 weeks, the median progression-free survival and overall survival were 2.2 months and 8.0 months, respectively. The progression-free survival rate at 6 months was 30.0%. The most common adverse event of grade 3 to 4 was neutropenia (32.5%). Grade 3 diarrhea was observed in 2 patients (5.0%). There was no treatment-related death. CONCLUSION:: Current combined biweekly irinotecan and monthly cisplatin treatment did not show activity comparable with other active regimens in AGC.
Phase II study of erlotinib in advanced non-small-cell lung cancer after failure of gefitinib.
Cho, Byoung Chul,Im, Chong-Kun,Park, Moo-Suk,Kim, Se Kyu,Chang, Joon,Park, Jong Pil,Choi, Hye Jin,Kim, Yu Jin,Shin, Sang-Joon,Sohn, Joo Hyuk,Kim, Hoguen,Kim, Joo Hang Grune Stratton ; American Society of Clinical Onco 2007 Journal of clinical oncology Vol.25 No.18
<P>This study was designed to evaluate the efficacy and toxicity of erlotinib in patients with advanced non-small-cell lung cancer (NSCLC) who experienced disease progression after treatment with gefitinib.</P>
Jeung, Hei‐,Cheul,Rha, Sun Young,Im, Chong Kun,Shin, Sang Joon,Ahn, Joong Bae,Yang, Woo Ick,Roh, Jae Kyung,Noh, Sung Hoon,Chung, Hyun Cheol Wiley Subscription Services, Inc., A Wiley Company 2011 Cancer Vol.117 No.10
<P><B>Abstract</B></P><P><B>BACKGROUND:</B></P><P>The purpose of this study was to compare 2 weekly docetaxel‐based regimens as first‐line treatments for advanced gastric cancer and to investigate the expression of secreted protein acidic and rich in cysteine (SPARC) and its abilities to predict treatment‐related clinical outcomes.</P><P><B>METHODS:</B></P><P>Patients were randomly selected to receive 3 weekly cycles of docetaxel (35 mg/m<SUP>2</SUP> on days 1 and 8) plus S‐1 (35 mg/m<SUP>2</SUP> each twice daily on days 1‐14) (DS), or docetaxel plus cisplatin (35 mg/m<SUP>2</SUP> each on days 1 and 8) (DC). Endpoints included overall response rate (primary), survival, toxicity, and quality of life (secondary). SPARC expression in prechemotherapy specimens of primary gastric tumors was evaluated via immunohistochemical analysis.</P><P><B>RESULTS:</B></P><P>Eighty patients were enrolled in the study. Confirmed overall response rates were 46% (95% confidence interval, 30%‐62%) for DS and 24% (95% confidence interval, 11%‐38%) for DC via intent‐to‐treat analysis. Median progression‐free survival was 7.3 and 4.9 months and overall survival was 16.0 and 8.3 months for DS and DC, respectively. The most common grade ≥3 toxicity was neutropenia. Grade ≥3 mucositis (18%) and hand‐foot syndrome (8%) were the toxicities most associated with DS, whereas anorexia (20%) and lethargy (20%) were more common with DC. High SPARC expression was related to early progression (hazard ratio, 3.67; <I>P</I> = .042) and poor overall survival (hazard ratio, 2.01; <I>P</I> = .010) in docetaxel chemotherapy on multivariate analysis.</P><P><B>CONCLUSIONS:</B></P><P>The outcomes in this study favored DS over DC for further phase 3 study. The findings suggest that split‐dose weekly docetaxel alleviates hematological toxicity without compromising efficacy, and that SPARC expression may help individualize therapy in advanced gastric cancer. Cancer 2011. © 2010 American Cancer Society.</P>
Slowed progression in models of huntington disease by adipose stem cell transplantation
Lee, Soon-Tae,Chu, Kon,Jung, Keun-Hwa,Im, Woo-Seok,Park, Jeong-Eun,Lim, Hun-Chang,Won, Chong-Hyun,Shin, Seung-Hyun,Lee, Sang Kun,Kim, Manho,Roh, Jae-Kyu Wiley Subscription Services, Inc., A Wiley Company 2009 Annals of Neurology Vol.66 No.5
<B>Objective</B><P>Adipose-derived stem cells (ASCs) are readily accessible and secrete multiple growth factors. Here, we show that ASC transplantation rescues the striatal pathology of Huntington disease (HD) models.</P><B>Methods</B><P>ASCs were isolated from human subcutaneous adipose tissue. In a quinolinic acid (QA)-induced rat model of striatal degeneration, human ASCs (1 million cells) were transplanted into the ipsilateral striatal border immediately after the QA injection. In 60-day-old R6/2 mice transgenic for HD, ASCs (0.5 million cells) were transplanted into each bilateral striata. In in vitro experiments, we treated mutant huntingtin gene-transfected cerebral neurons with ASC-conditioned media.</P><B>Results</B><P>In the QA model, human ASCs reduced apomorphine-induced rotation behavior, lesion volume, and striatal apoptosis. In R6/2 transgenic mice, transplantation of ASCs improved Rota-Rod performance and limb clasping, increased survival, attenuated the loss of striatal neurons, and reduced the huntingtin aggregates. ASC-transplanted R6/2 mice expressed elevated levels of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and reactive oxygen defense enzymes and showed activation of the Akt/cAMP-response element-binding proteins. ASC-conditioned media decreased the level of N-terminal fragments of mutant huntingtin and associated apoptosis, and increased PGC-1α expression.</P><B>Interpretation</B><P>Collectively, ASC transplantation slowed striatal degeneration and behavioral deterioration of HD models, possibly via secreted factors. Ann Neurol 2009;66:671–681</P>
Chang, Hyun,Rha, Sun Young,Jeung, Hei-Cheul,Im, Chong Kun,Noh, Sung Hoon,Kim, Jin Ju,Chung, Hyun Cheol National Hellenic Research Foundation 2010 ONCOLOGY REPORTS Vol.23 No.1
<P>We evaluated the frequency of ABCB1 polymorphisms (2677G/T>A and 3435C>T) and studied the association between the polymorphisms and clinical outcomes of paclitaxel-based chemotherapy in advanced gastric cancer patients. This study was performed in 43 gastric cancer patients and a control group consisting of 118 healthy volunteers. Patients were treated with paclitaxel combined with an infusional 5-fluorouracil and low-dose leucovorin. Genomic DNA from peripheral blood mononuclear cells was used to determine ABCB1 polymorphisms by direct sequencing. Genotypes were investigated for their association with survival and toxicity. The ABCB1 3435 C allele was more frequent in gastric cancer patients than healthy volunteers (p<0.001). The 2677G>T/A and 3435C>T polymorphisms were independent factors associated with shorter progression-free survival (PFS) (p=0.024, p=0.001, respectively). In combined analysis of 2677 and 3435 polymorphisms, the 3435C>T polymorphism was an independent factor for poor PFS (p=0.01). The 3435CT and TT genotypes were associated with mucositis (p=0.04), and the variant genotypes at 2677 loci were associated with diarrhea (p=0.034). Our data suggest that the ABCB1 polymorphism at 3435 is associated with clinical outcomes after paclitaxel-based combined chemotherapy in advanced gastric cancer patients.</P>
Gerelchuluun, Turmunkh,Lee, Young-Hee,Lee, Young-Ran,Im, Sun-A,Song, Suk-Gil,Park, Jeong-Sook,Han, Kun,Kim, Kyung-Jae,Lee, Chong-Kil 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.11
Biodegradable nanospheres generated from a biocompatible polymer, poly(D,L-lactide-co-glycolide) (PLGA), have been studied extensively as implantable reservoirs for sustained-release drug delivery. PLGA-nanospheres have also been studied as vehicles to deliver antigens to phagocytes. The intracellular ar processing pathway of antigens delivered to phagocytes by PLGA particles was studied in the present study. Ovalbumin (OVA) encapsulated with PLGA (OVA-nanosphere) was efficiently captured, processed and presented on class I major histocompatibility complex (MHC-I) by dendritic cells (DCs). The MHC-I processing of OVA-nano-spheres was resistant to lactacystin, a proteosome inhibitor, and brefeldin A, which blocks anterograde transport from the endoplasmic reticulum (ER) through the Golgi apparatus. Chloroquine, which inhibits phagolysosomal enzymes by increasing ph ago lysosomal pH, inhibited MHC-I processing of OVA-nanospheres. In addition, DCs generated from TAP-/- mice were markedly suppressed in MHC-I processing of OVA-nanospheres. These results demonstrate that DCs process phagocytosed OVA-nanospheres via a vacuolar alternate MHC-I pathway for presentation of OVA peptides to T lymphocytes.