Chi Hoon Maeng

Dr. Chi Hoon Maeng

Division of Medical Oncology and Hematology, Department of Internal Medicine, Kyung Hee University Hospital, Kyung Hee University College of Medicine, Seoul, Korea

Research Focus & Metrics

Academic Career Length

57Years (1970-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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11 March 2010 in Lung Cancer
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Journal Article
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JLJae Jin Lee
Jae Jin Lee
CMChi Hoon Maeng
Chi Hoon Maeng
SBSeon Kyung Baek
Seon Kyung Baek
GKGou Young Kim
Gou Young Kim
JYJee-Hong Yoo
Jee-Hong Yoo
SKSi-Young Kim
Si-Young Kim

1 April 2019 in Journal of Pain and Symptom Management
Verified
Journal Article
Closed access
HPHye Yoon Park
Hye Yoon Park
YKYoung Ae Kim
Young Ae Kim
JSJin-Ah Sim
Jin-Ah Sim
JLJihye Lee
Jihye Lee
HRHyewon Ryu
Hyewon Ryu
YYYoung Ho Yun
Young Ho Yun

22 April 2018 in Supportive Care in Cancer
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Journal Article
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YYYoung Ho Yun
Young Ho Yun
KKKyoung-Nam Kim
Kyoung-Nam Kim
JSJin-Ah Sim
Jin-Ah Sim
EKEunKyo Kang
EunKyo Kang
JLJihye Lee
Jihye Lee
KJKyung Hae Jung
Kyung Hae Jung

21 May 2012 in American Journal of Hematology
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Journal Article
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SPSilvia Park
Silvia Park
SMSeung Hwan Moon
Seung Hwan Moon
LPLee Chun Park
Lee Chun Park
DHDeok Won Hwang
Deok Won Hwang
JJJun Ho Ji
Jun Ho Ji
WKWon Seog Kim
Won Seog Kim
Taking a step forward from the IPI, attention is focused on the role of 18F-FDG PET/CT as a tool for guidance in risk stratification in patients with aggressive non-Hodgkin's lymphoma (NHL). Here, we analyzed the predictive value of various PET/CT parameters in patients with DLBCL. Particularly, we were interested in patients with an IPI score of 1, 2, or 3, whose prognosis are confusing. Between Jul 2008 and Feb 2010, a total of 100 patients (including 57 patients with an IPI score of 1-3) who were treated with R-CHOP for DLBCL, and had assessable PET/CT parameters were analyzed in this study. Absolute value of SUVmax, SUVsum(sum of SUVmax) and TLGsum(SUVmean x Volumemeta) from baseline and interim PET/CT, and ΔSUVsum, ΔSUVmax, and ΔTLGsum between baseline and interim PET/CT were selected as PET/CT parameters. The median number of R-CHOP cycles was 6, and interim PET/CT was performed after 2 or 3 cycles. None of the parameters which showed percentile change between initial and interim PET/CT were associated with prognosis. Instead, absolute value of SUVsum from baseline PET/CT, and SUVmax and SUVsum from interim PET/CT were significantly relevant to PFS in all patients, and in patients with an IPI score of 1–3.

20 August 2018 in The Oncologist
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Journal Article
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KLKeun-Wook Lee
Keun-Wook Lee
CMChi Hoon Maeng
Chi Hoon Maeng
TKTae-You Kim
Tae-You Kim
DZDae Young Zang
Dae Young Zang
YEUL KIMYEUL KIM
YEUL KIM
JCJae Yong Cho
Jae Yong Cho
Lessons Learned: Irinotecan could not be proven noninferior to paclitaxel as a second-line treatment for patients with metastatic or recurrent gastric cancer. The failure to demonstrate noninferiority may have been a result of insufficient patient enrollment. Both agents were tolerable but showed different toxicity profiles. Background: This phase III study compared the efficacy and safety of paclitaxel versus irinotecan in patients with metastatic or recurrent gastric cancer (MRGC) who had experienced disease progression following first-line chemotherapy. Methods: Patients were randomized to receive either paclitaxel (70 mg/m2; days 1, 8, 15, every 4 weeks) or irinotecan (150 mg/m2 every other week). The primary endpoint was progression-free survival (PFS). Results: This study was stopped early due to low accrual rate. A total of 112 patients were enrolled; 54 were allocated to paclitaxel and 58 to irinotecan. Median PFS for the paclitaxel and irinotecan groups was 3.5 and 2.1 months, respectively (hazard ratio [HR], 1.27; 95% confidence interval [CI], 0.86–1.88; p = .234). Noninferiority of irinotecan to paclitaxel was not proved because the upper boundary of the 95% CI (1.88) exceeded the predefined upper margin of noninferiority (1.32). Median overall survival (OS) was 8.6 months in the paclitaxel group and 7.0 months in the irinotecan group (HR, 1.39; 95% CI, 0.91–2.11; p = .126). Among toxicities greater than or equal to grade 3, neutropenia (11.5%) was the most common, followed by peripheral neuropathy (7.7%) in the paclitaxel group, and neutropenia (34.5%) followed by nausea, vomiting, and anemia (8.6%, respectively) in the irinotecan group. Conclusion: Although paclitaxel showed numerically longer PFS and OS compared with irinotecan, this was statistically insignificant. Both irinotecan and paclitaxel are valid second-line treatment options in MRGC.

3 August 2012 in PLOS ONE
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Journal Article
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CMChi Hoon Maeng
Chi Hoon Maeng
JLJeeyun Lee
Jeeyun Lee
PHPaul van Hummelen
Paul van Hummelen
SPSe Hoon Park
Se Hoon Park
EPEmanuele Palescandolo
Emanuele Palescandolo
YSYoung-Mog Shim
Young-Mog Shim
Given the high incidence of metastatic esophageal squamous cell carcinoma, especially in Asia, we screened for the presence of somatic mutations using OncoMap platform with the aim of defining subsets of patients who may be potential candidate for targeted therapy. We analyzed 87 tissue specimens obtained from 80 patients who were pathologically confirmed with esophageal squamous cell carcinoma and received 5-fluoropyrimidine/platinum-based chemotherapy. OncoMap 4.0, a mass-spectrometry based assay, was used to interrogate 471 oncogenic mutations in 41 commonly mutated genes. Tumor specimens were prepared from primary cancer sites in 70 patients and from metastatic sites in 17 patients. In order to test the concordance between primary and metastatic sites from the patient for mutations, we analyzed 7 paired (primary-metastatic) specimens. All specimens were formalin-fixed paraffin embedded tissues and tumor content was >70%. In total, we have detected 20 hotspot mutations out of 80 patients screened. The most frequent mutation was PIK3CA mutation (four E545K, five H1047R and one H1047L) (N = 10, 11.5%) followed by MLH1 V384D (N = 7, 8.0%), TP53 (R306, R175H and R273C) (N = 3, 3.5%), BRAF V600E (N = 1, 1.2%), CTNNB1 D32N (N = 1, 1.2%), and EGFR P733L (N = 1, 1.2%). Distributions of somatic mutations were not different according to anatomic sites of esophageal cancer (cervical/upper, mid, lower). In addition, there was no difference in frequency of mutations between primary-metastasis paired samples. Our study led to the detection of potentially druggable mutations in esophageal SCC which may guide novel therapies in small subsets of esophageal cancer patients.