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4 "Jung Eun Lee"
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Estimation of Population Attributable Fraction by Hormone and Reproductive Factors on Female Cancer in the Republic of Korea, 2015 to 2030
Youjin Hong, Soseul Sung, Woojin Lim, Sungji Moon, Kwang-Pil Ko, Jung Eun Lee, Inah Kim, Sun Ha Jee, Sun-Seog Kweon, Min-Ho Shin, Sangmin Park, Seung-Ho Ryu, Sun Young Yang, Jeongseon Kim, Sang-Wook Yi, Yoon-Jung Choi, Jeong-Soo Im, Hong Gwan Seo, Sue K. Park
Received July 26, 2024  Accepted November 18, 2024  Published online November 19, 2024  
DOI: https://doi.org/10.4143/crt.2024.707    [Epub ahead of print]
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
Population attributable fractions (PAFs) for hormone and reproductive factors have been estimated in several countries. International Agency for Research on Cancer (IARC) designated as group 1 and group 2A carcinogen for hormone factors in breast, ovarian, endometrial and uterine cervix cancer. This study aimed to estimate the PAFs of hormone/reproductive factor attributed to cancer incidence and deaths in Korean women and projected trends from 2015 to 2030.
Materials and Methods
The PAF was estimated with using the 2005 standardized prevalence rates and 2020 incidence and deaths with a 15-year latency. Based on the Levin’s formula, prevalence rates were calculated using the Korea National Health and Nutrition Examination Survey (KNHANES) and the relative risks, which were the risk of selected female cancer associated with oral contraceptive, hormone replacement therapy and duration of breastfeeding, were estimated from the meta-analysis of studies performed in Korean women population. Studies based on the Asian and Global populations were calculated as a sensitivity analysis.
Results
The estimation PAFs for hormone was 1.02% with 1,192 cases and reproductive was 2.67% with 3,112 cases. Moreover, 0.40% (125 deaths) and 1.09% (342 deaths) in female-related cancer deaths in order. Estrogen-progesterone combined hormone replacement therapy (HRT) accounted the most proportion in hormone factors and breastfeeding in reproductive factors. Also, the breast cancer had the highest percent in both hormone and reproductive factors.
Conclusion
Through this study, 1.02% and 2.67% of female-related cancer incidence will be reduced by encouraging avoiding the use of oral contraceptives and HRT and breastfeeding for more than 6 months in reproductive factors. Additionally, among four selected female cancers in this study, breast cancer was observed to be a significant level of prevention.
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Fraction of Cancer Attributable to Carcinogenic Drugs in Korea from 2015 to 2030
Woojin Lim, Soseul Sung, Youjin Hong, Sungji Moon, Sangjun Lee, Kyungsik Kim, Jung Eun Lee, Inah Kim, Kwang-Pil Ko, Sue K. Park
Received June 28, 2024  Accepted November 5, 2024  Published online November 6, 2024  
DOI: https://doi.org/10.4143/crt.2024.644    [Epub ahead of print]
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
This study aims to estimate and project the population attributable fraction (PAF) of cancer incidence and death due to carcinogenic drug use in Korea from 2015 to 2030, to estimate the degree of cancer prevention from exposure to carcinogenic drugs in Korea. Selected carcinogenic drugs were immunosuppressive and antineoplastic drugs classified as group I by the International Agency for Research on Cancer.
Materials and Methods
Systematic review and meta-analyses were conducted to estimate the relative risk of cancer associated with carcinogenic drug use. Age was standardized using the annual prevalence rate of the National Health Insurance Service sample cohort (NHIS-NSC) from 2002 to 2013 to calculate the standardized prevalence rate of carcinogenic drug use each year. The PAF of specific cancer incidence and death were calculated using Levin’s formula and Monte Carlo methods. The prevalence rates were extrapolated to estimate the trend of PAF from 2015 to 2030.
Results
In 2015, carcinogenic drugs attributed to 0.003% and 0.002% among the causes of cancer incidence and death in Korea. However, carcinogenic drugs attributed to 1.1% among the causes of both cancer incidence and death in patients with clinical indications of carcinogenic drugs.
Conclusion
The PAF in patients with clinical indications of carcinogenic drugs were significantly high and expected to increase rapidly over time. Since these drugs are listed as essential by the World Health Organization, and may be difficult to replace, a surveillance system on susceptible populations using group I carcinogenic drugs must be discussed and implemented.
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High-Dose Metformin Plus Temozolomide Shows Increased Anti-tumor Effects in Glioblastoma In Vitro and In Vivo Compared with Monotherapy
Jung Eun Lee, Ji Hee Lim, Yong Kil Hong, Seung Ho Yang
Cancer Res Treat. 2018;50(4):1331-1342.   Published online January 10, 2018
DOI: https://doi.org/10.4143/crt.2017.466
AbstractAbstract PDFSupplementary MaterialPubReaderePub
Purpose
The purpose of the study is to investigate the efficacy of combined treatment with temozolomide (TMZ) and metformin for glioblastoma (GBM) in vitro and in vivo.
Materials and Methods
We investigated the efficacy of combined treatment with TMZ and metformin using cell viability and apoptosis assays. A GBM orthotopic mice model was established by inoculation of 5×105 U87 cells and treatedwith metformin, TMZ, and the combination for 4weeks. Western blotting and immunofluorescence of tumor specimens were analyzed to investigate AMP-activated protein kinase (AMPK) and AKT pathway.
Results
The combination of TMZ and metformin showed higher cytotoxicity than single agents in U87, U251, and A172 cell lines. A combination of high-dose metformin and TMZ showed the highest apoptotic activity. The combination of TMZ and metformin enhanced AMPK phosphorylation and inhibited mammalian target of rapamycin phosphorylation, AKT phosphorylation, and p53 expression. The median survival of each group was 43.6, 55.2, 53.2, 65.2, and 71.3 days for control, metformin treatment (2 mg/25 g/day or 10 mg/25 g/day), TMZ treatment (15 mg/kg/day), combination treatment with low-dose metformin and TMZ, and combination treatment with high-dose metformin and TMZ, respectively. Expression of fatty acid synthase (FASN) was significantly decreased in tumor specimens treated with metformin and TMZ.
Conclusion
The combination of metformin and TMZ was superior to monotherapy using metformin or TMZ in terms of cell viability in vitro and survival in vivo. The combination of high-dose metformin and TMZ inhibited FASN expression in an orthotopic model. Inhibition of FASN might be a potential therapeutic target of GBM.

Citations

Citations to this article as recorded by  
  • Metformin and glioma: Targeting metabolic dysregulation for enhanced therapeutic outcomes
    Haneen A. Basheer, Nadeem M. Salman, Rami M. Abdullah, Lina Elsalem, Kamyar Afarinkia
    Translational Oncology.2025; 53: 102323.     CrossRef
  • Metformin as an Adjunct Treatment to Temozolomide for High-Grade Gliomas: A Systematic Review and Meta-Analysis
    Eloísa Bittencurt Thomaz de Assis, Marcio Yuri Ferreira, Jéssica Sales de Oliveira, Lucas Pari Mitre, Eduardo Mendes Correa da Silva, Luciano Lobão Salim Coelho, Daniel Antunes Moreno, Allan Dias Polverini
    World Neurosurgery.2025; 197: 123842.     CrossRef
  • Survival Impact of Combined Biguanide and Temozolomide in Glioblastoma Preclinical Models: A Systematic Review and Meta-Analysis
    Marcio Yuri Ferreira, Eloísa Bittencurt Thomaz de Assis, Savio Batista, Lucca B. Palavani, Gabriel Verly, Eduardo Mendes Corrêa, Lucas Pari Mitre, Jessica Sales de Oliveira, Raphael Bertani, Daniel Antunes Moreno, Allan Dias Polverini
    World Neurosurgery.2024; 183: 239.     CrossRef
  • Metabolic Contrasts: Fatty Acid Oxidation and Ketone Bodies in Healthy Brains vs. Glioblastoma Multiforme
    Corina Tamas, Flaviu Tamas, Attila Kovecsi, Alina Cehan, Adrian Balasa
    International Journal of Molecular Sciences.2024; 25(10): 5482.     CrossRef
  • Metformin and its potential influence on cell fate decision between apoptosis and senescence in cancer, with a special emphasis on glioblastoma
    Melika Hajimohammadebrahim-Ketabforoush, Alireza Zali, Mohammadreza Shahmohammadi, Amir Ali Hamidieh
    Frontiers in Oncology.2024;[Epub]     CrossRef
  • Combined metformin and simvastatin therapy inhibits SREBP2 maturation and alters energy metabolism in glioma
    Xiaolong Qiao, Zixuan Wang, Yinan Chen, Nan Peng, Hongwei Zhang, Chaoshi Niu, Chuandong Cheng
    Cell Death & Disease.2024;[Epub]     CrossRef
  • GBM Cells Exhibit Susceptibility to Metformin Treatment According to TLR4 Pathway Activation and Metabolic and Antioxidant Status
    Isabele Fattori Moretti, Antonio Marcondes Lerario, Paula Rodrigues Sola, Janaína Macedo-da-Silva, Mauricio da Silva Baptista, Giuseppe Palmisano, Sueli Mieko Oba-Shinjo, Suely Kazue Nagahashi Marie
    Cancers.2023; 15(3): 587.     CrossRef
  • Heterogeneity of Amino Acid Profiles of Proneural and Mesenchymal Brain-Tumor Initiating Cells
    Corinna Seliger, Lisa Rauer, Anne-Louise Wüster, Sylvia Moeckel, Verena Leidgens, Birgit Jachnik, Laura-Marie Ammer, Simon Heckscher, Katja Dettmer, Markus Riemenschneider, Peter Oefner, Martin Proescholdt, Arabel Vollmann-Zwerenz, Peter Hau
    International Journal of Molecular Sciences.2023; 24(4): 3199.     CrossRef
  • The Potential Therapeutic Impact of Metformin in Glioblastoma Multiforme
    Mehdi Sanati, Samaneh Aminyavari, Hamid Mollazadeh, Ali Motamed-Sanaye, Bahram Bibak, Elmira Mohtashami, Yong Teng, Amir R. Afshari, Amirhossein Sahebkar
    Current Medicinal Chemistry.2023; 30(7): 857.     CrossRef
  • Development and validation of a GC-MS method for determination of metformin in normal brain and in glioblastoma tissues
    Giorgia Ailuno, Sara Baldassari, Alice Balboni, Giuliana Drava, Cristina Spalletti, Elena Tantillo, Michele Mazzanti, Federica Barbieri, Stefano Thellung, Tullio Florio, Gabriele Caviglioli
    Journal of Pharmaceutical and Biomedical Analysis.2023; 234: 115503.     CrossRef
  • Efficacy and safety of metformin plus low-dose temozolomide in patients with recurrent or refractory glioblastoma: a randomized, prospective, multicenter, double-blind, controlled, phase 2 trial (KNOG-1501 study)
    Wan-Soo Yoon, Jong Hee Chang, Jeong Hoon Kim, Yu Jung Kim, Tae-Young Jung, Heon Yoo, Se-Hyuk Kim, Young-Cho Ko, Do-Hyun Nam, Tae Min Kim, Se Hoon Kim, Sung-Hae Park, Youn Soo Lee, Hyeon Woo Yim, Yong-Kil Hong, Seung Ho Yang
    Discover Oncology.2023;[Epub]     CrossRef
  • Targeted c-Myc Inhibition and Systemic Temozolomide Therapy Extend Survival in Glioblastoma Xenografts
    Laxmi Dhungel, Cayla Harris, Lauren Romine, Jan Sarkaria, Drazen Raucher
    Bioengineering.2023; 10(6): 718.     CrossRef
  • Could Metformin and Resveratrol Support Glioblastoma Treatment? A Mechanistic View at the Cellular Level
    Raghad Sabaawi Ibrahim, Shahad Sabaawi Ibrahim, Ahmed El-Naas, Lenka Koklesová, Peter Kubatka, Dietrich Büsselberg
    Cancers.2023; 15(13): 3368.     CrossRef
  • Dysregulated lipid metabolism in TMZ-resistant glioblastoma: pathways, proteins, metabolites and therapeutic opportunities
    Tzu-Jen Kao, Chien-Liang Lin, Wen-Bin Yang, Hao-Yi Li, Tsung-I Hsu
    Lipids in Health and Disease.2023;[Epub]     CrossRef
  • Drug Repurposing in Pediatric Brain Tumors: Posterior Fossa Ependymoma and Diffuse Midline Glioma under the Looking Glass
    Tiziana Servidei, Alessandro Sgambato, Donatella Lucchetti, Pierluigi Navarra, Antonio Ruggiero
    Frontiers in Bioscience-Landmark.2023;[Epub]     CrossRef
  • THERAPEUTIC USE OF METFORMIN IN THYROID CANCER
    Fatimah Haitham Fathi, Ammar A. Y. Almulathanon, Jehan A. Mohammad
    Military Medical Science Letters.2022; 91(4): 348.     CrossRef
  • Targeting Oncogenic Rewiring of Lipid Metabolism for Glioblastoma Treatment
    Haksoo Lee, Dahye Kim, BuHyun Youn
    International Journal of Molecular Sciences.2022; 23(22): 13818.     CrossRef
  • Amlexanox Enhances Temozolomide-Induced Antitumor Effects in Human Glioblastoma Cells by Inhibiting IKBKE and the Akt-mTOR Signaling Pathway
    Jinbiao Xiong, Gaochao Guo, Lianmei Guo, Zengguang Wang, Zhijuan Chen, Yang Nan, Yiyao Cao, Ruilong Li, Xuejun Yang, Jun Dong, Xun Jin, Weidong Yang, Qiang Huang
    ACS Omega.2021; 6(6): 4289.     CrossRef
  • Imaging Metformin Efficacy as Add-On Therapy in Cells and Mouse Models of Human EGFR Glioblastoma
    Silvia Valtorta, Alessia Lo Dico, Isabella Raccagni, Cristina Martelli, Valentina Pieri, Paolo Rainone, Sergio Todde, Bastian Zinnhardt, Elisabetta De Bernardi, Angela Coliva, Letterio S. Politi, Thomas Viel, Andreas H. Jacobs, Rossella Galli, Luisa Ottob
    Frontiers in Oncology.2021;[Epub]     CrossRef
  • Natural Compounds in Glioblastoma Therapy: Preclinical Insights, Mechanistic Pathways, and Outlook
    Kevin Zhai, Manaal Siddiqui, Basma Abdellatif, Alena Liskova, Peter Kubatka, Dietrich Büsselberg
    Cancers.2021; 13(10): 2317.     CrossRef
  • Role of Polymeric Local Drug Delivery in Multimodal Treatment of Malignant Glioma: A Review
    Yuan-Yun Tseng, Tai-Yuan Chen, Shih-Jung Liu
    International Journal of Nanomedicine.2021; Volume 16: 4597.     CrossRef
  • In Vitro and In Vivo Enhancement of Temozolomide Effect in Human Glioblastoma by Non-Invasive Application of Cold Atmospheric Plasma
    Vikas Soni, Manish Adhikari, Hayk Simonyan, Li Lin, Jonathan H. Sherman, Colin N. Young, Michael Keidar
    Cancers.2021; 13(17): 4485.     CrossRef
  • Landscape of the oncogenic role of fatty acid synthase in human tumors
    Xulei Huo, Lairong Song, Da Li, Ke Wang, Yali Wang, Feng Chen, Liwei Zhang, Liang Wang, Junting Zhang, Zhen Wu
    Aging.2021; 13(23): 25106.     CrossRef
  • Cetylpyridinium chloride is a potent AMP-activated kinase (AMPK) inducer and has therapeutic potential in cancer
    Sonia A. Allen, Sandipan Datta, Jose Sandoval, Alexey Tomilov, Thomas Sears, Kevin Woolard, James M. Angelastro, Gino A. Cortopassi
    Mitochondrion.2020; 50: 19.     CrossRef
  • Metformin treatment decreases the expression of cancer stem cell marker CD44 and stemness related gene expression in primary oral cancer cells
    Shankargouda Patil
    Archives of Oral Biology.2020; 113: 104710.     CrossRef
  • Metformin Treatment Sensitizes Human Laryngeal Cancer Cell Line Hep- 2 to 5-Fluorouracil
    Neslisah Barlak, Fatma Sanli, Ozel Capik, Elanur Tuysuz, Elanur Aydın Karatas, Hasan Turkez, Omer Faruk Karatas
    Clinical Cancer Drugs.2020; 7(1): 16.     CrossRef
  • An Experimentally Defined Hypoxia Gene Signature in Glioblastoma and Its Modulation by Metformin
    Marta Calvo Tardón, Eliana Marinari, Denis Migliorini, Viviane Bes, Stoyan Tankov, Emily Charrier, Thomas A McKee, Valérie Dutoit, Pierre-Yves Dietrich, Erika Cosset, Paul R Walker
    Biology.2020; 9(9): 264.     CrossRef
  • Repurposing old drugs in oncology: Opportunities with clinical and regulatory challenges ahead
    Rashmi R. Shah, Peter D. Stonier
    Journal of Clinical Pharmacy and Therapeutics.2019; 44(1): 6.     CrossRef
  • Repurposed Biguanide Drugs in Glioblastoma Exert Antiproliferative Effects via the Inhibition of Intracellular Chloride Channel 1 Activity
    Federica Barbieri, Ivan Verduci, Valentina Carlini, Gianluigi Zona, Aldo Pagano, Michele Mazzanti, Tullio Florio
    Frontiers in Oncology.2019;[Epub]     CrossRef
  • DrugR+: A comprehensive relational database for drug repurposing, combination therapy, and replacement therapy
    Yosef Masoudi-Sobhanzadeh, Yadollah Omidi, Massoud Amanlou, Ali Masoudi-Nejad
    Computers in Biology and Medicine.2019; 109: 254.     CrossRef
  • Role of Metformin and AKT Axis Modulation in the Reversion of Hypoxia Induced TMZ-Resistance in Glioma Cells
    Alessia Lo Dico, Silvia Valtorta, Luisa Ottobrini, Rosa Maria Moresco
    Frontiers in Oncology.2019;[Epub]     CrossRef
  • Repurposing drugs for the treatment of glioma
    Chengming Xu, Yaodong Zhao, Congyan Wu, Lei Li
    Glioma.2019; 2(4): 159.     CrossRef
  • Honokiol enhances temozolomide-induced apoptotic insults to malignant glioma cells via an intrinsic mitochondrion-dependent pathway
    Chung-Ching Chio, Yu-Ting Tai, Mahendravarman Mohanraj, Shing-Hwa Liu, Shun-Tai Yang, Ruei-Ming Chen
    Phytomedicine.2018; 49: 41.     CrossRef
  • Pleiotropic Effects of Metformin on Cancer
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    International Journal of Molecular Sciences.2018; 19(10): 2850.     CrossRef
  • Metformin attenuates cells stemness and epithelial‑mesenchymal transition in colorectal cancer cells by inhibiting the Wnt3a/β‑catenin pathway
    Chu Zhang, Yuchen Wang
    Molecular Medicine Reports.2018;[Epub]     CrossRef
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Optimal Timing for the Administration of Capecitabine with Preoperative Chemoradiation for Locally Advanced Rectal Cancer
Young Ju Noh, Won Sik Choi, Jong Hoon Kim, Jin Cheon Kim, Chang Sik Yu, Hee Cheol Kim, Tae Won Kim, Heung Moon Chang, Min Hee Ryu, Seung Do Ahn, Sang-wook Lee, Seong Soo Shin, Jung Eun Lee, Eun Kyung Choi
Cancer Res Treat. 2006;38(1):30-34.   Published online February 28, 2006
DOI: https://doi.org/10.4143/crt.2006.38.1.30
AbstractAbstract PDFPubReaderePub
Purpose

Capecitabine is an oral fluoropyrimidine carbamate and it is known as an effective radiosensitizer. Capecitabine and its metabolite reach their peak concentration in the plasma at 1~2 hours after a single oral administration of capecitabine and the levels fall rapidly thereafter. To verify the radiosensitizing effect of capecitabine that is based on such pharmacokinetic characteristics, we performed a retrospective analysis on the optimal timing of capecitabine administration with performing preoperative chemoradiation for locally advanced rectal cancer.

Materials and Methods

Among 171 patients who were treated with preoperative radiotherapy and concurrent capecitabine administration for rectal cancer, 56 patients were administered capecitabine at 1~2 hours before radiotherapy (group A), and at other time in the other 115 patients (group B). Total mesorectal excision was done at 4 to 6 weeks after the completion of chemoradiation. The radiosensitizing effect of capecitabine was evaluated on the basis of the pathological response.

Results

Complete pathological regression of the primary tumor was observed in 12 patients (21.4%) for group A and in 11 patients (9.6%) for group B (p=0.031). Residual disease less than 0.5 cm (a good response) was observed in 19 patients (33.9%) for group A and in 23 patients (20.0%) for group B (p=0.038). On multivariate analysis, the capecitabine ingestion time showed marginal significance.

Conclusion

When performing preoperative chemoradiation for locally advanced rectal cancer, the radiosensitizing effect of capecitabine was enhanced when it was administered 1 hour before radiotherapy.

Citations

Citations to this article as recorded by  
  • Systematic review of treatment intensification using novel agents for chemoradiotherapy in rectal cancer
    R Clifford, N Govindarajah, J L Parsons, S Gollins, N P West, D Vimalachandran
    British Journal of Surgery.2018; 105(12): 1553.     CrossRef
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