Oncology Research 22(5-6) Abstracts

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Oncology Research, Vol. 22, pp. 235–245, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14267282610858
E-ISSN 1555-3906
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Suppression of Cellular Proliferation and Invasion by HMGB1 Knockdown in Bladder Urothelial Carcinoma Cells

Haiqiu Liao,* Yang Xiao,* Yingbin Hu,† Yangming Xiao,* Zhaofa Yin,* and Liang Liu*

*Department of Urology, Loudi Central Hospital of Hunan Province, Loudi, China
†Department of Colorectal Surgery, the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan Province, China

HMGB1, which acts as a DNA chaperone to help maintain nuclear homeostasis, was reported to play a prominent role in cancer progression, angiogenesis, invasion, and metastasis development. Increased expression of HMGB1 has been observed in several tumor entities. However, the molecular mechanisms of HMGB1 in tumorigenesis of bladder cancer have rarely been reported. In the present study, real-time quantitative RT-PCR analysis revealed that the expression of HMGB1 in human bladder urothelial carcinoma (BUC) cells was much higher than that in human normal urethra epithelial cells. In order to investigate the role of HMGB1 in BUC cells, RNA interference and Talen-mediated gene knockout (KO) were used to knockdown and knockout HMGB1, respectively, in BUC cell lines BIU-87 and T24. HMGB1 knockdown/out greatly inhibited proliferation, invasion, and cell cycle G1/S transition of BUC cells. The decrease in cell viability caused by HMGB1 knockdown/out was due to an increase in apoptosis via Bax/Bcl-2, both of which were important molecules involved in the apoptotic pathway. We then investigated the effect of HMGB1 knockdown/out on the sensitivity of BUC cells treated with the anticancer drug cisplatin. Knockdown or knockout of HMGB1 rendered BUC cells more sensitive to cisplatin. The decreased expression of LC3-II and Beclin 1, which resulted in decreased levels of autophagy, could probably explain this phenomenon. Thus, HMGB1 may become a novel promising candidate for the prognosis and therapy for bladder cancer.

Key words: HMGB1; Bladder cancer; Proliferation; Invasion; Apoptosis; Autophagy

Address correspondence to Haiqiu Liao, Department of Urology, Loudi Central Hospital of Hunan Province, No. 51, Middle Changqing Street, Loudi City, Hunan, P.R. China 417000. Tel: +86-738-8230977, +86-738-8527012; Fax: +86-738-8215760; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 247–258, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14343704124430
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CXCL12-CXCR4 Axis Promotes Proliferation, Migration, Invasion, and Metastasis of Ovarian Cancer

Qing Guo,* Bu-Lang Gao,* Xue-Jing Zhang,* Guo-Chao Liu,* Feng Xu,* Qiong-Ying Fan,* Shao-Jing Zhang,* Bo Yang,* and Xiao-Hua Wu†

*Department of Obstetrics and Gynecology, Shijiazhuang First Hospital, Hebei Medical University, Shijiazhuang, China
†Department of Obstetrics and Gynecology, Bethune Peace Hospital, Shijiazhuang, China

The CXCL12-CXCR4 chemokine axis may play a very important role in ovarian cancer cells proliferation, migration, invasion, and peritoneal metastasis in vitro and in vivo. In this study, transfected SKOV3-CXCR4, transfected vector SKOV3-negative,nontransfected SKOV3 ovarian cancer cells, and human peritoneal mesothelial cells (HPMCs) were cultivated in vitro, and the proliferation, migration, and invasion of these ovarian cancer cells were investigated with or without the influence of the CXCL12-CXCR4 axis. Nude mice models of ovarian cancer were created by injection of ovarian cancer cells into the peritoneal cavity for investigation of ovarian cancer cells metastasis. Our results demonstrated that in the SKOV3-CXCR4 group, the cell number of proliferation, migration, or penetration through the Matrigel membrane treated with CXCL12 was significantly (p < 0.05) greater than those treated with CXCR4 antibody or CXCR4 antagonist AMD 3100 in a concentration-dependent manner. In the SKOV3-negative and the nontransfected SKOV3 groups, no significant (p > 0.05) differences existed in the cell number of proliferation, migration, or penetration. Coculture of HPMCs and SKOV3-CXCR4 had significantly (p < 0.05) higher migration and invasion rates than the SKOV3-CXCR4-only group. In nude mice seeded with ovarian cancer cells, the tumor weight in the nude mice injected with SKOV3-CXCR4 cells was significantly (p < 0.05) greater than in the group injected with the SKOV3-negative ornontransfected SKOV3 cells. Taken together, our results show that the CXCL12-CXCR4 chemokine axis can significantly promote the proliferation, migration, invasion, and peritoneal metastasis of ovarian cancer cells, and interference with this axis may serve as a new therapeutic target in treating ovarian cancers.

Key words: Chemokine CXCL12; Receptor CXCR4; Ovarian cancer; Tumor metastasis; Nude mice model

Address correspondence to Guo Qing, M.D., Ph.D., Department of Obstetrics and Gynecology, Shijiazhuang First Hospital, Hebei Medical University, 36 Fanxi Road, Shijiazhuang, Hebei Province, China 050011. Tel: +8613393019999; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it  or Xiao-Hua Wu, M.D., Department of Obstetrics and Gynecology, Bethune International Peace Hospital, 398 West Zhongshan Road, Shijiazhuang, Hebei Province, China 050000. Tel: +8631187978344; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 259–265, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14410238486603
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Knockdown of Peripheral Myelin Protein 22 Inhibits the Progression of Chronic Myeloid Leukemia

Hui Liu, Hui-qin Cao, Jin-bao Ta, Wen Zhang, and Yu-hong Liu

Department of Hematology, The Affiliated Hospital of Yan'an University, Yan'an, Shanxi, China

We aimed to explore the underlying mechanism of peripheral myelin protein 22 (PMP22) in the development of chronic myeloid leukemia (CML). The level of PMP22 expression in CD34
+ cells isolated from CML patients’ bone marrow samples (BMMCs) and peripheral blood samples (PBMCs) was determined by RT-PCR. In addition, PMP22-siRNA and scrambled control siRNA were transfected into human CML cell line K562 with Lipofectamine 2000 reagent. Cell viability and apoptosis were, respectively, determined by MTT assay and flow cytometry. Besides, the level of caspase 3 and Bcl-xL was then detected using Western blot. The level of PMP22 expression in CML patients’ CD34+ cells isolated from both PBMCs and BMMCs was significantly higher than the control group. PMP22 expression in K562 cells was successfully knocked down by siRNA. MTT analysis showed that knockdown of PMP22 inhibited the proliferation of CML cells. Flow cytometry showed that knockdown of PMP22 promoted the apoptosis of CML cells. Besides, Bcl-xL expression markedly decreased, while the expression of caspase 3 in CML cells significantly increased after knockdown of PMP22 expression. Our findings indicate that high expression of PMP22 may promote cell proliferation and inhibit cell apoptosis via upregulation of Bcl-xL or inhibition of caspase 3 activation, and thus may contribute to the development of CML. PMP22 may serve as a novel therapeutic target for the treatment of CML.

Key words: Chronic myeloid leukemia (CML); Peripheral myelin protein 22 (PMP22); Proliferation; Apoptosis; Bcl-xL; Caspase 3

Address correspondence to Yu-hong Liu, Department of Hematology, The Affiliated Hospital of Yan'an University, #43 North Street, Yan'an, Shanxi 716000, China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 267–273, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14410238486685
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Ursolic Acid Inhibits the Proliferation of Gastric Cancer Cells by Targeting miR-133a

Fenfen Xiang,*1 Chunying Pan,†1 Qianqian Kong,* Rong Wu,* Jiemin Jiang,* Yueping Zhan,‡ Jian Xu,‡ Xingang Gu,† and Xiangdong Kang*

*Department of Laboratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China
†Department Ultrasound, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China
‡Department of Central Lab, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China

Ursolic acid (UA), a potential chemotherapeutic agent, has the properties of inhibition of the growth of many human cancer cell lines. Whether UA can inhibit the growth and metastasis of human gastric cancer cells remains unknown. In this study, it was found that UA inhibited the growth and metastasis of human gastric cancer cells in vitro. Our results showed the increase of the percent of apoptotic cells and G1
phase, the inhibition of cell migrations well as the decrease of the expression of Bax, caspase 3 and Bcl-2 in BGC-823 cells after the treatment with UA. Real-time quantitative PCR analysis showed that UA treatment upregulated the level of miR-133a in BGC-823 cells. Overexpression of miR-133a increased the G1 phase of cell cycle and decreased Akt1 expression in BGC-823 cells. These outcomes might be secondary to the increased expression of miR-133a after the treatment with UA.

Key words: Ursolic acid (UA); Gastric cancer; miR-133a; Akt1

1These authors provided equal contribution to this work.
Address correspondence to Xiangdong Kang, Department of Laboratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it  or Xingang Gu, Department of Ultrasound, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 275–281, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14344177566282
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Inhibition of Glioblastoma Cell Growth In Vitro and In Vivo by Brucine, a Component of Chinese Medicine

Wang Ruijun,*†1 Meng Wenbin,1 Wang Yumin,§ Zhang Ruijian,¶ Huang Puweizhong,# and Li Yulin*

*Department of Pathology, Norman Bethune School of Medicine, Jilin University, Changchun, P. R. China
†Department of Neurosurgery, The First Affiliated Hospital of Inner Mongolia Medical University, Huimin District, Hohhot, P. R. China
‡Department of Gynecology and Obstetrics, The First Affiliated Hospital of Inner Mongolia Medical University, Huimin District, Hohhot, P. R China
§Department of Clinical Laboratory, The First Affiliated Hospital of Inner Mongolia Medical University, Huimin District, Hohhot, P. R. China
¶Department of Neurosurgery, People’s Hospital of Inner Mongolia Autonomous Region, Hohhot, P. R. China
#Department of Geriatrics, The First Affiliated Hospital of Inner Mongolia Medical University, Huimin District, Hohhot, P. R. China

Glioblastoma multiforme (GBM) is one of the most common glial cell tumors and has drawn more and more attention in the clinic in recent years.
Brucine has been reported to significantly suppress gastric cancer, lung cancer, and prostate cancer growth in vivo by inducing cell apoptosis. Here, the effects of brucine on U251 human glioma cell growth were investigated in vitro by cell proliferation assay, FACs, and qPCR in a xenograft tumor model. Treatment with brucine reduced the expression of BCL-2 and cyclooxygenase-2 (COX-2), while upregulated BAX expression in U251 human glioma cells resulted in reduced glioma cell survival rate and inhibited the growth of xenograft tumors. We concluded that brucine has a suppressive effect on U251 human glioma cells in vitro and in vivo, which could help in understanding the role of brucine in glioma cells and guiding drug use in the clinic.

Key words: Brucine; Glioma; Apoptosis; Glioblastoma multiforme (GBM)

1These authors provided equal contribution to this work.
Address correspondence to Li Yulin, Department of Pathology, Norman Bethune School of Medicine, Jilin University, 126 Xinmin Avenue, Changchun, 130021, China. Tel: +8604716621186; Fax: +8604716621186; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 282–292, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14410238486720
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Mechanistic Study on Triptorelin Action in Protecting From 5-FU-Induced Ovarian Damage in Rats

Ying Wang,* Xiaoyu Tian,* Lingxia Liang,† Yan Wang,‡ Ruifang Wang,* Xiaolin Cheng,* Zhen Yan,* Yawei Chen,* and Pengwei Qi*

*Obstertrics and Gynaecology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, China
†Medical Oncology, The First People’s Hospital of Nanyang, Nanyang, China
‡Agricultural College, GuangXi University, Nanning, China

Triptorelin, a kind of GnRH agonist, is widely used in the treatment of hormone-responsive cancers in the clinic. This study aimed to discover the underlying mechanism of triptorelin in protection from 5-fluorouracil (5-FU)-induced ovarian damage in Sprague–Dawley rats. In the present study, after using 5-FU to induce ovarian damage in rats, body weight and wet ovaries were weighed, the levels of estradiol (E2), follicle-stimulating hormone (FSH), and anti-Mullerian hormone (AMH) in blood were detected, and the expression of Bcl-2, Bax, and NF-κB was determined. It suggested that, compared to the control, body weight gain, the ratio of ovarian wet weight to body weight, primary follicle numbers, and the levels of AMH were significantly decreased, while the concentration of E2 and FSH was heavily increased following 5-FU administration. In contrast, after coadministration of triptorelin with 5-FU, the ratio of ovarian wet weight to body weight and the levels of AMH were significantly increased, whereas the level of E2 and FSH was decreased significantly when compared with the 5-FU group. Furthermore, at indicated times, 5-FU led to the reduced Bcl-2 and NF-κB expression and increased Bax expression while triptorelin plus 5-FU increased Bcl-2 and NF-κB expression and decreased Bax expression. It was indicated that triptorelin could protect rats from 5-FU-induced ovarian damage by modulation of hormones, Bcl-2, Bax, and NF-κB. These results might highlight the mechanism oftriptorelin as a protective agent in clinical chemotherapy for ovarian damage.

Key words: Triptorelin; 5-Fluorouracil (5-FU); Rat; Ovarian damage; Bcl-2; Bax; NF-κB

Address correspondence to Xiaoyu Tian, Obstetrics and Gynaecology, The First Affiliated Hospital of Henan University of Science and Technology, No. 24 of Jinghua Road, Jianxi District, Luoyang, Henan Province, 471003 China. Tel/Fax: +8637969823006; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 293–300, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14424348426035
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Overexpression of SMAR1 Enhances Radiosensitivity in Human Breast Cancer Cell Line MCF7 via Activation of p53 Signaling Pathway

Heng-chao Liu,*1 Fang Ma,†1 Yong Shen,* Yong-quan Hu,* and Shaojun Pan†

*Department of Nuclear Medicine, First Affiliated Hospital, Bengbu Medical College, Bengbu, Anhui, China
†Department of Medical Laboratory, Bengbu Medical College, Bengbu, Anhui, China

This study sought to investigate the effect of overexpression of SMAR1 (scaffold/matrix-associated region-binding protein 1) on cell radiosensitivity in breast cancer, as well as elucidate its regulatory mechanism. We constructed a lentiviral expression system to successfully overexpress SMAR1 in human breast cancer cell line MCF7. In addition, overexpression of SMAR1 in MCF7 cells enhanced the radiosensitivity to 89SrCl2. Moreover, overexpression of SMAR1 significantly induced cell apoptosis rate and G2/M phase arrest under the irradiation of 89SrCl2. In addition, Western blot analysis showed that overexpression of SMAR1 in MCF cells significantly increased the expression levels of pP53 (ser15), pP53 (ser20), acP53, and p21 and obviously decreased the expression of MDM2 under the irradiation of 89SrCl2. Notably, these expression changes could be neutralized by PFTa, an inhibitor of p53 signaling pathway that could inhibit p53-dependent transactivation of p53-responsive genes. Therefore, overexpression of SMAR1 may increase radiosensitivity to 89SrCl2
in breast cancer cell line MCF7 by p53-dependent G2/M checkpoint arrest and apoptosis. Enhanced expression of SMAR1 in tumors will help to improve the clinical efficiency of radiation therapy.

Key words: Breast cancer; Scaffold/matrix-associated region-binding protein 1 (SMAR1); Radiosensitivity; p53; G2/M checkpoint arrest; Apoptosis

1These authors provided equal contribution to this work.
Address correspondence to Fang Ma, Department of Medical Laboratory, Bengbu Medical College, Xuefu Road, Longzihu District, Bengbu, Anhui 233030, P.R. China. Tel: 0552-3175244; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 301–309, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14424348425991
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Calcitriol Inhibits Cervical Cancer Cell Proliferation Through Downregulation of HCCR1 Expression

Guoqing Wang,*† Lei Lei,† Xixia Zhao,† Jun Zhang,† Min Zhou,† and Kejun Nan*

*Department of Oncology, the First Affiliated Hospital of Medical College, Xi’an Jiaotong University, Xi’an, Shaanxi, China
†Department of Gynecologic Neoplasms, Cancer Hospital of Shaanxi Province, Xi’an, Shaanxi, China

Calcitriol (1α,25-dihydroxyvitamin D3) has demonstrated anticancer activity against several tumors. However, the underlying mechanism for this activity is not yet fully understood. Our experiment was designed and performed to address one aspect of this issue in cervical cancer. HeLa S3 cells were cultured in media with various concentrations of calcitriol. Cell proliferation and cell cycle were assessed by spectrophotometry and flow cytometry, respectively. The mRNA and protein expression levels of human cervical cancer oncogene (HCCR-1) and p21 were determined by RT-PCR and Western blot, respectively. Results indicated that calcitriol inhibited HeLa S3 cell proliferation and induced cell cycle arrest at the G1
phase. Calcitriol decreased HCCR-1 protein expression in a dose- and time-dependent manner. Furthermore, promoter activity analyses revealed that transcriptional regulation was involved in the inhibition of HCCR-1 expression. Overexpression of HCCR-1 in HeLa S3 cells reversed the inhibition of cell proliferation and G1 phase arrest that resulted from calcitriol treatment. In addition, calcitriol increased p21 expression and promoter activity. HCCR-1 overexpression decreased p21 expression and promoter activity. Thus, our results suggested that calcitriol inhibited HeLa S3 cell proliferation by decreasing HCCR-1 expression and increasing p21 expression.

Key words: Calcitriol; HeLa S3 cells; Human cervical cancer oncogene (HCCR-1)

Address correspondence to Kejun Nan, M.D., Ph.D., Department of Oncology, the First Affiliated Hospital of Medical College, Xi’an Jiaotong University, No. 77 West Yanta Street, Xi’an, Shaanxi 710061, China. Tel: +862985324086; Fax: +862985324086; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 311–319, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14424348426152
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Cost-Effectiveness Analysis of Adjuvant Stage III Colon Cancer Treatment at Veterans Affairs Medical Centers

Amy Soni,* Sherrie L. Aspinall,†‡§ Xinhua Zhao,‡ Chester B. Good,†‡§¶ Francesca E. Cunningham,† Gurkamal Chatta,# Vida Passero,** and Kenneth J. Smith††

*University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA
†VA Pharmacy Benefits Management Services, Hines, IL, USA
‡VA Center for Health Equity Research and Promotion, VA Pittsburgh Healthcare System, Pittsburgh, PA, USA
§University of Pittsburgh, School of Pharmacy, Pittsburgh, PA, USA
¶University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA
#Virginia Mason Medical Center, Seattle, WA, USA
**VA Pittsburgh Healthcare System, Pittsburgh, PA, USA
††University of Pittsburgh, Division of Clinical Modeling and Decision Sciences, Pittsburgh, PA, USA

The objective of this study was to evaluate the real-world cost effectiveness of adjuvant stage III colon cancer chemotherapy regimens, given that previous analyses have been based on data from clinical trials. The study was designed using integrated decision tree and Markov model, which was developed to evaluate the cost effectiveness of 5-fluorouracil/leucovorin (5-FU/LV), capecitabine, and the combination of each with oxaliplatin. The analysis was performed from a US Veterans Affairs perspective via retrospectively collected data, over a 5-year model time horizon. Outcome and cost data were used to calculate cost per quality adjusted life year (QALY), and one-way and probabilistic sensitivity analyses were performed. In the base case analysis,capecitabine and capecitabine plus oxaliplatin both cost more and were less effective than other regimens, and 5-FU/LV plus oxaliplatin, compared to 5-FU/LV alone, resulted in a cost of $25,997 per QALY gained. Model results were generally robust to parameter variation. Capecitabine plus oxaliplatin could be economically reasonable if full dosing occurred ≥76% of the time (base case 42%). In a real-world setting, the addition of oxaliplatin to 5-FU/LV is more effective but also more costly than 5-FU/LV alone. If full dosing of capecitabine-containing regimens can be assured, they may also be cost-effective strategies.

Key words: Colon cancer; 5-Fluorouracil (5-FU); CapecitabineOxaliplatin; Cost-effectiveness

Address correspondence to Amy Soni, M.D., Palo Alto Medical Foundation, Sunnyvale Center, 301 Old San Francisco Road, Level 1, Sunnyvale, CA 94086, USA. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 321–324, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14400775740416
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Radiation Recall Pneumonitis During Systemic Treatment With Everolimus

Douglas
Clark, Dron Gauchan, Ryan Ramaekers, Max Norvell, and Mehmet Sitki Copur

Saint Francis Cancer Treatment Center, Grand Island, NE, USA

Radiation recall syndrome is an acute inflammatory reaction developing at anatomical sites of previously irradiated tissue, weeks to months after the completion of radiation therapy. The distribution pattern of inflammation typically involves, and remains limited to, the boundaries of prior radiation treatment fields. Several classical chemotherapy drugs have been reported to have the potential for causing radiation recall syndrome. With the increasing availability and expanding use of novel biologic and targeted therapy anticancer drugs, isolated reports of radiation recall syndrome secondary to this class of agents are starting to appear in the literature. We describe a case of everolimus-induced radiation recall pneumonitis in a patient with metastatic renal cell cancer.

Key words: Radiation recall; Everolimus; Pneumonitis

Address correspondence to Mehmet Sitki Copur M.D., Saint Francis Cancer Treatment Center, 2116 W Faidley Ave, Grand Island, NE 68803, USA. Tel: +1-3083985450; Fax: +1-3083985351; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 325–331, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14410238486522
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Efficacy and Safety of Capecitabine and Oxaliplatin (CapOX) as an Adjuvant Therapy in Japanese for Stage II/III Colon Cancer in a Group at High Risk of Recurrence in Retrospective Study

Hiroshi Osawa, Naoko Handa, and Kunihiko Minakata

Department of Oncology and Hematology, Edogawa Hospital, Tokyo, Japan

A number of large-scale clinical trials have demonstrated that using a combination of oxaliplatin and fluoropyrimidines as an adjuvant chemotherapy for stage II/III colon cancer improved the prognosis. However, there has only been experience in Japanese patients with using CapOX therapy, in which capecitabine and oxaliplatin are used in combination. Therefore, our objective was to evaluate the efficacy and safety of CapOX in Japanese patients as an adjuvant chemotherapy for colon cancer in a single institute retrospective study. The efficacy and safety of CapOX as an adjuvant chemotherapy for patients with stage III colon cancer and stage II patients who had a signature for high risk of recurrence were evaluated in patients who had undergone surgery at our institution between December 1, 2009 and March 31, 2013. Forty-one patients received CapOX therapy during the study period: 23 men and 18 women with median age of 68.0 years (35–79 years). Performance status was 0 for 33 patients, and PS 1 for eight patients. The clinical stages were stage II in 14 patients, stage IIIA in 15 patients, and stage IIIB in 12 patients. The median number of CapOX cycles was eight (two to eight courses). The treatment completion rate was 82.9%. Five-year DFS rates were 63.8%. Five-year OS rates were 71.0%. In terms of adverse events, the serious adverse events of grade 3 or higher seen among all patients were neutropenia in four patients, thrombocytopenia in one patient, and peripheral sensory neuropathy in seven patients. However, hand–foot syndrome, which is characteristic of capecitabine, was not observed. Efficacy and tolerability of CapOX in Japanese patients as an adjuvant chemotherapy after colon cancer surgery was demonstrated.

Key words: CapecitabineOxaliplatin; Adjuvant chemotherapy; Colon cancer

Address all correspondence to Hiroshi Osawa, Department of Oncology and Hematology, Edogawa Hospital, 2-24-18 Higashikoiwa, Edogawa-ku, Tokyo 133-0052, Japan. Tel: 03-3673-1221; Fax: 03-3673-1229; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 333–338, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14410238486568
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Review

BLID: A Novel Tumor-Suppressor Gene

Xin Yu*1 and Zheng Li†1

*Department of Dermatology, Peking Union Medical College Hospital, Peking Union Medical College, Beijing, China
†Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Beijing, China

BLID (BH3-like motif containing, cell death inducer), also known as breast cancer cell 2 (BRCC2), was first reported in the human breast cancer cell line in 2004. BLID is a BH3-like motif containing apoptotic member of the Bcl-2 family. Recently, the BLID tumor-suppressor roles have been fully established. Several studies have found that BLID is frequently downregulated in many human cancers and the downregulation is often associated with tumor progression. Multivariate analysis indicated that BLID is an independent prognostic factor for overall survival and distant metastasis-free survival. Moreover, BLID can inhibit breast cancer cell growth and metastasis and promote apoptosis. BLID can regulate the expression of various tumor-related genes and proteins, such as AKT and MMP. In this review, we provide an overview of current knowledge concerning the role of BLID in tumor development and progression. To our knowledge, this is the first review about the role of this novel tumor-suppressor gene in tumor development and progression.

Key words: BH3-like motif containing, cell death inducer (BLID); Cancer; Tumor-suppressor gene (TSG)

1These authors provided equal contribution to this work.
Address correspondence to Zheng Li, Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Peking Union Medical College, 9 Dongdan 3rd Alley, DongchengBeijing, China. Tel: 86-010-69152812; Fax: 86-010-69152812; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 339–348, 2015
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DOI: http://dx.doi.org/10.3727/096504015X14424348426116
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Review

TIP30: A Novel Tumor-Suppressor Gene

Xin Yu,*1 Zheng Li,†1 and William K. K. Wu‡

*Department of Dermatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
†Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Beijing, China
‡Institute of Digestive Disease and State Key Laboratory of Digestive Disease, LKS Institute of Health Sciences and Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong

TIP30/CC3 was first identified and characterized as a “candidate” tumor-suppressor gene in 1997. Recently, the TIP30 tumor-suppressor status has been fully established since several studies have described that TIP30 protein expression is frequently downregulated in diverse types of human tumors, and the downregulation is often associated with tumor progression. TIP30 is involved in the control of cell apoptosis, growth, metastasis, angiogenesis, DNA repair, and tumor cell metabolism. Moreover, TIP30−/−
mice spontaneously develop hepatocellular carcinoma and other tumors at a higher incidence than that of wild-type mice. In this review, we provide an overview of current knowledge concerning the role of TIP30 in tumor development and progression. To our knowledge, this is the first review about the role of novel tumor-suppressor gene TIP30 in tumor development and progression.

Key words: TIP30; Cancer; Tumor-suppressor gene (TSG)

1These authors provided equal contribution to this work.
Address correspondence to Zheng Li, Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Beijing, China. Tel: +86-010-69152812; Fax: +86-010-69152812; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it