Oncology Research 22(2) Abstracts

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Oncology Research, Vol. 22, pp. 67–74, 2015
0965-0407/15 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504014X14024160459168
E-ISSN 1555-3906
Copyright © 2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Adjuvant Chemotherapy With Sequential Cytokine-Induced Killer (CIK) Cells in Stage IB Non-Small Cell Lung Cancer

Da-Peng Li,1 Wei Li,1 Jun Feng, Kai Chen, and Min Tao

Department of Oncology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People’s Republic of China

For non-small cell lung cancer (NSCLC) patients at stage IB, adjuvant chemotherapy does not improve survival. Evidence suggests that dendritic cell (DC)-activated cytokine-induced killer (DC-CIK) cell therapy in addition to chemotherapy improves survival for stage I–IIIA NSCLC patients after surgery, but there are not enough data to confirm this benefit specifically for those at stage IB. Herein, we retrospectively evaluated the efficacy and safety of this therapy administered to stage IB NSCLC patients. Sixty-six patients were treated with four-cycle adjuvant chemotherapy initiated 3 weeks after surgical resection. In addition, 28 of these patients underwent DC-CIK therapy on a trimonthly basis (average 3.1 times, range 1–6) beginning 1 month after chemotherapy. The disease-free survival (DFS) rates of the two groups were statistically similar, although patients who received DC-CIK therapy showed slightly higher 1- and 2-year DFS rates (100.0% and 96.4%, respectively, compared with 81.6% and 76.3%). More importantly, patients in the DC-CIK therapy group had significantly longer overall survival (p = 0.018). For patients who received treatment after recurrence, the DC-CIK therapy group had longer progression-free survival compared with the chemotherapy-only group. In addition, patients given DC-CIK therapy experienced less fatigue and appetite loss. The rate of adverse side effects was similar between the two groups. In conclusion, for these stage IB NSCLC patients, DC-CIK therapy significantly improved 2-year DFS rates compared with those who received chemotherapy only. DC-CIK

therapy also benefited patients’ quality of life, and adverse events were acceptable.

Key words: Chemotherapy; Cytokine-induced killer (CIK) cells; Natural killer cells; Non-small cell lung cancer (NSCLC)

1These authors provided equal contribution to this work.
Address correspondence to Min Tao, Department of Oncology, First Affiliated Hospital of Soochow University, 188 Shizi Road, 215006 Suzhou, Jiangsu, People’s Republic of China. Tel: +86 0512-67780310; Fax: +86 0512-67781716; E-mail:  This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 75–84, 2015
0965-0407/15 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504014X14024160459203
E-ISSN 1555-3906
Copyright © 2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

MicroRNA-181a Inhibits Tumor Proliferation, Invasiveness, and Metastasis and Is Downregulated in Gastric Cancer

Feng Lin, Ye Li, Shuai Yan, Shaoping Liu, Wenjun Qian, Dong Shen, Qingfeng Lin, and Weidong Mao

Department of Oncology, the Affiliated Jiangyin Hospital of Southeast University Medical College, Jiangyin, Jiangsu, PR China

MicroRNAs (miRNAs) play crucial roles in the development and progression of human cancers, including gastric cancer. The discovery of miRNAs may provide a new and powerful tool for studying the mechanism, diagnosis, and treatment of gastric cancer. Here we show that miR-181a levels were significantly downregulated in gastric cancer tissues compared with the adjacent normal regions in 80 paired samples. Moreover, the lower levels of miR-181a were associated with the pM or pTNM stage in clinical gastric cancer patients. In addition, the ectopic expression of miR-181a in the gastric cancer cell line HGC-27 inhibited cell proliferation, cell migration, and invasion by directly interacting with the mRNA encoding the oncogenic factor Prox1. Taken together, our results indicate that miR-181a might act as a tumor suppressor in gastric cancer, which may provide a novel diagnostic and therapeutic option for human gastric cancer in the near future.

Key words: Gastric cancer; miR-181a; Tumor suppressor; Prox1

Address correspondence to Weidong Mao, Department of Oncology, the Affiliated Jiangyin Hospital of Southeast University Medical College, Jiangyin, Jiangsu, PR China. Tel: +86-0510-86275861; Fax: +86-0510-86275861; E-mail:  This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 85–92, 2015
0965-0407/15 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504014X14146137738547
E-ISSN 1555-3906
Copyright © 2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Intensive Chemotherapy in Patients Aged 70 Years or Older Newly Diagnosed With Acute Myeloid Leukemia

Kelly Ross, Amanda L. Gillespie-Twardy, Mounzer Agha, Anastasios Raptis, Jing-Zhou Hou, Rafic Farah, Robert L. Redner, Annie Im, Shrina Duggal, Fei Ding, Yan Lin, and Michael Boyiadzis

Division of Hematology and Oncology, University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA

Acute myeloid leukemia (AML) represents a major therapeutic challenge in the elderly. Because of the high treatment-related mortality and poor overall outcomes of remission induction therapy, many older patients are not considered candidates for intensive chemotherapy. The current study evaluated prognostic factors for achievement of complete remission (CR) in newly diagnosed elderly AML patients who were treated with initial intensive chemotherapy. The study included 62 newly diagnosed AML patients≥70 years who were treated with intensive chemotherapy. The overall response rate (CR and CRp) was 56%. Patients with favorable or intermediate cytogenetics (p = 0.0036) as well as those with primary AML (p = 0.0212) had a higher response rate. The median overall survival for all patients was 6.85 months (95% CI 3.7–13.5 months). The median overall survival for patients achieving remission after intensive induction chemotherapy was significantly higher than those who did not respond to therapy (20.4 months vs. 3.5 months, p < 0.001). The all-cause 4-week mortality rate was 11%, and the all-cause 8-week mortality rate was 17.7%. A subgroup of elderly patients may benefit more from initial intensive induction chemotherapy, specifically those patients with performance status able to tolerate induction chemotherapy and favorable cytogenetic status. However, despite high rates of initial CR, relapse rates are still high, suggesting that alternative strategies of postremission therapy are warranted.

Key words: Acute myeloid leukemia (AML); Induction chemotherapy; Elderly patients; Prognostic factors; Survival

Address correspondence to Michael Boyiadzis, M.D., M.H.Sc., Division of Hematology and Oncology, University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, 5150 Center Ave, Suite 572, Pittsburgh, PA 15232, USA. Tel: +1-412-648-6589; Fax: +1-412-648-6579; E-mail:  This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 93–103, 2015
0965-0407/15 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504014X14146137738583
E-ISSN 1555-3906
Copyright © 2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

RNA Interference of Biot2 Induces G1 Phase Arrest and Apoptosis in Mouse Colorectal Cancer Cell Line

Cong Zhou,*1 Peng Zhang,†1 Guang-chao Xu,* Dong-ming Wu,* Ru-yan Liu,‡ Qi Zeng,* and Chun-ting Wang*

*State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University, Chengdu, P. R. China
†Department of Radiation Oncology, Sichuan Cancer Hospital, Chengdu, Sichuan, P. R. China
‡Guangxi Medical University, People’s Republic, Nanning, Guangxi, P. R. China

Biot2 is a tumor-associated antigen, and it is a novel gene (GenBank EF100607) that was first identified with the SEREX technique and named by our laboratory. It is highly expressed in cancer cells and testis, with low or no expression in normal tissues. In our previous study, RNA interference of human Biot2 can inhibit tumor cell growth, and it is associated with poor prognosis of patients in clinical study; however, the mechanism of Biot2 that effects tumor growth is not yet clear. Here, in this study, we explore further the mechanism of Biot2 by silencing Biot2 in CT26 cells. It provides some theoretical basis for Biot2 as a new target for gene therapy. In CT26 cells, the expression of Biot2 was downregulated by Biot2-shRNA. It also promoted G1 phase arrest, the expression of p16 and p21, and cell apoptosis. In the mouse model, the tumor volume and the expression of PCNA of the Biot2-shRNA group significantly decreased. These results suggest that silencing Biot2 in CT26 cells by RNA interference can inhibit cell growth in vitro and in vivo. It also induces cell cycle arrest in the G1 phase and apoptosis throughout regulation of p16 and p21. Taken together, our data demonstrate that Biot2 can be a potential target of gene therapy.

Key words: Biot2; RNA interference; CT26; Gene therapy

1These authors provided equal contribution to this work.
Address correspondence to Chun-Ting Wang, State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, Gaopeng Street, Keyuan Road 4, Chengdu 610041, China. Tel: +86-028-85164063; Fax: +86-028-85164060; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 105–115, 2015
0965-0407/15 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504014X14146137738628
E-ISSN 1555-3906
Copyright © 2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Inhibition of Canonical NF-κB Nuclear Localization by (−)-DHMEQ via Impairment of DNA Binding

Kana Horie,* Jun Ma,† and Kazuo Umezawa‡

*Department of Applied Chemistry, Faculty of Science and Technology, Keio University, Yokohama, Japan
†Shenzhen Wanhe Pharmaceutical Co., Ltd., Hi-tech Industrial Park, Nanshan District, Shenzhen, China
‡Department of Molecular Target Medicine, Aichi Medical University School of Medicine, Nagakute, Japan

We previously discovered (−)-DHMEQ as a selective inhibitor of NF-κB, and it was shown to suppress many cancer and inflammation models in animals. (−)-DHMEQ directly binds to NF-κB components to inhibit DNA binding, and moreover, it often inhibits nuclear translocation of NF-κB. The mechanism of inhibiting nuclear translocation has been elucidated for RelB, a main noncanonical NF-κB component. However, it was not elucidated for p65, a main canonical NF-κB component. In the present research, we studied how (−)-DHMEQ inhibits nuclear localization of p65. First, (−)-DHMEQ inhibited p65 nuclear accumulation in adult T-cell leukemia MT-2 cells in which canonical p65 is constitutively activated. But there was no change in the stability and importin-α3 affinity of p65. Then, we prepared a p65 mutant protein with Arg35Ala and Tyr36Ala (AA) mutations having no DNA-binding ability in HeLa cells. The p65 AA mutant showed reduced nuclear localization without changing the stability andimportin affinity. Taken together, the mechanism of inhibition is different between RelB and p65, and inhibition of p65 nuclear localization is likely to be due to the inhibition of DNA binding changing the equilibrium between the nuclear and cytoplasmic amounts of p65.

Key words: (−)-DHMEQ; Canonical NF-κB; Nuclear localization; Adult T-cell leukemia; DNA binding; IκBα

Address correspondence to Dr. Kazuo Umezawa, Department of Molecular Target Medicine, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan. Tel/Fax: +81-561-61-1959; E-mail:  This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 117–121, 2015
0965-0407/15 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504014X14174484758503
E-ISSN 1555-3906
Copyright © 2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Chondroitin Sulfate Proteoglycan-4 (CSPG4)-Specific Monoclonal Antibody 225.28 in Detection of Acute Myeloid Leukemia Blasts

Moon Fenton,* Theresa L. Whiteside,* Soldano Ferrone,† and Michael Boyiadzis*

*Division of Hematology and Oncology, University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
†Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA

Chondroitin sulfate proteoglycan-4 (CSPG4), a membrane-bound proteoglycan known to be expressed on the surface of malignant cells, has a restricted distribution in normal tissues. CSPG4 is a potential candidate tumor marker. We investigate CSPG4 expression on blasts in newly diagnosed acute myeloid leukemia (AML) patients and its relation with cytogenetic abnormalities and molecular markers known to have prognostic significance in this disease. Using hybridoma technology, we generated a specific monoclonal antibody (mAb), mAb 225.28, reactive with CSPG4. Blast samples obtained from the peripheral blood of newly diagnosed AML patients were analyzed for CSPG4 expression using the CSPG4-specific mAb and multiparameter flow cytometry. The results were correlated with cytogenetic and molecular characteristics of AML. CSPG4 was found to be expressed on a variable fraction of leukemic blasts in all AML patients with different leukemia morphology, including monoblastic cases. Reactivity of CSPG4-specific mAb with leukemic blasts was not limited to those with the rearranged MLL gene. CSPG4 was also expressed on AML blasts with a complex karyotype, FLT3 mutation, or NPM1 mutation. The results indicate that CSPG4 is expressed and detectable by flow cytometry using the mAb 225.28 on a proportion of blasts of all subtypes of AML irrespective of cytogenetic and molecular abnormalities. mAb 225.28 could be useful in detecting AML blasts by flow cytometry.

Key words: Chondroitin sulfate proteoglycan-4 (CSPG4); Acute myeloid leukemia (AML); Monoclonal antibody (mAb) 225.28; Cytogenetic and molecular abnormalities

Address correspondence to Dr. Michael Boyiadzis, M.D., M.H.Sc., Division of Hematology and Oncology, University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, 5150 Center Ave., Suite 564, Pittsburgh, PA 15232, USA. Tel: +1-412-648-6589; Fax: +1-412-648-6579; E-mail:  This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 22, pp. 123–128, 2015
0965-0407/15 $90.00 + .00
DOI: http://dx.doi.org/10.3727/096504014X14198596979742
E-ISSN 1555-3906
Copyright © 2015 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Cullin7 Is Required for Lung Cancer Cell Proliferation and Is Overexpressed in Lung Cancer

Xuelin Men,*† Lingcheng Wang,† Wenfei Yu,‡ and Yuanrong Ju*

*Department of Respiratory, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, P.R. China
†Department of Respiratory Medicine, Jinan No. 4 People’s Hospital, Jinan, Shandong, P.R. China
‡Shandong University School of Medicine, Jinan, Shandong, P.R. China

Ubiquitin ligase Cullin7 has been identified as an oncogene in some malignant diseases such as choriocarcinoma and neuroblastoma. However, the role of Cullin7 in lung cancer carcinogenesis remains unclear. In this study, we explored the functional role of Cullin7 in lung cancer cell proliferation and tumorigenesis and determined its expression profile in lung cancer. Knocking down Cullin7 expression by small interfering RNA (siRNA) in lung cancer cells inhibited cell proliferation and elevated the expression of p53, p27, and p21 proteins. The enhanced p53 expression resulted from activation of the DNA damage response pathway. Cullin7 knockdown markedly suppressed xenograft tumor growth in vivo in mice. Moreover, Cullin7 expression was increased in primary lung cancer tissues of humans. Thus, Cullin7 is required for sustained proliferation and survival of tumor cells in vitro and in vivo, and its aberrant expression may contribute to the pathogenesis of lung cancer. Thus, our study provided evidence that Cullin7 functions as a novel oncogene in lung cancer and may be a potential therapeutic target for lung cancer management.

Key words: Cullin7; Lung cancer; Proliferation

Address correspondence to Dr. Yuanrong Ju, Department of Respiratory, Shandong Provincial Hospital Affiliated to Shandong University 324#, Jingwu Road, Jinan, Shandong 250021, P.R. China. E-mail:  This e-mail address is being protected from spambots. You need JavaScript enabled to view it