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学科主题: 临床医学
题名:
Anti-HDGF Targets Cancer and Cancer Stromal Stem Cells Resistant to Chemotherapy
作者: Zhao, Jun1,3; Ma, Mark Z.1; Ren, Hening1,2; Liu, Zhenqiu2; Edelman, Martin J.2; Pan, Hong1,4; Mao, Li1,2
刊名: CLINICAL CANCER RESEARCH
发表日期: 2013-07-01
DOI: 10.1158/1078-0432.CCR-12-3478
卷: 19, 期:13, 页:3567-3576
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Oncology
研究领域[WOS]: Oncology
关键词[WOS]: GROWTH-FACTOR ; LUNG-CANCER ; TUMOR MICROENVIRONMENT ; BREAST CARCINOMAS ; ANGIOGENESIS ; FIBROBLASTS ; BEVACIZUMAB ; INHIBITORS ; EXPRESSION ; PACLITAXEL
英文摘要:

Purpose: Approximately one third of the patients with advanced non-small cell lung carcinoma(NSCLC) will initially respond to platinum-based chemotherapy, but virtually all tumors will progress (acquired resistance). The remainder will progress during initial treatment (primary resistance). In this study, we test whether the treatment can be improved by inhibiting hepatoma-derived growth factor (HDGF).

Experimental Design: Thirteen primary NSCLC heterotransplant models were used to test four treatment regimens, including platinum-based chemotherapy with and without bevacizumab (VEGF-neutralizing antibody) or HDGF-H3 (HDGF-neutralizing antibody) and chemotherapy with bevacizumab and HDGF-H3. Expression of stem cell-related genes was measured using quantitative reverse transcription PCR (qRT-PCR) and immunohistochemistry.

Results: Among 13 primary NSCLC heterotransplant models, three (23%) responded to chemotherapy but all relapsed within 20 days. The residual tumors after response to the chemotherapy exhibited an increased expression in 51 (61%) of 84 genes related with stem cell proliferation and maintenance, particularly those in Notch and Wnt pathways, suggesting enrichment for stem cell populations in the residual tumors. Interestingly, tumors from two of three models treated with HDGF-H3, bevacizumab, and chemotherapy combination did not relapse during 6 months of posttreatment observation. Importantly, this treatment combination substantially downregulated expression levels in 57 (68%) of 84 stem cell-related genes, including 34 (67%) of 51 genes upregulated after the chemotherapy.

Conclusion: These data support the hypothesis that cancer stem cells (CSC) are a mechanism for chemotherapy resistance and suggest HDGF may be a target for repressing CSCs to prevent relapse of NSCLC sensitive to chemotherapy. (C)2013 AACR.

语种: 英语
所属项目编号: R01 CA126818 ; P30 CA134274
项目资助者: National Cancer Institute
WOS记录号: WOS:000321095900024
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/60631
Appears in Collections:北京大学临床肿瘤学院_胸部肿瘤内科_期刊论文

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作者单位: 1.Univ Maryland, Sch Dent, Dept Oncol & Diagnost Sci, Baltimore, MD 21201 USA
2.Univ Maryland, Marlene & Stewart Greenebaum Canc Ctr, Baltimore, MD 21201 USA
3.Peking Univ, Canc Hosp & Inst, Dept Thorac Med Oncol, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100871, Peoples R China
4.Guangxi Univ, Affiliated Tumor Hosp, Dept Thorac Surg, Nanning 530004, Guangxi, Peoples R China

Recommended Citation:
Zhao, Jun,Ma, Mark Z.,Ren, Hening,et al. Anti-HDGF Targets Cancer and Cancer Stromal Stem Cells Resistant to Chemotherapy[J]. CLINICAL CANCER RESEARCH,2013,19(13):3567-3576.
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