学术投稿
中国癌症研究(英文版)杂志

中国癌症研究(英文版)杂志

(非官网)

  • 主管单位:中国癌症研究
  • 主办单位:中国科学技术协会
  • 国际刊号:11-2591/R
  • 国内刊号:凌启柏
  • 影响因子:1.59
  • 创刊:1989
  • 周期:
  • 发行:
  • 语言:中文
  • 邮发:北京市海淀区阜成路52号
  • 全年订价:0.00
期刊收录 期刊荣誉 期刊标签
  • 1998年中国科协择优支持基础性、高科技学术期刊资助
  • 肿瘤学
  • 还需要咨询该刊物的详情?->
相关期刊
期刊级别:
产品参数:
主管单位:中国癌症研究
主办单位:中国科学技术协会
出版地方:
期刊标签:肿瘤学
国际刊号:11-2591/R
国内刊号:凌启柏
邮发代号:北京市海淀区阜成路52号
创刊时间:1989
发行周期:

中国癌症研究(英文版)杂志简介

本刊主要是及时报道我国在肿瘤防治研究领域包括癌症基础理论研究和癌症预防、临床治疗研究方面的新进展、新成果,内容涉及肿瘤病因学与浒病学,实验肿瘤学、肿瘤细胞分子生物学,肿瘤病理学以及肿瘤影像诊断、肿瘤外科治疗、化学治疗、放射治疗、介入治疗、生物治疗和中西医结合治疗肿瘤等各分支学科,旨在促进国内外学术交流,提高我国癌症研究与癌症治疗水平。

栏目设置

杂志收录/荣誉

/ 1998年中国科协择优支持基础性、高科技学术期刊资助

中国癌症研究(英文版)杂志投稿要求

中国癌症研究(英文版)杂志社征稿要求

  1. 稿件应可靠、准确、有创意、科学、实用。论点要新颖,论点要有充分可靠的数据,要自负(抄袭),文章要简洁。

  2. 名称在正文标题下的订单,安排应在提交时确定。作者姓名、单位、详细地址和邮政编码必须写清楚,作者必须征得作者的同意,其他作者同意,行序后,通知不再更改。

  3.为了缩短出版时间,减少错误,图纸为word格式,请详细说明我的联系方式。

  4. 编辑部已删除修稿,不同意稿件中的声明,请修改稿件。

  5.期刊名称应根据医学索引中使用的格式缩写。作者对参考文献的准确性负责。

  6.作者及所属机构:

  所有作者的全名;

  进行该项工作的机构的地址,连同包括邮政编码的完整邮政地址;

  (iii)作者的电子邮件地址、电话和传真号码,有关稿件的信件应寄给作者。


杂志分析报告

名词解释:

影响因子:指该期刊近两年文献的平均被引用率,即该期刊前两年论文在评价当年每篇论文被引用的平均次数

被引半衰期:衡量期刊老化速度快慢的一种指标,指某一期刊论文在某年被引用的全部次数中,较新的一半被引论文刊载的时间跨度

期刊发文量:通常是指在特定时间内,一个学术期刊所发表的论文数量。计算期刊发文量是评估期刊生产力和影响力的一个重要指标,也是学者选择投稿期刊时常常考虑的因素之一。

期刊他引率:期刊被他刊引用的次数占该刊总被引次数的比例用以测度某期刊学术交流的广度、专业面的宽窄以及学科的交叉程度

总被引频次:指该期刊自创刊以来所登载的全部论文在统计当年被引用的总次数。这是一个非常客观实际的评价指标,可以显示该期刊被使用和受重视的程度,以及在科学交流中的作用和地位。

平均引文率:在给定的时间内,期刊篇均参考文献量,用以测度期刊的平均引文水平,考察期刊吸收信息的能力以及科学交流程度的高低

中国癌症研究(英文版)杂志影响因子
中国癌症研究(英文版)杂志发文量
中国癌症研究(英文版)杂志总被引频次

杂志文章摘录

  • Objective: To investigate the antitumor mechanisms of the streptococcal preparation OK-432. Methods: Using C57BL/6 mouse bearing B16 melanoma, we observed the antitumor activity of OK-432 and investigated the effect of OK-432 on multi-cytokine (IL-2, IL-4, IL-6, IL-10, IL-12, IFN-() production of mouse splenocyte both in vitro and in vivo. Results: As compared with control, OK-432 significantly inhibited B16 melanoma growth and lengthened mice survival time (P<0.05). In vitro OK-432 could stimulate splenocyte from tumor bearing mice to secrete IL-6, IL-12, IFN-( and IL-10 remarkably (P<0.01). In vivo OK-432 led to the increased production of IL-2, IL-12 and IFN-( but decreased production of IL-10 (P<0.05). When the splenocytes harvested from OK-432 treated mice were stimulated with OK-432 again in vitro, the production of IFN-( increased and IL-10 decreased significantly (P<0.05). Conclusion: OK-432 could boost multiple cytokines production, especially IL-12 which skewed T cells in a Th1 dominant state and enhanced the host antitumor activities.

    作者:王湘辉;藤本敏博;张滨;磨伊正义;柴福录 刊期: 2002年第01期

  • To study the killing effect of suicide gene CD on mouse gastric cancer. Methods: CD gene was transduced with the retroviral vector. The killing effect and bystander effect of CD gene on mouse gastric cancer cell line MFC were observed. The mouse gastric cancer model was used for in vivo study. The CD gene containing virus was injected into the tumors. The volumes of the tumors in every group were measured in time. Results: Significant killing effect and bystander effect were observed by CD gene in vitro, 70~80% cell death resulting from 20% of CD gene transduction. In vivo, CD/5-Fc caused tumor to diminution. Conclusion: CD/5-Fc system has significant killing effect on mouse gastric cancer

    作者:郭善禹;顾琴龙;朱正纲;林言箴 刊期: 2001年第04期

  • Objective: To clone multidrug resistance (MDR) related genes in lung adenocarcinoma cell lines. Methods: The differentially expressed cDNA fragments between A549 and A549DDP cells were analyzed by mRNA differential display PCR(DD RT-PCR). The fragments thus obtained were further analyzed by DNA sequencing and Northern blotting. Results: Three differentially expressed cDNA fragments were obtained and confirmed by Northern blot. Sequence analysis revealed that two of them were novel and one was 100% identical with ICE gene. Conclusion: Analyzing differentially expressed fragment between A549 and A549DDP cells may be helpful for finding new MDR related genes. The drug resistance of A549DDP cells may be related to the inhibition or down-regulation of ICE gene.

    作者:王洁;刘叙仪;李西平;李振甫;张宏 刊期: 2001年第02期

  • Objective: Ajoene, a major compound extracted from crashed garlic, has been shown to have antitumor, antimycotic, antimicrobial, antimutagenic functions in vivo or in vitro and treated as a potential antitumor drug. However, the molecular mechanisms underlying the tumor cytotoxicity of ajoene and even garlic substances are poorly defined. In the present study, we aimed to generate gene expression profiles of HL-60 cell treated by ajoene. Methods: A cDNA microarray presenting 2400 of genes amplified from human leukocyte cDNA library was constructed and the gene expression profiles of HL-60 cell induced by ajoene were generated. Results: After data analysis, 28 differentially expressed genes were identified and sequenced. These genes include 21 known genes and 7 ESTs. Most of the known genes are related to cell apoptosis, such as secretory granule (PRG1), beta-2 microglobulin (B2M), 16S ribosomal RNA gene and ribosomal protein S12. Several genes are related to cell differentiation, including the genes similar to H3 histone and ribosomal protein L31. Northern blot analysis was used to verify and quantify the expression of selected genes. Conclusion: Ajoene can induce HL-60 cell apoptosis significantly and may play a role in differentiation. cDNA microarray technology can be a valuable tool to gain insight into molecular events of pharmacological mechanism of herbal medicine.

    作者:方志俊;黄文秀;黄明辉;梁润松;崔景荣;王夔;杨梦苏 刊期: 2002年第01期

  • Objective:The Fas and Fas ligand (FasL) play an important role in maintaining immune privilege on malignant tumors. In present study, we investigated the expression of FasL in SW480 and LS174 human colon carcinoma cell lines and twenty primary colon carcinoma specimens. Methods: The expression of FasL in human colon carcinoma cell lines and primary colon carcinomas specimens was detected by immunohistochemistry and Reverse Transcription-PCR (RT-PCR). Results: We found that all of detected human colon carcinoma cell lines and primary colon carcinoma specimens constitutively expressed FasL at the mRNA and protein level. However, the expression of FasL was not found in normal colon epithelial cells. Conclusion: The expression of FasL may occur during malignant transformation from normal colon epithelial cells to colon carcinoma cells. Our results suggest that tumor cells kill cytotoxic T lymphocytes (CTLS) and natural killer (NK) cells by expression of FasL. It may be a new mechanism for tumor cells to escape the host's immune surveillance. The expression of FasL may contribute to the formation of colon carcinomas.

    作者:邢宝才;王怡;S Wimmenauer;E H Farthmann;黄信孚 刊期: 2002年第01期

  • To investigate the regulation effect of protein kinase A on IL-6-induced STAT3 activation in myeloma cells. Methods: Two human myeloma cell lines-Sko-007 and U266 were pretreated with Forskolin, a protein kinase A antagonist, and then stimulated by IL-6. The activation state of STAT3 in these two cells were examined by electrophoretic mobility shift assay (EMSA). Results: Although PKA pathway itself doesn't participate in IL-6 signal transduction in Sko-007 and U266 cells, activation of protein kinase A can inhibit IL-6-induced STAT3 activation in these two cell lines. Conclusion: There exists an inhibitory effect of protein kinase A on STAT3 activation in human myeloma cells treated by IL-6.

    作者:宋伦;黎燕;沈倍奋 刊期: 2001年第04期

  • Objective: To understand whether verapamil (VER) resistance development in the multidrug-resistant cell line and its mechanism. Methods: K562/ADM/VER cell subline resistant to verapamil was established through a gradual increase of VER concentration in the media. MTT method was used to assay resistance to VER, cross resistance to dipyriamole (DPM), cyclosporin A (CsA) in the cells, and HPLC and spectrofluorometer to detect intracellular accumulation of VER or ADM respectively, as well as S-P immunocytochemical technique for detection of genes expression. Results: It were observed that 7.9-fold increase in VER resistance, significantly reduced intracellular accumulation of VER or ADM and also develop across resistance to DPM and CsA in K562/ADM/VER cells, compared with its parent cell, K562/ADM. High-level of p-glycoprotein(pgp), middle-level of p53, p16, was present in two cell lines without expression of GSTPI, C-myc, C-myc, C-fos and C-erbB-2. Bc1-2 protein expression was found only in K562/ADM cells. Conclusion: K562/ADM cells were capable of being induced to develop resistance to VER.

    作者:谢佐福;周冬梅;林贤东;林声;吴允昆 刊期: 2001年第02期

  • Objective: This study was designed to investigate differential pattern of G1-cyclins (D1 and E) in transitional cell carcinoma (TCC) of human urinary bladder with or without human papillomavirus-18 (HPV-18) infection. Methods: Immunohistochemistry method was used in the detection of the expression of G1-cyclins in 57 cases of TCC (7 normal bladders as control), and HPV-18 DNA was found in 29 cases by polymerases chain reaction (PCR). Results: Cyclin D1 expression was found in 41 of 57 (71.93%) TCCs and it was reverse associated with HPV (x2=8.21, P<0.05). And cyclin D1 expression was found in 16 of 29 (55.17%) in HPV-18 infection group and 25 of 28 (89.29%) in non-HPV infection group. Cyclin E expression was detected in 36 of 57 (63.16%) and the association between the cyclin E expression and HPV infection was not found (x2=0.52, P>0.05). Cyclin E expression was found in 17 of 29 (56.82%) in HPV-18 infection group and 19 of 28 (67.86%) in non-HPV infection group. There was obvious difference in the cyclin D1 and cyclin E expression between the TCC and normal tissue (x2=7.46, P<0.05; x2=7.45, P<0.05, respectively). Conclusion: These data demonstrated that HPV infection altered the control of G1 cell cycle. And changes of G1 cell cycle regulatory proteins, either by interaction of cellular protein with viral oncoproteins or by changes in the cellular proteins themselves, may be critical for carcinogenesis of TCC of urinary bladder.

    作者:郑闪;何祖根;刘海涛;王顺宝 刊期: 2002年第01期

  • To observe the synergistic efficacy between Adenovirus-mediated bcl-Xs(Adv-bcl-Xs) gene transfer and chemotherapy on ovarian cancer cell growth. Methods: NuTu-19 cells were infected by different titers of Adv-bcl-Xs and treated with topotecan in the meantime. Cell proliferation was measured 3 days later by MTT. Graphical representations and statistical analyses for their interaction in tumor cells were done. Results: The statistical result and Graphical representations of the statistical modeling showed synergy effect on cell growth inhibition (P<0.01). Conclusion: There were synergistic efficacies between Adv-bcl-Xs gene therapy and Topotecan in ovarian cancer cell growth.

    作者:王和;Vicki V Baker 刊期: 2001年第04期

  • To investigate the influence of consecutive immunization on cellular and humoral immunity in mice. Methods: We evaluated a consecutive immunization strategy of priming with recombinant fowlpox virus vUTALG and boosting with plasmid DNA pcDNAG encoding HIV-1 capsid protein Gag. Results: In immunized mice, the number of CD4+ T cells from splenic lymphocytes increased significantly and the proliferation response of splenocytes to ConA and LPS elevated markedly and HIV-1-specific antibody response could be induced. Conclusion: Consecutive immunization could increase cellular and humoral immunity responses in mice.

    作者:罗坤;金宁一;郭志儒;秦云龙;郭炎;方厚华;安汝国;殷震 刊期: 2001年第04期

杂志往期目录

更多评论>>

网友反馈(不代表本站观点)

nblove** 的反馈:

9月中旬在投中国癌症研究(英文版)杂志的稿,10月就通知录用啦,速度杠杠的。需要说的是,这本杂志的编辑排版很严格,录用后会有多次排版校对,编排质量很高,编辑工作非常严谨认真,值得赞扬!

一江春水** 的反馈:

中国癌症研究(英文版)杂志 这个刊物免审稿费,版面费正常,效率高

一江春水** 的反馈:

文章接收速度还可以,我投稿的时间有些尴尬,恰逢是在放假的时候,耽误了一段时间。中国癌症研究(英文版)杂志在学术界还是有一定地位,还是不错的。编辑老师也很不错,比较推荐大家投此杂志。

明哥** 的反馈:

等得好心急哟,编辑大哥大姐们,能不能快点审下我的稿子

谢正勇** 的反馈:

请问一下,中国癌症研究(英文版)杂志 投稿授权证明要不要盖单位的章,录用了,说要搞个什么授权证明。

小小小硕** 的反馈:

五天了还是已发回执状态 什么情况?有人知道么

steven0281** 的反馈:

感觉还是挺难投的,不过编辑老师挺好的。去年八月份投了一篇文章,修改后录用了,今年投了篇,个人感觉比上一次写的好,却退稿了,可能这就是命吧

小荷** 的反馈:

等了好几个月,终于收到书了,悬着的心终于放下了,感谢中国癌症研究(英文版)杂志编辑部大大,感谢~~感谢

嘟噜噜~** 的反馈:

退修了三四次,基本都是格式和缩减字数,可能文章比较符合期刊主题。样刊是平邮,大家一定要写好自己的详细地址,越细越好流泪

春风沉醉de早上** 的反馈:

求助各位学友,还有3天就投稿满一个月了,但是现在目前仍然是初稿待处理,请问这样是不是就没希望了呀。现在想撤稿了,官网也没有撤稿的选项,请问该如何撤稿呢?