2006年在一个德国网络杂志 EXCLI Journal上发表了一篇综述文章EXCLI Journal 2006;5:79-92 –Received: 12. July 2006, accepted: 31. July 2006, published 3. August 2006 Review article:The molecular mechanisms of esophageal cancer Yun ping Zhao 1,2, Ruwen Wang2, Daiming Fan1,*

被人发现，是彻头彻尾抄袭 一篇发表2005年International Immunopharmacology上的南非一个大学发表的综述文章，该文章2004年就可以在网络上获得。

Received 27 September 2004; revised 19 November 2004; accepted 29 November2004. Available online 24 December 2004.

The molecular mechanisms of oesophageal cancerM.L. McCabe and Z. Dlamini,

两篇文章的标题不但一模一样，文章整个内容也完全一样，是赤裸裸的抄袭之作。樊代明是文章的通讯作者，第一作者赵云平同时写了第四军医大学和第三军医大学单位地址。

樊代明作为中科院的院士，国家重点实验室的教授，国家教育部"长江学者奖励计划"的特聘教授和国家自然科学基金委首批"创新研究群体"的学术带头人，如此抄袭行为，实在令人发指。

樊代明文章的抄袭，开头部分，在句子上，有点小改动，後来就是赤裸裸100%的抄袭了。

有趣的是，樊代明文章的参考文献部分，许多都用了新的参考文献，没有采用抄袭原文的参考文献。也就是说，【Dlamini文】和樊代明文章用一模一样的内容，但是二文采用不同的参考文献。一般来说，樊代明文章的参考文献是2004年以后发表的。也许考虑到他们文章的发表时间是2007年，而原文是2004 年，所以，原文没有2004年以后的参考文献，而樊代明文章大量采用了2005年和2006年的文章作为参考文献，遮人耳目。

下面举例比较两文，读者自己明鉴【樊代明院士文】

【Dlamini文】

AbstractApoptosis is a process of programmed cell death, which is as essential ascell growth, for the maintenance of homeostasis. When these processes looseintegration such as cancer, then uncontrolled cell growth occurs. Cancer ofthe oesophagus ranks as the ninth most common malignancy in the world, andrecent evidence shows that its incidence is increasing. Prognosis of thisdisease is poor, with an overall 5-year survival rate of less than 10%.Unraveling the mechanisms or developing animal models for oesophagealcarcinoma have thus far not been successful. It is believed that oesophagealcancer has an intricate molecular mechanism of evading apoptosis by the down-regulation of Bax, up-regulation of Bcl-2, Bcl-xl and Survivin, mutation ofp53 and alteration in Fas expression. A great deal of research has been performed in order to determine the key genes that initiate and promote thegrowth of oesophageal cancer. This review focuses on apoptosis and candidategenes linked to the development of oesophageal cancer, which it is hoped mayprovide diagnostic and therapeutic tools, and potential therapeuticstrategies for the management of this carcinoma.

【樊代明院士文】

ABSTRACTEsophageal Cancer ranks among the 10 most frequent cancers in the world, andrecent evidence shows that its incidence is increasing. Prognosis of thisdisease is poor, with an overall 5-year survival rate of less than 10%.Unraveling the mechanisms or developing animal models for esophagealcarcinoma have thus far not been successful. Many genes have been found thatare believed to play a role in the development of esophageal cancer but theunderlying mechanism by which this disease develops is still not clear. It isbelieved that esophageal cancer has an intricate molecular mechanism ofevading apoptosis by the down-regulation of Bax, up-regulation of Bcl-2, Bcl-xl and Survivin, mutation of p53 and alteration in Fas expression. A greatdeal of research has been performed in order to determine the key genes thatinitiate and promote the growth of esophageal cancer. This review focuses onapoptosis and candidate genes linked to the development of esophageal cancer,which it is hoped may provide diagnostic and therapeutic tools, and potentialtherapeutic strategies for the management of this carcinoma.

【Dlamini文】

Keywords: Human oesophageal cancer; Molecular genetics; Apoptosis signallingpathway; Genomics; Oesophageal cancer therapeutics

【樊代明院士文】

Keywords: Human esophageal cancer, molecular genetics, apoptosis signallingpathway, genomics, esophageal cancer therapeutics

【Dlamini文】

1.3. Molecular genetics of oesophageal cancer

As oesophageal carcinogenesis is poorly understood, much research is beingcarried out to understand the precise mechanisms causing the metaplasia–dysplasia sequence of oesophageal carcinoma at a molecular level [9]. It isknown that tumour suppressor genes, oncogenes, and apoptotic genes areinvolved in the initiation and development of oesophageal cancer, but to dateno gene directly related to oesophageal cancer has been identified [10].

Many candidate genes and their role in the development of oesophageal cancerare still to be revealed before a human oesophageal carcinogenesis model canbe developed. Key tumour related genes and their specific role played in thedevelopment of oesophageal cancer are discussed in more detail.

【樊代明院士文】

Molecular genetics of esophageal cancer

As esophageal carcinogenesis is poorly understood, many research works arebeing carried out to discover the precise mechanisms causing the metaplasia–dysplasia sequence of esophageal carcinoma at a molecular level. It is knownthat tumor suppressor genes, oncogenes, and apoptotic genes are involved inthe initiation and development of esophageal cancer, but to date no genedirectly related to esophageal cancer has been identified (Kwong et al.,

2005). The key tumor related genes and their specific role which played inthe development of esophageal cancer are discussed in more detail infollowing chapters.

【Dlamini文】

3.4. p16INK4a and p15INK4bThese are tumour suppressor genes and are localized to 9p21. This region hasbeen shown to undergo hemizygous or homozygous deletion in a variety oftumour types [29]. These two genes encode two cyclin dependent kinase (CDK)inhibitors which negatively regulates the cell from G1-S phase inproliferating cells, contributing to active pRb maintenance [30]. During theG1-S phase p16INK4a binds and inhibits CDK4/6 activity [31], and p15INK4bbinds to cyclin D-dependent kinase and prevents p27 association. [32] p27then binds to E-CDK2 complex, blocking the cell cycle at the G1-S boundary,risking cells to abnormally proliferate [32]. Aberrant methylation ofp16INK4a has been found to be a key feature in human carcinogenesis andalthough aberrant methylation of p15INK4b also occurs it is found to occurless frequently in human oesophageal cancer in Lixian, China [29]. A commonfeature of p15INK4b is homozygous deletion, which also takes place inp16INK4a.

【樊代明院士文】

(3) p16INK4a and p15INK4bTwo tumor suppressor genes are localized at 9p21, Which has been shown toundergo hemizygous or homozygous deletion in a variety of tumor types. Thesetwo genes encode two cyclin dependent kinase (CDK) inhibitors whichnegatively regulate the cell from G1-S phase in proliferating cells,contributing to active pRb maintenance (Morgan D, 1995). During the G1-Sphase p16INK4a binds and inhibits CDK4/6 activity (Retnisdottir et al.,

1997), and p15INK4b binds to cyclin D-dependent kinase and prevents p27association(Kunisaki et al., 2004). p27 then binds to E-CDK2 complex,blocking the cell cycle at the G1-S boundary, risking cells to abnormallyproliferate(Kunisaki et al., 2004). Aberrant methylation of p16INK4a has beenfound to be a key feature in human carcino-genesis, and although aberrantmethylation of p15INK4b also occurs it is found to occur less frequently inhuman esophageal cancer in Lixian county, China (Xing et al., 1999). A commonfeature of p15INK4b is homozygous deletion, which also takes place inp16INK4a.

【Dlamini文】

6. AngiogenesisAngiogenesis is the development of new blood vessels, which provide blood andnutrient supply to tumours to survive. Once the tumour is stable, it can theninvade neighbouring cells leading to metastasis.

In oesophageal cancer cells the increased expression of vascular endothelialgrowth factors (VEGFs) stimulates endothelial proliferation and migration.Increased expression of VEGFs and VEGFRs (receptors) were detected inmetaplastic tissues of the lower oesophagus but not in normal oesophagealepithelium, indicating sustained neovascular development early in Barrett'scarcinogenesis [25].

【樊代明院士文】

AngiogenesisAngiogenesis is the development of new blood vessels, which provide blood andnutrient supply to tumors to survive. Once the tumor is stable, it can theninvade neighbouring cells leading to metastasis.

In esophageal cancer cells the increased expression of vascular endothelialgrowth factors (VEGFs) stimulates endothelial proliferation and migration.Increased expression of VEGFs and VEGFRs (receptors) were detected inmetaplastic tissues of the lower esophagus but not in normal esophagealepithelium, indicating sustained neovascular development early in Barrett’scarcinogenesis (Feagins et al., 2005).

【Dlamini文】

7. Invasion and metastasis

Invasion and metastasis of oesophageal cancer is poorly understood. The cell–cell adhesion molecules (CAMs) hold cells together, and believed to play animportant role in metastasis of the cancer cell [25].

β-Catenin has been found to play a role in squamous oesophageal cancer cells,by its cell–cell adhesion function and interactions with the cytoskeletonand cadherin junctions of cells. β-Catenin has been implicated in the transciption of oncogenes such as c-myc, c-jun and cyclin D1, which areoncogenes frequently active in oesophageal cancer cells.

The APC gene product targets β-catenin for degradation and prevents β-catenindependent degradation. Increased β-catenin dependent transcription due to β-catenin binding to Fz receptors, mutations in β-catenin, APC, and increased β-catenin expression due to Fz receptor mutations, have all been found inadenocarcinomas and squamous oesophageal carcinomas [67].

It is therefore believed that down-regulation of β-catenin expression byantisense technology could be an effective treatment for oesophageal cancer[79].

【樊代明院士文】

Invasion and metastasisInvasion and metastasis of esophageal cancer is poorly understood. The cell–cell adhesion molecules (CAMs) hold cells together, and believed to play animportant role in metastasis of the cancer cell (Kleespies et al., 2004).

B-Catenin has been found to play a role in squamous esophageal cancer cells,by its cell–cell adhesion function and interactions with the cytoskeletonand cadherin junctions of cells. B-Catenin has been implicated in thetranscription of on cogenes such as c-myc, c-jun and cyclin D1, which areoncogenes frequently active in esophageal cancer cells.

The APC gene product targets B-catenin for degradation and prevents h-catenindependent degradation. Increased B-catenin dependent transcription due to B-catenin binding to Fz receptors, mutations in B-catenin, APC, and increased B-catenin expression due to Fz receptor mutations, have all been found inadenocarcinomas and squamous esophageal carcinomas.

It is therefore believed that down-regulation of hcatenin expression byantisense technology could be an effective treatment for esophageal cancer(Kuwano et al., 2005)