中國科學院院士樊代明赤裸裸剽竊國外綜述
樊代明（1953.11.7－ ）2001年當選為中國工程院院士。1989年畢業於第四軍醫大
學，獲博士學位。現任第四軍醫大學西京醫院教授、主任醫師、腫瘤生物學國家重點實驗
室主任和國家臨床藥理基地主任。現任國家教育部"長江學者獎勵計劃"的特聘教授和國家
自然科學基金委首批"創新研究群體"的學術帶頭人。
2006年在一個德國網絡雜誌 EXCLI Journal上發表了一篇綜述文章
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
Yunping Zhao1,2, Ruwen Wang2, Daiming Fan1,*
被人發現，是徹頭徹尾抄襲 一篇發表2005年International Immunopharmacology上的南
非一個大學發表的綜述文章，該文章2004年就可以在網絡上獲得。
Received 27 September 2004; revised 19 November 2004; accepted 29 November
2004. Available online 24 December 2004.
The molecular mechanisms of oesophageal cancer
M.L. McCabe and Z. Dlamini,
兩篇文章的標題不但一模一樣，文章整個內容也完全一樣，是赤裸裸的抄襲之作。樊代明
是文章的通訊作者，第一作者趙雲平同時寫了第四軍醫大學和第三軍醫大學單位地址。
樊代明作為中科院的院士，國家重點實驗室的教授，國家教育部"長江學者獎勵計劃"的特
聘教授和國家自然科學基金委首批"創新研究群體"的學術帶頭人，如此抄襲行為，實在令
人髮指。
樊代明文章的抄襲，開頭部分，在句子上，有點小改動，後來就是赤裸裸100%的抄襲了。
有趣的是，樊代明文章的參考文獻部分，許多都用了新的參考文獻，沒有採用抄襲原文的
參考文獻。也就是說，【Dlamini文】和樊代明文章用一模一樣的內容，但是二文採用不
同的參考文獻。一般來說，樊代明文章的參考文獻是2004年以後發表的。也許考慮到他們
文章的發表時間是2007年，而原文是2004年，所以，原文沒有2004年以後的參考文獻，而
樊代明文章大量採用了2005年和2006年的文章作為參考文獻，遮人耳目。
下面舉例比較兩文，讀者自己明鑑【樊代明院士文】
【Dlamini文】
Abstract
Apoptosis is a process of programmed cell death, which is as essential as
cell growth, for the maintenance of homeostasis. When these processes loose
integration such as cancer, then uncontrolled cell growth occurs. Cancer of
the oesophagus ranks as the ninth most common malignancy in the world, and
recent evidence shows that its incidence is increasing. Prognosis of this
disease is poor, with an overall 5-year survival rate of less than 10%.
Unraveling the mechanisms or developing animal models for oesophageal
carcinoma have thus far not been successful. It is believed that oesophageal
cancer has an intricate molecular mechanism of evading 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 great deal of research has been
perxxxxed in order to determine the key genes that initiate and promote the
growth of oesophageal cancer. This review focuses on apoptosis and candidate
genes linked to the development of oesophageal cancer, which it is hoped may
provide diagnostic and therapeutic tools, and potential therapeutic
strategies for the management of this carcinoma.
【樊代明院士文】
ABSTRACT
Esophageal Cancer ranks among the 10 most frequent cancers in the world, and
recent evidence shows that its incidence is increasing. Prognosis of this
disease is poor, with an overall 5-year survival rate of less than 10%.
Unraveling the mechanisms or developing animal models for esophageal
carcinoma have thus far not been successful. Many genes have been found that
are believed to play a role in the development of esophageal cancer but the
underlying mechanism by which this disease develops is still not clear. It is
believed that esophageal cancer has an intricate molecular mechanism of
evading 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 great
deal of research has been perxxxxed in order to determine the key genes that
initiate and promote the growth of esophageal cancer. This review focuses on
apoptosis and candidate genes linked to the development of esophageal cancer,
which it is hoped may provide diagnostic and therapeutic tools, and potential
therapeutic strategies for the management of this carcinoma.
【Dlamini文】
Keywords: Human oesophageal cancer; Molecular genetics; Apoptosis signalling
pathway; Genomics; Oesophageal cancer therapeutics
【樊代明院士文】
Keywords: Human esophageal cancer, molecular genetics, apoptosis signalling
pathway, genomics, esophageal cancer therapeutics
【Dlamini文】
1.3. Molecular genetics of oesophageal cancer
As oesophageal carcinogenesis is poorly understood, much research is being
carried out to understand the precise mechanisms causing the metaplasia–
dysplasia sequence of oesophageal carcinoma at a molecular level [9]. It is
known that tumour suppressor genes, oncogenes, and apoptotic genes are
involved in the initiation and development of oesophageal cancer, but to date
no gene directly related to oesophageal cancer has been identified [10].
Many candidate genes and their role in the development of oesophageal cancer
are still to be revealed before a human oesophageal carcinogenesis model can
be developed. Key tumour related genes and their specific role played in the
development 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 are
being carried out to discover the precise mechanisms causing the metaplasia–
dysplasia sequence of esophageal carcinoma at a molecular level. It is known
that tumor suppressor genes, oncogenes, and apoptotic genes are involved in
the initiation and development of esophageal cancer, but to date no gene
directly related to esophageal cancer has been identified (Kwong et al.,
2005). The key tumor related genes and their specific role which played in
the development of esophageal cancer are discussed in more detail in
following chapters.
【Dlamini文】
3.4. p16INK4a and p15INK4b
These are tumour suppressor genes and are localized to 9p21. This region has
been shown to undergo hemizygous or homozygous deletion in a variety of
tumour types [29]. These two genes encode two cyclin dependent kinase (CDK)
inhibitors which negatively regulates the cell from G1-S phase in
proliferating cells, contributing to active pRb maintenance [30]. During the
G1-S phase p16INK4a binds and inhibits CDK4/6 activity [31], and p15INK4b
binds to cyclin D-dependent kinase and prevents p27 association. [32] p27
then binds to E-CDK2 complex, blocking the cell cycle at the G1-S boundary,
risking cells to abnormally proliferate [32]. Aberrant methylation of
p16INK4a has been found to be a key feature in human carcinogenesis and
although aberrant methylation of p15INK4b also occurs it is found to occur
less frequently in human oesophageal cancer in Lixian, China [29]. A common
feature of p15INK4b is homozygous deletion, which also takes place in
p16INK4a.
【樊代明院士文】
(3) p16INK4a and p15INK4b
Two tumor suppressor genes are localized at 9p21, Which has been shown to
undergo hemizygous or homozygous deletion in a variety of tumor types. These
two genes encode two cyclin dependent kinase (CDK) inhibitors which
negatively regulate the cell from G1-S phase in proliferating cells,
contributing to active pRb maintenance (Morgan D, 1995). During the G1-S
phase p16INK4a binds and inhibits CDK4/6 activity (Retnisdottir et al.,
1997), and p15INK4b binds to cyclin D-dependent kinase and prevents p27
association(Kunisaki et al., 2004). p27 then binds to E-CDK2 complex,
blocking the cell cycle at the G1-S boundary, risking cells to abnormally
proliferate(Kunisaki et al., 2004). Aberrant methylation of p16INK4a has been
found to be a key feature in human carcino-genesis, and although aberrant
methylation of p15INK4b also occurs it is found to occur less frequently in
human esophageal cancer in Lixian county, China (Xing et al., 1999). A common
feature of p15INK4b is homozygous deletion, which also takes place in
p16INK4a.
【Dlamini文】
6. Angiogenesis
Angiogenesis is the development of new blood vessels, which provide blood and
nutrient supply to tumours to survive. Once the tumour is stable, it can then
invade neighbouring cells leading to metastasis.
In oesophageal cancer cells the increased expression of vascular endothelial
growth factors (VEGFs) stimulates endothelial proliferation and migration.
Increased expression of VEGFs and VEGFRs (receptors) were detected in
metaplastic tissues of the lower oesophagus but not in normal oesophageal
epithelium, indicating sustained neovascular development early in Barrett's
carcinogenesis [25].
【樊代明院士文】
Angiogenesis
Angiogenesis is the development of new blood vessels, which provide blood and
nutrient supply to tumors to survive. Once the tumor is stable, it can then
invade neighbouring cells leading to metastasis.
In esophageal cancer cells the increased expression of vascular endothelial
growth factors (VEGFs) stimulates endothelial proliferation and migration.
Increased expression of VEGFs and VEGFRs (receptors) were detected in
metaplastic tissues of the lower esophagus but not in normal esophageal
epithelium, indicating sustained neovascular development early in Barrett’s
carcinogenesis (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 an
important 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 cytoskeleton
and cadherin junctions of cells. β-Catenin has been implicated in the
tranxxxxion of oncogenes such as c-myc, c-jun and cyclin D1, which are
oncogenes frequently active in oesophageal cancer cells.
The APC gene product targets β-catenin for degradation and prevents β-catenin
dependent degradation. Increased β-catenin dependent tranxxxxion 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 in
adenocarcinomas and squamous oesophageal carcinomas [67].
It is therefore believed that down-regulation of β-catenin expression by
antisense technology could be an effective treatment for oesophageal cancer
[79].
【樊代明院士文】
Invasion and metastasis
Invasion and metastasis of esophageal cancer is poorly understood. The cell–
cell adhesion molecules (CAMs) hold cells together, and believed to play an
important 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 cytoskeleton
and cadherin junctions of cells. B-Catenin has been implicated in the
tranxxxxion of oncogenes such as c-myc, c-jun and cyclin D1, which are
oncogenes frequently active in esophageal cancer cells.
The APC gene product targets B-catenin for degradation and prevents h-catenin
dependent degradation. Increased B-catenin dependent tranxxxxion 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 in
adenocarcinomas and squamous esophageal carcinomas.
It is therefore believed that down-regulation of hcatenin expression by
antisense technology could be an effective treatment for esophageal cancer
(Kuwano et al., 2005).
