樊代明院士剽窃M.L. McCabe and Z. Dlamini的论文的两文的

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樊代明院士剽窃M.L. McCabe and Z. Dlamini的论文的两文的逐段比较

方舟子先生，

记不得多少年以前您一身正气地维护科学的真理，批判伪造，令人敬佩。最近见到您揭发了樊代明论文造假。我谨向你提供樊代明的论文严重剽窃事件。附件是樊代明发表的文章和被剽窃的论文。

樊代明的论文 Yunping Zhao1,2, Ruwen Wang2, Daiming Fan1* （赵云平 王汝文 樊代明），The molecular mechanisms of esophageal cancer 2006年发表于EXCLI杂志

ABSTRACT　　Esophageal Cancer ranks among the 10（说明，Dlamini 的原文是: the ninth）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 andalteration 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.　　Key Words: Human oesophageal cancer; Molecular genetics; Apoptosis signaling pathway; Geneomics; Oesphageal cancer therapeutics

M.L. McCabe and Z. Dlamini的论文，Mini review　　The molecular mechanisms of oesophageal cancer.2005年发表于International Immunopharmacology。

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.　　Key words: Human oesophageal cancer; Molecular genetics; Apoptosis signaling pathway; Geneomics; Oesphageal cancer therapeutics

【樊代明文章】　　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. 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 . 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.

【Dlamini文章】　　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. 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 . 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.

【樊代明文章】　　(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 83 　　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文章】　　3.4. p16INK4a and p15INK4b　　These are tumor suppressor genes and are localized to 9p21. This region has been shown to undergo hemizygous or homozygous deletion in a variety of tumour types. 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. During the G1-S phase p16INK4a binds and inhibits CDK4/6 activity , and p15INK4b binds to cyclin D-dependent kinase and prevents p27 association， then binds to E-CDK2 complex, blocking the cell cycle at the G1-S boundary, risking cells to abnormally proliferate. 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 . A common feature of p15INK4b is homozygous deletion, which also takes place in p16INK4a.

【樊代明文章】　　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

【Dlamini文章】　　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

【樊代明文章】　　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. h-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. h-Catenin has been implicated in the transcription 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 h-catenin for degradation and prevents h-catenin dependent degradation. Increased h-catenin dependent transcription due to hcatenin binding to Fz receptors, mutations in h-catenin, APC, and increased h-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.

【Dlamini文章】　　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. 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. It is therefore believed that down-regulation of β-catenin expression by antisense technology could be an effective treatment for oesophageal cancer.

(XYS20190129)

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