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12.09.22-23ûи
12.09.24, ӡһϸ
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12.09.24, ·ߡԡϵ⡷һĵۡ
12.09.24, ܡ˵˵˿Ρ
12.09.24, ָС麺ƴĸĴϡ
12.09.24, ת°ǿ
12.09.24, 조ӡҪ20˾רαն

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ԹƳһ˿ǻڵϸ25000֡ЩϸֲҺ
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γʯʯһγɣûͨˢȥˣר
ҵ豸ϴȥһ㲢޶ϴϰߣΪϴϴ
ȥϴǻԱ֣Ҳѹֹ˶͡ϻ𡱡

2012.9.19

»ÿյѶ2012.9.21

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ת°ܱʵĿ

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ڣǾͿɳԵξ档⣬ʱר


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ǵӡǣȻɶֻ֧򹤳ֵ̼Ȥ
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ƪû㹻ֵ֤֧£ĵԿζѧJohn 
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׷ױΪϲһ棬ȻBT
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ۣȴܳԵʳ˭Ҳܲˣ෴׻Ϊ
ṩ㹻ĵʣĸáJohn LoseyԼҲ
˼ƪˡȤǣһΰƪͶѧ־ʱ
ľܾȻȴܷ˵־
ɱӰ죬˵ҲϲͶͨաá־Ҳ
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ߣVetiver010

˵ںҵĵ˶֮⽯΢
д֮

۵΢صǡϡ١ϡָ΢
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仰У㵱ܴͨ󣬿԰ʮ
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ĸܻǵġһøʵһЩЩʧȥŮ
ûмļͥô죿봨ɱߣʧȥԭֵء
Դ΢βҵֶ֧ã

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⣬ڱɴ֮Լ߲ɷĴȻֻСӦ
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do more, care lessǽʱߴΪԼ
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ǣ۵дˮƽȺעJuniorSeniorǿһ㣬
ǲ࣬Ҫ˵ѧġߡ̸ϣʵҲ治
ת΢΢תóö࣬ԭ٣ȥǿţ
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һǣڷǰܿȻҪļӹɫ
ĸɱ༭ڴŽվ֤֤α

Ű˵Ҫ硣ĸа׷ǵġ
ƻǷǽ⣬ĸŮ˲ں

ԣŰңֲܸ󣻶أдVɡ

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ԺʿĳϮģΪʲôһֱأ

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ҽƴѧëҽѧƼ¹ʱƽ      
ǳϮ˼ҵģҺ˲ƪ£2007ָ
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ӰɲãҲ֪ԺʿǷ֪

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            ͨ¼ AND Dlaminiƪ¶գ
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ëڣá
ƪҿˣ֪ԺʿǷ֪ǵµ귢Ϊ
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һߣYunping Zhao1,2, Ruwen Wang2, Daiming Fan1,* 
.PDF
       ƽ                 
EXCLI Journal. (Experimental and Clinical Sciences) (Text in English) 
(Online Only)ʵٴѧ־(). The journal publishes 
original research ...
2006һ¹־EXCLI JournalϷһƪ 
EXCLI Journal 2006;5:79-92 C Received: 12. July 2006, accepted: 31. 
July 2006, published 3. August 2006 Review article: 
The molecular mechanisms of esophageal cancer 
ߣM.L. McCabe and Z. Dlamini, Dlamini PMID 
15914317

Ϸһѧ·2005International Immunopharmacology
־ϣ2004Ϳϻá 
Received 27 September 2004; revised 19 November 2004; accepted 29 
November 
2004. Available online 24 December 2004. 
mechanisms of oesophageal cancer PMID 15914317
    ƪµıⲻһģһҲȫһµ
ͨѶߣһƽͬʱд˵ľҽѧ͵ҽѧλַ 
    µĿͷ֣ھϣеСĶ100%ĳϮˡȤ
ǣµĲοײ֣඼µĲοףûвԭĵĲοס
Ҳ˵DlaminiġͷһģһݣǶĲòͬ
Ĳοסһ˵µĲο2004Ժ󷢱ġҲ
µķʱ2007꣬ԭ2004꣬ԣԭû2004Ժ
Ĳοף´20052006Ϊοס 
Ҳ˵任ԭĵĲοס ȻˣԺʿĵĲο
ǾûСDlaminiġġ 
    Ƚ
Dlamini¡ 
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. 
¡ 
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¡ 
Keywords: Human oesophageal cancer; Molecular genetics; Apoptosis 
signalling pathway; Genomics; Oesophageal cancer therapeutics 
¡ 
Keywords: Human esophageal cancer, molecular genetics, apoptosis 
signalling pathway, genomics, esophageal cancer therapeutics 
Dlamini¡ 
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 metaplasiaC 
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. 
¡ 
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 
metaplasiaC 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¡ 
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. 
¡ 
(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¡ 
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]. 
¡ 
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 Barretts carcinogenesis 
(Feagins et al., 2005). 
Dlamini¡ 
7. Invasion and metastasis 
Invasion and metastasis of oesophageal cancer is poorly understood. 
The cellC cell adhesion molecules (CAMs) hold cells together, and 
believed to play an important role in metastasis of the cancer cell 
[25]. -Catenin has been found to play a role in squamous oesophageal 
cancer cells, by its cellCcell adhesion function and interactions 
with the cytoskeleton and cadherin junctions of cells. -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 -catenin for degradation 
and prevents -catenin dependent degradation. Increased -catenin 
dependent tranxxxxion due to - catenin binding to Fz receptors, 
mutations in -catenin, APC, and increased - 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 -catenin expression by antisense technology could 
be an effective treatment for oesophageal cancer [79]. 
¡ 
Invasion and metastasis 
Invasion and metastasis of esophageal cancer is poorly understood. The 
cellC 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 cellCcell 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

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