                         ˿µϣ20060416գ

06.04.16, ˾ҶĴѧκȫԺʿеŷĸ
06.04.16, Բ԰ܡ˾κ֮ǡͬѧ۵顱𣿡
06.04.16, ˡԡĴѧӦпԺʿκȫ¼ĶС
06.04.16, HonestXԡпԺʿκȫ¼ һЩ
06.04.16, wupiĴѧѡ
06.04.16, ġɡڷκȫ방֢롱Ĵ𸴡뵽
06.04.16, ũô¶
06.04.16, lijunӹκȫNature-Medicineĵʵԡ
06.04.16, 㽭ѧԺĳУʦҿĴѧκȫ¼ĻӦ
06.04.16, trusκȫ4ֻС⡷
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ҶĴѧκȫԺʿеŷĸ

˾

ϤĴѧκȫԺʿŷᣬڻɢ
һͨ档κԺʿҲڻϽڶýŲɷáڶ
֮ҽ˵

1ҶκȫԺʿѧɣҸб¶
⣬˵ѧµĻɣһѧ۵֮ҵɼ
޸˶ԹҲǣڵѧλҵΪȲҶ
κҲǶĴѧɣκҲĴѧ

2ĴѧУɢĲͼһѧɣ
Ϊѧ۵ۣͽ͵ģġĴѧɢĲУκ
ɵĹᵽ־δܷҵĶĵ
ʵصΪĴѧĳЩ쵼ֲʵΪе衣

3κȫԺʿҵûнĻش𣬶ǲȡ˼ģ
Ҷʵַͼһ⵭Ϊ˶Թ
¶Լвɸ˵ܡ޹ص⣬κ֮
УκҪ˽ˣ100Ԫµȵȣκȡһ˵ѵİ취
һʹԼ¶Ŀ֮¡

4֣Ҫ󣬿ѧԺ֯ר飬Ŷ񣬶Կѧ
̬ȶκԭʼʵ飬¼йϽ飬Ҷκ
ɡ֤κȷû٣ԸκȫԺʿǸ

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˾κ֮ǡͬѧ۵顱

Բ԰

ͨѧ˾ڹĴѧκȫһ£
ѧԹķʽʽĹٷ¼Ϊ˾
зӳҪڲͬѧ۵飬˾ھݴ˶κȫ
ѧ١ָĿǰȱʵݡ

ʵϣϵУҲһЩذⳡս˵
ǡѧۡ˾κλڵѧˮƽκڵ׫дˮƽ˾
ڵˮƽӲʿˮƽ۷׷ס

ȷָǣ˾κ֮¼ıǲҽκڱ
Ƿм١⣬˾κ֮˵ǡͬѧ۵
顱ǻ¼ıʡĵȻ˾ڴһʼȷָ
κȫԺʿġˣٵʽʲô磺ݣ
޸ݣɸѡݶɾݣȵȣҲٵν̶ȡ
ΣҲ֮Ƿ˾ָժһģһֻҪκ
ڵıеȷм٣ô˾ڵָؾ100%ġ֮κ
ڵıеȷûм٣ô˾ڵָؾ100%ܸ档ֻ
СС͡ޡ򡰺ڡ͡ס⣬һУ磺˾κλ
ѧˮƽκڵ׫дˮƽ˾ڵˮƽκĵ˼룬
۵ӱԺȷԣκĵıȵȣ˱
޹ء

κοѧоĿĶΪ˷ֺʶ͹ˣǶһ
ѧһǶɸÿѧҷ˵ʵضԴͷʵԿѧ
оҪҪκѧٵıʶƭ֪ʷѧ
ٺѧıѧǺѧˮƽйصѧ⣬
ѧѧˮƽ޹صľԵ⡣ѧǷмٵ
۵ȻҪõѧֶΣıȫѧǵ¡

Ϊ˾κ֮¼ıǲҽκڱɵǷм٣
ֻ֤Ƿм١ͨʵѧо˵
ñ֧оɹԭʼݵԭʼ¼ǿѧĳʶҪ֤κ
ڵıеȷûм٣Ψһȷķκڹõ
оɹԭʼݵԭʼ¼ЩԭʼΪ˵
ݺͳɹǿԴЩԭʼݵõġȻκ
ڱ˹ԭʼݵʵҲǱҪ֤ġñı
˵û߼ǲͨҲЧġǡʵʱʹ
ѧһɹѧѧȨרɵĴ֤ᣬ
κȫں˾ڳԵĹ۵֤ݣκڲԭʼ
ݵԭʼ¼Ҳκڱ˹ԭʼݵʵԽִ֤
֤ҲǺģרҵרҶԴѧ顱ܡѧ
жϡ

ǰ˵һ䣬ڿѧȽңĳʵоɹʵԵ
κɾܾṩԭʼݵԭʼ¼ʱһ㶼Ϊ١
ԭʼݵԭʼ¼ʧʱô޶ʱظʵ
ԭʼݣһʵɲԭʼݣһ㶼Ϊ١

⣬ˣرǵˣⳡ˵ǡ˶Թ֮
ĻǾͲǻ¼ʣһ޳ܵΪˡ

ԡϽʵĿѧ̬ȡĴѧĹС
ųİ취ṫںۡ仰ʼ⡣1998
ĴѧԱ׫дκȫڵһϵŸЩԹ
ƭĲʵݣĴѧǷҲΪǡáųİ취
ṫںۡأǣΪ˭ڡáųİ취
ṫںۡأΪǷϺ±׼⣬Ϊ
˲ĵĴѧΪѵûǷϺ±׼

עΪѧʿѧڣȫѧҽѧ

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ԡĴѧӦпԺʿκȫ¼Ķ



϶ˡĴѧӦпԺʿκȫ
¼һģебҪ˵䡣ܵĸоĴѧڻ
жΡ

ȣĴѧѧ١͡ѧ۵顱ѿΪ
ȫûйϵΪѧٺѧ۵鲢ìܣʵϣ
ǰ߷ıҪѧ۵鲻һ漰ѧ٣ѧٱȻ
ѧ۵顣л־༭Ϊ˾κȫѧ۵飬
ֻ˵༭ûжĶԴ˵鷳֤
κûѧ١Ĵѧñ༭֤κû٣ⱾͲԡû
˾κȫ֮ȷʵѧ۵飬Ҫһ˾Ϊκ
ٵɣôڶҲ˷ĴѧԴ
ЩͲᷢƪЦˡ

ΣκȫıùҲ˵κû٣˰
κṩķʵԤ⡣һеӦ
ֻܶIntroductionһ¡ĴѧӦøЩκµ
κĹ

ĴѧƣûŪʵ֮ǰͬѧ۵¶
Ϊѧ١Խѧ򵥻ữáųİ취
ṫںۡΪЩѧۣҲڴٽ¡
ѧٺͿѧչô֪Ĵѧôжκȫ˾
֮Ǵѧ۵飬ôжκȫû٣Ĵѧܸܲ
һЩеݣ֪ϵǲ̫ϿЦˣ
ǸУĴѧЩɶá

˷ĴѧûŪʵ֮ǰ֮󣬽ܵġѧ١
жΪѧ۵顱Խѧ򵥻Ĵѧѧ
١͡ѧ۵顱ṫںۡΪЩ
ѧۣҲڴٽ¡ѧٺͿѧչҲԲ
ϰպȫ

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ԡпԺʿκȫ¼ һЩ

ߣHonestX

1˾ڡסκԺʿⲻŲԭһǶ
ġЭѰڹȥļﲢδκԺʿ
˼·õһչ֤ʵǡɡʵϣ
ѧģǷڡȻߡѧֻǡлϵУ
֮ҪҪ۵ʵ͹ۡıɣϸо
̫ùɴӱϽҲǶߵһְо仰˵ԽԽ
 𣿵Ȼ߿ܸܻ᲻ܻͬرܵǽѧĴ
࣬Ȼ͡ѧ־¼ϡ
ԶıʵҡÿѧҶӦнѯ
׼ڡһġĿѧһΪҪźκԺʿڹȥļ
ƺûԴƴ˾()ɣҲ˽ġ


2Դˡ¼ġٳɡӳְܲ(Ȼѧί
ܿе쵼Ĵѧ) ְ֮Ȼѧίר
Ľ(2001) κڵĳɹʱе鲢ۣ
е쵼ʱܲ˾ʩѹƪڷǻݱɽ
¼𣿶Ĵѧġ½ġ塱Ÿһ
ࡣ״ϡɡԴ2001֪꣬ιδӣΪѳܵ
Ǿ2003˾ڵƪ(NMȻҽѧ)δܷԭΪѧ
ûվסţԴΪ֧֤κĵȷΪʡ
֤ƪδԭǷǿѧصӰ¡ΪȵĴѧ
֤ĳᣬΪڲ׼(κԺʿԼ) ڽ
ĳ(û)ʱ֤ᣬʵһжýලĽԴҺ
ԲŴýأԷڵʵĴѧûͿŷ
塱óһЩΪѧ֤ݺӦɣȴҪƻ
֤ᡱȻδ֤硱ܹ塱ᷨǵ
ѧ߼ͨ

3»Ӧˣѵġд衱
κԺʿϧԼԼ̫Уһ
ڱ˵ĻϡƩȥݷá˾֮£ӳ˵̬
ڡԺʿѡꡱɳгϻ̳ϿֵԼڴ̬ʹ
һЩϵ鷴ǿġľʹ±(κԺʿĴ
ѧ) ÷СС˵־(ʿ) ֮ݡ˰֮
˭һŲ㡱ĿѧĿгɹܡɫ㡱أ
ԣϽԺʿԼԺʿĹܵλܲȡʵЧľٴ뾡컹
ߵĳڹڡҪгĹĨڡ

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Ĵѧ

ߣwupi

ĴѧУʽκȫԺʿѧˡǿд
ģ׼֤ģġӼд
ѶҿҪʵʵ߳߹ˡ

ҺɣȥκȫԺʿǿԱĴ
ѧУرǣ֮󣬶Դǵ֮


֮ҾͲ̸ˡ˵ڲ֮ġ

ԼºһУ֪ͨҲԷסУڸʿ졣
Ǹɶ˿ϣڵձϡ
˶ŷôѧȦڵЩͬǣй˽
˾վֱκԺʿ˻֮٣Ǵ
ﶼԼжϡǴҪŰµİɣҪͬд
İɡҸѡ

ôڿʼҽѧ硰رǰ֢оߡ
۾עйκоչãһ棬ڲס
Ҫ㣺ǴǸκԺʿоչôˣôش𣿣ѵ˵
ǻģǴġǶϲöˣּҲɣ

ôҪдĿİɣҪͬȥ
İɣںˣһĴѧĸ־ͻرעĿ
汾ͲãǾͲ˵˰ɡдеȣԭڡͬ
֮ͬ͡еԥһ뵽𵼵κԺʿ¾Ҫд¸
ͬˡĿд÷ǳã˿¾Ҫ뵽ֱ
κԺʿʵ

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ɡڷκȫ방֢롱Ĵ𸴡뵽



    ڷȭ֮£κԺʿǼһмܵġ𸴡
ááҿһ㶼֡

    ȣٵЩݲλģԴǼϡ
ôⱾЩϵʲô˭Ƶģͳ˱
⡣ҷǳ޳ɡˡ(XYS20060413)еĹ۵㣬 Щٻ
ΣʼٸֻκԺʿ򸾶ˣ˵ôḻҲ˵
бۡλȴҪȻֹµ©ν
Σٵ³ǰκԺʿΪѰζһ
Ҫ¡ջ־ٲȻһʵ˾ӣһڱ־
粢δ¡ջ־²֮硰֮ܡԣһ
µ¶Ҫ־翯ǣʵ׾ٵ飩κԺ
ʿǾýȥָµֻ֮ڳ͵̬
÷Ͽɵӣһպ󶫴·Ҳֲͷϣ
£ҲûǸҪЩµ˻ǶҺ֪
ĸطűͿѧĵ𡱶ű׼
ȷݲ10% ʹǿ͹ԭɵʧʵ˶ҪʱԳ壬
ʵǻҪűġλ˵ְҵ¾
ôߣǵġ𸴡Űٷ֮أģΪȣ
λʾԸеһκͺЩηšǣǲ
ҪеһСµߡһӦóеΣң
⡰һСǳе֮ԸڲԸ˵Ϊڶ
κԺʿܹȥǰκԺʿİӾǸ߸߾𲢲£
ԺֻҪκԺʿ͸Уٵǵĺã

    ôκԺʿܹȥ𣿴ѧ˵κǰ
¡Ĳѧҽѧ֪˵ĵ뷽跨ֹ˷
£ߵҶҪܲ֯󣬲ʵ
̺ݵԭʼϣ֣ӡ֤һƲ⡣Ҫ֤ʵ
ƲҲ̫ۡȻͻκԺʿȥ𣿲һؼ
ͷʱͷҪһԼѧܵľģκ
̫ԾҩκԺʿΣˡ 413աձһƪ
Ծ֡Ǹ֮סҪȶΪأκͲ
д¡õĹٳͬһߣܱ
ȴҲܲ޹ʵ
κԺʿɣ

    ĴѧһҵԴУ쵼С졢κȫ¼еĲΪ
ʹļףĸж鲢ô򵥡ѧУôص飬
ǱȾ֪öҪ磬ǲͲȡĳж
Ҫͷ˼ҪǸͷһǾͲ»ẦԼ
ͷЩ¼֮֮ǵѡȻǱĳѧ
ΪάѧУֶֻΣĿǱԼĳ֮ܳ
ܴϸҫ۵Ĺ⻷ǰ쵼ҪЩתΪٶ
ʹ쵼ǲڴԼĶ𣿳Ȼദ߲֮ڣ
ǿҵľʾãҲάѧУǣ쵼أҪ֪
ѡŲһѧУ̨ϿˣҲˣǰ;
λãˡǿ޴֮٣ȱලĻ˭
סģԣǵѡǺȻģβȫǡҪıЩǲ
׵ģˣҪͷһŬ

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ô¶

ũ

缸˿пԺĴѧκԺʿ¼
׵

1κԺʿĴѧĸУĴѧ顣ûлرܣ
ûйĽκԺʿû⣬Գ̬ȣʵ
κԺʿҲƽκԺʿ⣬ȡԺʿͷΣֹĿ
Ĵѧʸ

2ĴѧûͬɡĴѧܷһ
κԺʿûֱϵġ߱ӦҵˮƽרίԱᣬǴҵ
⡣޺ϸ֮٣޺֮ͬȻ

3˾пԺⲢҪпԺġпԺְܣ
ѧйع£пԺκпԺԺʿоѧ
ʱöйصǲεġΪпԺûλ
͸˿ԻһסֻпԺԴʸۡпԺǽ
ϽĴѧƸĴѧƺ⡣

4˾пԺĿǰ飬пԺѧ
ϼѯҪѭйع涨

5κԺʿǿѧѧߣв졣ɹ
ҶϣȨѧͬˡļƷԱ¶
ŵļиء͹ҲӦйصġпԺҲ̫㣬
˶ҲǸ취ѧǰͬԺʿܲȥ
ʵְ֮ڣ֮СҲ飬ҷġ

6¼ѾʹעϵпԺѧܲⱵ
죬пԺԴмί참Ҫмίʲôһ
䷶󳬹¼õû⻹һף
嵱ǰѧ˵磬ġ

ͨ׵ıȷװͬѧѧУٱҰ೤ס೤
أѧУʲôġͬѧ˵ƾоݣͬѧҲͣ
ܴѧУȴҰİί鴦̫˰ɡ

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ӹκȫNature-Medicineĵʵ

ߣlijun

һ¡ձı[ꣳ£գߵκȫ
ĵκȫᵽԼ˾ָƪģڿѧ
վסŵġĿǰѧϵ ⣬Ӧ˵úˡΪǸ
ǹʹϵġΪʲô˵ǹʹأϣַһϵ
£оУƪ˼ˣҵġ
ܶġκȫʾûһ ˵ҵģ˼һá
ڷǳ𡣡 ]

򷢱Nature-MedicineһκԺʿҪģǾ
ʵʹһ򵥷ͬʱĽصԿԭϡ

2000 귢񣬸ıڿ49ΡУ15Σ
14Σо20Ρ͹˵ü¼
µĿйءͨԣоԱϲڸߵε־Ϸ
¡ھͿһ20омƪһ
ϵ⣬ýֻᵽһ¶ѣǼ֤乤
ʵϣκԺʿᵽ֧乤ƪ(̸)⣬е
ظκĽǼӵطĽҪԿԭ档
Щ½м򵥷Ӱ·5ƪĶκĵ
ƪκΪ֧۵ģǣĿǰûܹ
ظκĵĽһЩĵóκĽȻͬĽۣκ
ȫĹá֤ʵͬк͹ڡ

1. This paper is the one mentioned the most, either positively as a 
support or negatively as a piece of evidence, by Professor Wei and 
other accusers. This paper was published by Scappaticci, FA et al. in 
2003 (Scappaticci, FA, et al. 2003, Polyclonal antibodies to 
xenogeneic endothelial cells induce apoptosis and block support of 
tumor growth in mice. 21:2667-2677). Previously, other people already 
pointed out that this paper cannot be used to support Weis work 
because of the differences in experimental design, results and 
mechanism. Now, lets look at how Weis publication was actually 
cited in this paper. I quote here Until now, there has been little 
evidence that endothelial cells or their products can be exploited for 
immunotherapeutic strategies in the tumor-bearing host [14]. Wei et al. 
have recently demonstrated that active vaccination of mice with human 
endothelial cells can break tolerance and induce a specific 
antiangiogenic immune response with broad antitumor activity [15]. 
While this strategy may result in a protective immune response for a 
variety of cancers, the use of endothelial cells to induce an immune 
response could potentially lead to toxic side effects. These include 
autoimmune responses against quiescent endothelium as well as 
inhibitory effects on angiogenesis during wound healing and 
revascularization. The use of passive immunotherapy, however, can be 
controlled more readily allowing the option of discontinuing therapy 
as required. From this paragraph, Wei is the only group doing active 
vaccination with endothelial cells; even if Weis strategy works, 
there is high risk for therapeutic use; and the reason why passive 
immunotherapy is needed instead of active vaccination. I couldt see 
any supportive language in this paragraph. So, Weis claim of which 
his work was supported by this paper is false. In fact, there are many 
differences in the results compared to Weis paper as well: a. The 
antibody showed cross reactivity even to human non-endothelial cell 
types (DLD-1). I quote here Although the avidity of the antibody was 
slightly greater, the results indicate cross-reactivity of the immune 
antibody to these divergent cell lines suggesting common antigenic 
epitopes on these cell lines (as would be expected if the targets 
recognized by these polyclonal antibodies were such molecules as 
histocompatibility molecules). b. No specific antigen(s) could be 
detected and identified by Western blots, and the protein bands did 
not have any specificity. I quote here Tumor cell lysates were then 
probed on Western blots with either pre-immune or immune IgG. Multiple 
bands were identified by immune IgG but not the pre-immune IgG. 
Futheremore, these bands were present in endothelial (SVR) and 
non-endothelial cell types (L1210, B16F10, and Phoenix A). Therefore, 
rather than supporting Weis paper, their results were contradictory 
a lot to Weis results.

2. Second paper is the one published in 2004 (Corsini, E. et al. 2004, 
Immunotherapy with bovine aortic endothelial cells in subcutaneous and 
intracerebal glioma models in rats: effects on survival time, tumor 
growth and tumor necovascularization. Cancer Immunol. Immunother. 
53:955-962.). This paper has been cited as supportive to Weis work 
at many occasions. First of all, it would be suspicious if one has to 
use a paper published at a very low impact journal to support his/her 
work published at a high profile journal, and unfortunately this one 
is the case. Secondly, lets look at how they cited Weis paper. I 
quote A study by Wei [14] suggested that in a murine model, 
vaccination with actively proliferating xenogenic endothelial cells 
was effective in reducing tumor progression in mice bearing various 
types of tumor lines (i.e., Meth A fibrosarcoma, H 22 heptoma, MA 
782/5s, FM3A mammary carcinoma, and Lewis lung carcinoma). However, no 
glioma lines were used in the work by Wei et al [14], leaving the 
impact of this kind of treatment on glioma development unexplored. 
This citation clearly indicated that their work was only a 
supplemental to Weis observation, which was absolutely not a 
validation of Weis study. Thirdly, although its not scientifically 
reasonable to compare rats with mouse models, it clearly indicated 
that there were significant difference between this paper and Weis 
paper. The efficacy of their endothelial cells was not as good as Wei
s results as shown in Fig. 1 and Fig. 2 in which vaccinated tumor 
growth was inhibited only after day 17 and the difference between 
treated group and controls was not significant (Fig. 2). Finally, they 
were unable to identify any specific antigens causing the antitumor 
effects without any proteins like VEGFR II, alpha v integrin in Weis 
paper. I quote here By Western blot analysis, endothelial cell 
extracts showed two bands with molecular sizes of 11 and 19 kDa when 
probed with serum from rats with tumor immunized with bovine 
endothelium (Fig. 8),. In fact, not only their results did not 
support Weis publication, but they also displayed different activity 
and molecular mechanism. Then, how can someone claim such results to 
support Weis paper? The only explanation is that the intention was 
to fool people without basic knowledge in biosciences.

3. The third paper cited Weis publication was published in 2004. 
(Okaji, Y. et al. 2004, Vaccination with autologous endothelium 
inhibits angiogenesis and metastasis of colon cancer through 
autoimmunity. Cancer Sci. 95:85-90). Based on Weis hypothesis, 
quoting from his paper The breaking of immune tolerance to 
autologous angiogenic endothelial cells should be a useful approach 
for cancer therapy. However, immunity to angiogenic vessels is 
presumably difficult to clicit by autologous or syngeneic endothelial 
cells or their proteins as vaccine because of the immune tolerance 
acquired during the development of the immune system., it is 
unlikely to use own endothelial cells to produce antitumor activity. 
Unfortunately, this paper was directly contradictory to Weis 
hypothesis, and showed superior antitumor activity by vaccination of 
syngeneic endothelial cells, which resulted in greater antitumor 
activity compared to HUVES (Fig. 2). In addition, the immunoglobulins 
had no specificity. I quote here Although the increase in serum 
concentration of immunoglobulins was small, in the ELISA assay, the 
antibodies showed a strong affinity for endothelial membrane antigens. 
In addition, the antibodies present in the sera of HSE-vaccinated mice 
strongly bound not only proteins of HSE membranes, but also those of 
HUVEC membranes (Fig. 4A), and vice versa (Fig. 4B). Thus, the 
antibodies induced by endothelial vaccines were cross-reactive with 
both murine and human antigens. Furthermore, the sera of mice of both 
groups did not react with membrane proteins of tumor cells (Fig. 4C), 
in accordance with the flow-cytometry analysis. Now, lets take a 
look what they cited from Weis paper. I quote here Wei et al have 
reported that immunization with xenogeneic, but not autologous, 
endothelial cells, was effective in inducing an antiangiogeneic 
immunity and protecting mice from tumor growth... The present study, 
however, autologous endothelial vaccines were more active than the 
xenogeneic ones in inducing specific humoral and cellular immunities 
against tumor endothelium, and they consequently provided greater 
tumor inhibition. Therefore, the difference is very obvious, which 
directly challenged Weis results, at least on the basis of his 
hypothesis of breaking tolerance of own immune system by xenogeneic 
antigens. Moreover, this paper was unable to identify specific 
antigens for the antitumor activity either, not mentioning about VEGF 
II and alpha v integrin.

4. It has been extensive interest in discovering novel 
anti-angiogeneic targets for therapies by both proteins and small 
molecules. The following paper was an attempt to identify new 
therapeutic target by establishing phage display technique in order to 
identify specific markers in endothelial cells. This paper was 
published by Mutuberria, R. et al. in 2004 (Mutuberria, R. et al. 2004, 
Isolation of human antibodies to tumor associated endothelial cell 
markers by in vitro human endothelial cell selection with phage 
display libraries. Journal of Immunological Methods, 287:31-47). First 
of all, lets see what they say on Weis work. I quote here 
Immunotherapy of tumors using fixed proliferating HUVEC as a vaccine 
has resulted in the inhibition of angiogenesis and regression of solid 
tumors (Wei et al., 2000). Thats the only place mentioned Weis 
work in the entire article. Since the same cells (HUVEC) were used and 
the molecular basis of antigens was explored in this paper, its 
quite reasonable to compare their results with Weis. Also, phage 
display is a powerful tool to probe specific peptide regions in the 
antigens. Any significant antigens would be picked up, such as the 
VEGFR-2 and alpha v integrin shown in Weis Fig. 7. However, in the 
results section, I quote here We have used commercially available 
antibodies to compare these antigens with the molecular weights of 
possible target antigens such as CD31 (PECAM), Tie-1, Tie-2, VEGFR-1 
and VEGFR-2. None of the those commercial antibodies detected the 
exact same molecular weights as the selected phage antibodies (Fig. 2b 
and data not shown). In fact, what they observed were the bands with 
molecular weights of 175 kDa and 110-125 kDa. Thus, the conclusion is 
that there must be somebody wrong, either the group in Netherlands or 
Professor Wei according to this paper.

5. Finally, lets examine another paper published by Mittleman, A. et 
al. in 2002 on analysis of immune responses based on peptide 
similarity (Mittleman, A. et al. 2002, Monoclonal and polyclonal 
humoral immune response to EC Her-2/neu peptides with low similarity 
to the hosts proteome. International Journal of Cancer, 98:741-747). 
The intention of this paper was to rationalize the relationship 
between peptide sequences and hosts proteome in order to better 
predict the epitopic peptide sequence and corresponding immunogeneicity. 
In this paper, they cited Weis publication in the discussion as In 
an effort to improve the ability of predicting disease relevant 
epitopic peptides, the present work has taken into consideration the 
self-character of TAAs and the matter of fact that immune tolerance 
appears as the main obstacle to an effective immune recognition and 
destruction of human cancers. 30-32. Their results showed that there 
is a relationship between disease associated epitopes and the host 
proteome, but human brest/prostate cancer sera preferentially react 
with synthetic HER-2/neu peptides having low/medium level of 
similarity to human patients. In addition, the highest level of 
peptide immunogeneicity was shown in the peptides with no similarity 
at all to human proteome. Their conclusion was We suggest that a low 
level of similarity to the hosts proteome might play a significant 
role in determining peptide immunogeneicity.. In contrast, what Wei 
described in his paper and his theoretical basis of choosing peptides 
for synthesis and test their activity was Sequence comparison 
analysis using the SwissPort database in NCBI indicated that the 
primary sequences of VEGFR II and alpha v integrin of mice and humans 
were homologs that were 82% and 89% identical, respectively, at 
amino-acid level. Next, we selected pairs of peptides for synthesis 
from the regions that shared the most-identical amino-acid sequences 
between humans and mice. In his case, human peptides are immunogens 
whears mouse sequences represent the host proteome. Therefore, there 
is an obvious discrepancy between Weis theoretical basis and this 
papers experimental data.

In conclusion, to date, there has been no report on the detection and 
identification of VEGFR-II and alpha v integrin as antigens from 
endothelial cells when they were vaccinated in animals in literature. 
Its fair to say that Professor Wei has mislead colleagues and the 
public on the actual citations of his paper published at 
Nature-Medicine in 2000. Nobody has been able to repeat his work in 
any scholastic publications so far, and the truth is that there are 
some publications that observed very different results and made 
opposite conclusions. If it were possible to repeat or verify his work, 
I would suggest to use his peptides listed in the paper to observe 
their antitumor activity, which is the simplest and most convenient 
way to draw a conclusion to determine whether he faked or manipulated 
the data in this very important publication.

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