來自麻省理工Koch綜合癌癥研究所,，霍華休斯醫(yī)學(xué)研究所,，白頭生物醫(yī)學(xué)研究所等處的研究人員在Nature雜志提前在線版上發(fā)表節(jié)食與癌癥發(fā)生,，以及節(jié)食對癌癥治療方面的影響,。節(jié)食究竟能否達到餓死腫瘤的目的呢？
限制熱量的飲食被認為能夠保護人類抵抗癌癥,，具有抑制腫瘤生長的功能,。但是，這一觀點并不適用于所有的癌癥類型,，據(jù)說,，限制熱量飲食對有些癌癥患者確實有幫助，但是對某些癌癥患者卻沒有幫助,。是個體的差異還是所患癌癥類型的差異所致呢？科學(xué)家們通過試驗為您解開謎底,。
據(jù)哈佛大學(xué)醫(yī)學(xué)院癌癥遺傳學(xué)家Pier Paolo Pandolfi介紹,，約一個世紀以來，研究者都認為節(jié)食有助延長動物的壽命,，并且能有助治療癌癥,。但是，哪些癌癥類型用節(jié)食的方法有效,，具體要如何操作研究者們卻所知甚少,，目前這還是個開放性問題，有待科研工作者去解決,。
霍華休斯醫(yī)學(xué)院的研究員David Sabatini帶領(lǐng)的研究團隊對該問題進行了探索,，研究小組將6種人類癌細胞系注入生物模型小鼠體內(nèi)，包括,，乳腺癌細胞,，結(jié)腸癌細胞，腦癌細胞,，前列腺癌細胞等,。接種同一類型癌細胞的小鼠分別分成兩組，一組自由采食,，自組限制飼養(yǎng)（減少40%食物攝?。?/p>
研究小組發(fā)現(xiàn)，節(jié)食并不對所有的癌癥有效,。6種癌癥中只有乳腺癌和結(jié)腸癌對節(jié)食有效,。與自由采食的小鼠相比，節(jié)食組小鼠（乳腺癌和結(jié)腸癌）的腫瘤大小大約是自由采食組小鼠腫瘤大小的2/3或1/5大,。
研究者對這些癌細胞株進行對比,，結(jié)果發(fā)現(xiàn)表達PI3K的癌細胞對節(jié)食抗癌具有抵抗作用。也就意味著,，癌細胞一旦表達PI3K則節(jié)食對其沒有影響,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature advance online publication 11 March 2009 | doi:10.1038/nature07782;
Tumours with PI3K activation are resistant to dietary restriction
Nada Y. Kalaany1,2,3 & David M. Sabatini1,2,3,4
1 Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 02142, USA
2 Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
3 Koch Institute for Integrative Cancer Research at MIT, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA
4 Broad Institute, Seven Cambridge Center, Cambridge, Massachusetts 02142, USA
Dietary restriction delays the incidence and decreases the growth of various types of tumours, but the mechanisms underlying the sensitivity of tumours to food restriction remain unknown. Here we show that certain human cancer cell lines, when grown as tumour xenografts in mice, are highly sensitive to the anti-growth effects of dietary restriction, whereas others are resistant. Cancer cells that form dietary-restriction-resistant tumours carry mutations that cause constitutive activation of the phosphatidylinositol-3-kinase (PI3K) pathway and in culture proliferate in the absence of insulin or insulin-like growth factor 1. Substitution of an activated mutant allele of PI3K with wild-type PI3K in otherwise isogenic cancer cells, or the restoration of PTEN expression in a PTEN-null cancer cell line, is sufficient to convert a dietary-restriction-resistant tumour into one that is dietary-restriction-sensitive. Dietary restriction does not affect a PTEN-null mouse model of prostate cancer, but it significantly decreases tumour burden in a mouse model of lung cancer lacking constitutive PI3K signalling. Thus, the PI3K pathway is an important determinant of the sensitivity of tumours to dietary restriction, and activating mutations in the pathway may influence the response of cancers to dietary restriction-mimetic therapies.
