来自麻省理工Koch综合癌症研究所，霍华休斯医学研究所，白头生物医学研究所等处的研究人员在Nature杂志提前在线版上发表节食与癌症发生，以及节食对癌症治疗方面的影响。节食究竟能否达到饿死肿瘤的目的呢？
限制热量的饮食被认为能够保护人类抵抗癌症，具有抑制肿瘤生长的功能。但是，这一观点并不适用于所有的癌症类型，据说，限制热量饮食对有些癌症患者确实有帮助，但是对某些癌症患者却没有帮助。是个体的差异还是所患癌症类型的差异所致呢？科学家们通过试验为您解开谜底。
据哈佛大学医学院癌症遗传学家Pier Paolo Pandolfi介绍，约一个世纪以来，研究者都认为节食有助延长动物的寿命，并且能有助治疗癌症。但是，哪些癌症类型用节食的方法有效，具体要如何操作研究者们却所知甚少，目前这还是个开放性问题，有待科研工作者去解决。
霍华休斯医学院的研究员David Sabatini带领的研究团队对该问题进行了探索，研究小组将6种人类癌细胞系注入生物模型小鼠体内，包括，乳腺癌细胞，结肠癌细胞，脑癌细胞，前列腺癌细胞等。接种同一类型癌细胞的小鼠分别分成两组，一组自由采食，自组限制饲养（减少40%食物摄取）。
研究小组发现，节食并不对所有的癌症有效。6种癌症中只有乳腺癌和结肠癌对节食有效。与自由采食的小鼠相比，节食组小鼠（乳腺癌和结肠癌）的肿瘤大小大约是自由采食组小鼠肿瘤大小的2/3或1/5大。
研究者对这些癌细胞株进行对比，结果发现表达PI3K的癌细胞对节食抗癌具有抵抗作用。也就意味着，癌细胞一旦表达PI3K则节食对其没有影响。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
