看過一些數據，一年中死於化療的數字比本身癌症還多。
【美國終於承認手術或化療後癌細胞反而加速擴散】 - 路透社報道
科學家一項最近研究發現，有些癌症患者在接受手術、化療或放療後，癌細胞反而加速擴散，造成這種現象的原因之一是人體一種名為TGF-be-ta物質。因此，控制TGF-be-ta物質在人體內的含量，才是治癒癌症的關鍵。
來自美國田納西州範德比爾特大學的研究人員在老鼠身上試驗發現，患有乳腺癌的老鼠在服用化療物質“阿黴素”或接受放療後，體內的TGF-be-ta物質含量提高，刺激癌細胞向肺部轉移。而使用某種抗體抑制它們體內的TGF-be-ta含量則能夠遏制癌細胞擴散。
參考連結：Inhibition of TGF-β with neutralizing antibodies prevents radiation-induced acceleration of metastatic cancer progression
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1838926/
此前有科學家提出，動物體內的原發性腫瘤可能會抑制其他腫瘤生長，但一旦原發性腫瘤被從體內清除，其他被抑制腫瘤可能會就此瘋長。而科學此次研究顯示，TGF-be-ta就是這樣一種既能抑制腫瘤生長，也能刺激癌細胞擴散的物質。
主持研究的卡洛斯.。啊特亞加博士補充說，可能還有其他物質與TGF-be-ta一樣對癌症的治療有類此的影響。他們希望通過對TGF-be-ta的研究得出更多結論。 以上訊息在10月8日的《參考訊息》報也有報導。
看來主張手術或放化療治療癌症的人，良心終於被發現了。 人類自從3000年前發明瞭藥物以來，200年前發現了抗生素，人類的疾病就更複雜，更多，更難治。
很多慢性病，免疫系統紊亂症，都與藥物和抗生素的濫用有很大的關係。人的耐藥性越強。人就更難戰勝病魔。而癌症自然也有它的天敵。眾所周知醫學界對癌症束手無策。
醫學界奪命奪錢三招“手術、化療、放療”。目前醫學科技很發達，世界各國投入無數財力物力去研究醫學，但是卻對絕大多數的慢性疾病無能為力，這不能不說是個人類天大的笑話。
1、成年人每人每天都有3000-6000個癌細胞產生（由於基因突變而讓正常細胞變成癌細胞，基因突變原因很多，化學藥物，肉類，動物荷爾蒙、空氣汙染等等）。
２、但人每一天誕生的癌細胞幾乎都被人體自身自然殺手細胞（NK細胞）殺滅了。所以不是人人都會患上癌症.當免疫系統下降，也就是自然殺手細胞弱了，癌細胞就佔上風。久而久之5-10年以上就會得到癌症.如果我們能讓癌症病人身體裡的自然殺手細胞變強，恢復活力，對付癌症是簡單的事。
所以癌症病人只能靠自己也就是自身免疫細胞－自然殺手細胞（NK細胞）來對付癌症。
３、讓自然殺手細胞（NK細胞）恢復活力的唯一途徑是營養70%、心情10%、運動10%、休息10%（世界衛生組織的健康的四大基石）。
４、只要有充足的營養,自然細胞就能恢復到以前的活力來殺滅癌細胞。（這個世界一物降一物，但一物應該是人體的細胞而不是藥物，也不是植物，更不是動物。人的免疫細胞是可以對付世界上所有的病毒和細菌，比如非典病毒，艾滋病毒，埃博拉病毒，流感病毒，關鍵是人的免疫細胞要足夠的強。例外：但人的免疫細胞沒有辦法對付毒藥。
５、醫學上常規不得已用藥物和化療、放療、電療方法，除了把癌細胞部分殺滅外，反而把正常的大量的自然殺手細胞殺滅.醫學界奪命奪錢三招“手術、化療、放療”！所以手術藥物和化療放療有時能減輕病人的痛苦同時反而加速癌症病人的死亡.
６、為什麼國內的癌症研究者都是研究藥物如何殺滅癌細胞（治標）。為什麼不能研究讓人體內的自然殺手細胞增強來殺滅癌細胞呢（治本）?只有0.5%的經過化療放療的病人能活過超過5年！！
７、世界上最好的醫生是自己的免疫系統、免疫細胞，而不是醫生和藥物！！只有本人的免疫系統（自然殺手免疫細胞）才能殺滅癌細胞。可是藥物和化放療卻會快速讓人的免疫系統下降。
８、請癌症病人去新華書店購買《營養免疫學》陳昭妃癌症研究博士著，《不要讓不懂營養學的醫生殺了你》雷.D.斯全德醫學博士著。《別讓醫生殺了你》, 《食物是最好的醫生》,《醫生對你隱瞞了什麼》...等最新學科書籍。但是闡述得最完整最好的還是《營養免疫學》這本書。
９ 四大基石裡的休息和運動促使免疫力提高。晚上安靜下來睡覺的時候，是人體內免疫細胞正在大量修復身體破損的細胞的時候，所以晚上也是最需要休息和營養的時候。
１０、偶然我們在報上看到有些極少數癌症病人得了癌症不治,反而過了幾年後身體的癌症症狀全無,經檢測沒有癌細胞的存在.這是因為這個癌症病人平常的飲食心情運動休息讓體內的自然殺手細胞得到增強來殺滅癌細胞.也就是自愈力了——自已治病的能力。治癌不能靠高科技，而只能靠自然的力量、自身的力量。
Inhibition of TGF-β with neutralizing antibodies prevents radiation-induced acceleration of metastatic cancer progression
Abstract
We investigated whether TGF-β induced by anticancer therapies accelerates tumor progression. Using the MMTV/PyVmT transgenic model of metastatic breast cancer, we show that administration of ionizing radiation or doxorubicin caused increased circulating levels of TGF-β1 as well as increased circulating tumor cells and lung metastases. These effects were abrogated by administration of a neutralizing pan–TGF-β antibody. Circulating polyomavirus middle T antigen–expressing tumor cells did not grow ex vivo in the presence of the TGF-β antibody, suggesting autocrine TGF-β is a survival signal in these cells. Radiation failed to enhance lung metastases in mice bearing tumors that lack the type II TGF-β receptor, suggesting that the increase in metastases was due, at least in part, to a direct effect of TGF-β on the cancer cells. These data implicate TGF-β induced by anticancer therapy as a prometastatic signal in tumor cells and provide a rationale for the simultaneous use of these therapies in combination with TGF-β inhibitors.
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Introduction
TGF-β is both a tumor suppressor and a tumor promoter. The TGF-β ligands bind to cognate serine/threonine kinase transmembrane receptors, which in turn phosphorylate and activate the Smad family of signal transducers. Once activated, Smad2 and Smad3 associate with Smad4 and translocate to the nucleus, where they regulate the transcription of genes involved in cell cycle arrest and apoptosis (1), essential for the tumor suppressor role of the TGF-βs. Indeed, loss or attenuation of TGF-β signaling in epithelial cells and stroma is permissive for epithelial cell transformation (2, 3). On the other hand, introduction of dominant-negative TGF-β receptors into metastatic cancer cells has been shown to inhibit epithelial-to-mesenchymal transdifferentiation, motility, invasiveness, and survival, supporting the tumor promoter role in TGF-β in fully transformed cells (reviewed in ref. 4). Most carcinomas retain TGF-β receptors but attenuate or lose the Smad-dependent antimitogenic effect while, in some cases, gaining prometastatic abilities in response to TGF-β. In addition, excess production and/or activation of TGF-β by cancer cells can contribute to tumor progression by paracrine mechanisms involving modulation of the tumor microenvironment (2, 5, 6). These data have provided a rationale in favor of blockade of autocrine/paracrine TGF-β signaling in human cancers with a therapeutic intent.
In addition to Smads, TGF-β can stimulate several transforming signaling pathways (7). TGF-β has previously been shown to protect transformed cells from apoptosis (8–10). One possible mechanism for this cellular response is TGF-β–induced activation of PI3K and its target, the serine-threonine kinase Akt (11, 12), a signaling program associated with resistance to anticancer drugs. Some tumors resistant to conventional anticancer chemotherapy overexpress TGF-βs (13, 14), and inhibitors of TGF-β have been shown to reverse this resistance (15). In addition, overexpression of TGF-β ligands have been reported in most cancers, and high levels of these in tumor tissues and/or serum are associated with early metastatic recurrences and/or poor patient outcome (16–21).
In transgenic models of breast cancer, TGF-β signaling enhances the metastatic progression of established mammary tumors induced by oncogenes such as Neu/ErbB2 or polyomavirus middle T antigen (PyVmT) (22–24). Furthermore, in transgenic mice expressing the PyVmT oncogene under the control of the MMTV/LTR mammary promoter, conditional induction of active TGF-β1 for as little as 2 weeks increases lung metastases by more than 10-fold (10). Some anticancer therapies have been shown to induce TGF-β systemically or in situ (25–28). Therefore, we speculated that in tumors resistant to anticancer therapies or in resistant subpopulations within those tumors, treatment-induced TGF-β would provide a survival signal to cancer cells potentially accelerating tumor progression immediately after therapy. Using the MMTV/PyVmT transgenic model of metastatic breast cancer, we show here that administration of ionizing radiation or doxorubicin caused increased circulating levels of TGF-β1 as well as increased circulating tumor cells and lung metastases. These effects were abrogated by administration of a neutralizing pan–TGF-β antibody. Radiation did not increase lung metastases in mice bearing tumors that lack the type II TGF-β receptor (TβRII). These data implicate TGF-β induced by anticancer therapy as a prometastatic signal in tumors and thus provide a rationale for the simultaneous use of these therapies in combination with TGF-β inhibitors.
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Results
Thoracic radiation and chemotherapy increase circulating TGF-β1.
We administered 10 Gy to the thoraxes or pelvises of 8-week-old FVB virgin female mice. Blood was collected 24 hours after irradiation. We observed an approximate 2-fold increase in plasma TGF-β1 in irradiated mice over controls regardless of the site of radiation (thorax, P = 0.03; pelvis, P = 0.02; Figure Figure1A),1A), while TGF-β2 levels did not change (data not shown). Similar results were obtained in 8-week-old MMTV/PyVmT transgenic mice and in nontransgenic mice transplanted with MMTV/PyVmT tumor cells stably transfected with a luciferase expression vector (P = 0.015 and P = 0.007, respectively, versus controls; Figure Figure1B).1B). Levels of TGF-β1 remained higher than controls 7 days after radiation (data not shown). To expand these results to other anticancer therapies, we examined the effect of the DNA-intercalating agent and topoisomerase II inhibitor doxorubicin (Adriamycin). Transgenic mice were treated 3 times with doxorubicin (5 mg/kg i.p.) at 21-day intervals starting at week 8. In plasma collected on week 15, TGF-β1 was also elevated 2-fold compared with untreated mice (P = 0.009; Figure Figure1C),1C), whereas TGF-β2 levels remained constant. To measure activated TGF-β1 in the lung tissue harvested 5 weeks after radiation, we used a TGF-β1 bioassay that uses mink lung epithelial cells stably expressing a plasminogen activator inhibitor–1/luciferase reporter (PAI-1/luciferase reporter) (29). Tissue lysates from irradiated mouse lungs induced a 2-fold increase in active TGF-β1 compared with nonirradiated lung tissue lysates (P = 0.0008; Figure Figure1D). 1D).
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