廿一世紀癌症防治大突破–自律神經調控法

   

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廿一世紀癌症防治大突破–
自律神經調控法

楊維邦 博士 2011.08

摘要：

根據近年來發表在世界頂尖學術期刊上的百餘篇論文顯示，癌症之發生、惡化及轉移與交感神經過度亢奮及副交感神經低下有關。若能降低交感神經之活性，且同時提升副交感神經活性，對於癌症之預防治療，降低復發及轉移率均有令人挀奮的效果。

（摘要撰稿：王群光醫師　中華自律神經醫學會 理事長）

一、人類自律神經與免疫系統之關聯性

人類的免疫淋巴系統、血管及源自中樞神經的自律神經系統有緊密的連接。中樞神經就是經由自律神經來管理免疫系統，並對目標物進行攻擊消滅及正常細胞之維護。免疫系統攻擊的目標物包括入侵的細菌、黴菌、病毒、大分子蛋白質、自身老化受損的細胞或是自體免疫疾病中的自身細胞。

交感神經系統是經由釋放一種叫做正腎上腺素(Norepinephrine，NE) 的神經傳導因子來刺激免疫系統的運作。其運作方法如下：(1)

入侵外物或受損細胞表面會有一層叫LPS(Lipopolysacharide)脂多醣體的化合物，這些LPS 便會把淋巴系統中的單核白血球(monocytes)吸引過來，到達現場後，單核白血球就會自我轉變為巨噬細胞macrophages( MΦ)。這些MΦ 便開始產生一種叫腫瘤壞死因子(Tumor Necrosis Factor-α，TNF-α)的蛋白質，以執行消滅入侵外物或受損細胞的動作。一連串的發炎過程及副產物都因TNF-α 之產生而引起，諸如cytokines(細胞激素)IL-1，IL-8 等之合成便是。但這些過程中最重要的一項就是NF-KB被活化了，抗癌科學家也已發現，最有力量活化NF-KB的就是TNF-α。NF-KB被活化後，細胞便不容易死亡，且容易增殖，這便是身體發炎及細胞自我修復之常見現象。

二、發炎與消炎，癌化與去癌化的主角 – NK-KB與P53

NF-KB即細胞核轉錄因子(Nuclear Factor - Kappa B，簡稱NF-KB)；P53即是腫瘤抑制蛋白(Protein 53，簡稱P53)。NF-KB 是造成身體發炎的主要調節物質，而P53則是抑制腫瘤產生的主要物質。這兩種物質相互影響而造成身體發炎及癌化與否的一連串事件，也是癌症形成的重要因素。(2)

NF-KB是一蛋白質的複合體，在很多動物(包括人類)的細胞裏都存在著。NF-KB平常都很安靜地躲在細胞質裏，但當其被激發喚醒後，會立刻跑到細胞核及粒腺體裏面。細胞核及粒腺體裏面有著生物的整個基因體，因此NF-KB 便會使得個別基因體產生免疫效果的基因表現出來，同時那些會保護細胞不致於死亡的基因也會表現出來，更甚者那些使細胞增殖的基因亦被表現出來。這原本是件好事，是我們身體為了對抗受傷或是對抗外界入侵的一種自我保護措施。這種NF-KB 所造成身體局部的反應便是所謂發炎的現象。但問題是：如果NF-KB 這些動作一直被激發著，則細胞都將呈現快速增殖及抗拒死亡的特質，這就是細胞癌化及癌症進行的模式。所以，NF-KB 長期被激發就會造成慢性發炎現象；也就會形成了癌症。此種進行模式目前已普遍被醫界所接受。(3)

至於P53，它是一53千道頓的蛋白質分子，它被稱為基因體的守護神，也被稱為天使基因。因為它守護著基因體，使其保持穩定，不被破壞。當細胞要分裂複製時，P53會先把基因體巡視一遍，如果發覺基因體有被破壞時，則會請基因修補分子對基因體進行修補動作。如果基因體被破壞過大或該細胞已夠老化(分裂50~60 次)，則P53便會啟動另一程序，使細胞自行死亡，即所謂細胞凋零。所以如果我們身體的P53 都沒有被抑制或被破壞時，則細胞便不能抗拒死亡，所以癌症也就不會產生了。但問題是：NF-KB和P53之活化都需要同一種叫做P300(and CBP) 的伙伴。這個P300(and CBP) 伙伴若被NF-KB搶走，則NF-KB 就被活化，但P53便因沒有伙伴而會被抑制。反過來如果P53 搶走了P300(and CBP) 伙伴，則P53 會活化而NF-KB則被抑制。(4)

萬一NF-KB 搶到了P300(and CBP) 伙伴而活化，而抑制了P53的活性，身體就會引起慢性發炎，而NF-KB 也將使得P53不再行使對基因體作為守護天使的天職。因此此現象發生後細胞不再凋零，這便是細胞抗拒死亡、癌化及癌症進行的原因。所以如前面所說的癌症的產生及進行模式更準確的表述如下圖所示：

所以慢性發炎和癌症可說是無法切割的連嬰。(5), (6)

究竟NF-KB 或P53 是如何搶得它們的P300(and CBP) 伙伴而使其活化呢？這就要靠身體的自律神經系統來決定了！如果交感神經活躍就會幫助NF-KB 取得P300(and CBP)，反過來，若副交感神經活躍時，則P53 會取得P300(and CBP)。所以可以說，交感神經的活躍將使發炎加劇，而健全的副交感神經則會抑制炎症的發生與進展。

三、自律神經過度活躍會激化發炎及癌症

如果我們的交感神經過度的活躍，則發炎的故事就會繼續演下去，過度活躍的交感神經會產生大量的去甲腎上腺素，去甲腎上腺素正好是TNF-α 的激化分子；濃度越高的去甲腎上腺素會激化越多的TNF-α。在活躍的交感神經下，去甲腎上腺素飆高，TNF-α 之濃度因而變得超高；NF-KB亦會跟著被大量的活化。以前所說之NF-KB 和P53 之平衡便被打破：NF-KB 被大量地活化，而P53 則被嚴重的壓抑。交感神經之過度活躍便是打破平衡的這隻手！

更甚者，NF-KB 及IL-8 等都會啟動一些叫VEGF 因子，這些因子會使血管增生；有足夠的營養，細胞長得更快，又不會凋零，最後還會轉移，這就是癌。說到轉移，最近的研究已指出乳癌細胞的遠程轉移，也是交感神經闖的禍。有一篇文獻的標題是「交感神經是原發乳癌轉移的開關」，由此可見交感神經對於癌症形成及轉移是何等的重要。(7)

上面的過程可以歸納如下：

巨噬細胞及其產生之TNF-α 在癌症發展中所扮演的角色早在臨床上被詳細深入及評估過。在很多癌體裏都有被滲透進去的巨噬細胞；并且都有很多的TNF-α 及其他的cytokines 如IL-1 等。這些滲透到癌體裏的巨噬細胞被稱為Tumor-Associated-Macrophages(TAM)。TAM 濃度被發現跟癌症的預後成反比，即TNF-α 愈多則癌發展愈不樂觀。(8)

四、交感神經活性過高的可能原因

以HRV自律神經檢測儀可分別定量出交感及副交感神經的活性。最理想的狀態是交感神經活性（LF）、副交感神經活性（HF）以及LF/HF比例都在正常範圍內。交感神經活性 / 副交感神經活性（LF/HF）比例越大，表示交感神經活性越活躍。

交感神經活性過高的可能原因有下列各項：

1、病原菌入侵

當人體遭受細菌、黴菌、病毒等病原入侵時，人體便會啟動交感神經，再驅動巨噬細胞來防衛。

有許多種類的癌症已被證實與慢性感染發炎有關，如EB Virus之於鼻咽癌、B型肝炎病毒之於肝癌等，這都是因為發炎的結果導致NF- KB受到激發而P53受到了抑制。

2、大分子蛋白質入侵

大分子蛋白質經由呼吸道或消化黏膜入侵人體，導致IgG、IgE抗體產生，這屬非感染的入侵方式。雖然它也同樣會激化交感神經及NF- KB，同時抑制P53，但到目前為止，尚未有充份證據可證明罹患黏膜滲漏症之患者有較高的罹癌率。

3、精神性因素

情緒上易動怒的人，交感神經活性普遍偏高（LF/HF比值高）。當一個人面對巨大壓力或無法如期完成設定的目標時，身體會自動提升交感神經進入備戰狀態。有些人交感神經活性過高，但其LF/HF比正常，這是因為其副交感也同步提高，進入「超飽和狀態」（Allostatic State），這樣對身體的健康同樣也是不利的。

五、副交感神經是人體的滅火部隊

自律神經可分為交感神經及副交感神經，大家都知道交感與副交感是處於對立及拮抗狀態，例如交感神經亢奮時，會使心跳加快；副交感則會令心跳變慢；但是對於腸胃道而言，副交感則扮演促進功能的角色，而交感神經則表現出抑制的功能。

在「發炎」這課題上，交感神經是扮演促進的角色，而副交感神經則負責「消炎」。

六、副交感神經 – 抗癌的最新希望(9), (10)

最近幾年，副交感神經能快速、自然地控制發炎的功能被發現了，於是「癌症的神經生物學」(11) 說法蔚為流行。這個消炎的反射功能被稱為膽鹼消炎途徑(Cholinergic Anti-inflammatory Pathway)，如果我們的迷走神經功能還健全，則它會自動感應到發炎因子(即TNF-α、IL-1 等)的存在。如果發現這些發炎因子濃度過高時，即會通知大腦，大腦便會透過自律神經，在發炎地區附近釋放出一種叫乙醯膽鹼(Acetycholine,Ach)的神經傳遞物質(neurotransmitter)。這些Ach 會非常有效地抑制巨噬細胞，使其不再分泌TNF-α、IL-1 等細胞激素。發炎現象便會自然地停止。這其實就是身體去除消炎最常用的方法。

身體發炎現象痊癒後，TNF-α、IL-1 等也會隨之消失，而NF-KB 又會回到細胞質裏，不再進行激化的活動。由於P53 沒有抑制者，便會重新活躍地巡視、守護我們的基因體，就有更大的機會可遠離癌症。所以過度活躍的交感神經會引起慢性發炎，會增進癌症之發展。活化副交感神經會抑制發炎及有害之細胞激素的產生，進而也可抑制癌症的發生與發展。

臨床上如果能提升副交感神經活性並降低交感神經活性，對癌症之治療就會有正面意義。很可惜目前能長時間提升副交感，降低交感神經活性，又沒有副作用的藥物幾乎無處尋覓。倒是有許多天然非藥物的方式可以達到上述目的，將另行為文介紹。

References （英文文獻全文請至「自律神經文獻部落格」下載）

(1) Bellinger DL, Millar BA, Perez S, Carter J, Wood C, ThyagaRajan S, Molinaro C, Lubahn C, Lorton D. Sympathetic Modulation of Immunity: Relevance to disease. Cellular Immunology, 252, p27, 2008.

(2) A.V. Gudkov , K.V. Gurova , and E.A. Komarova. Inflammation and P53: A Tale of TwoStresses. Genes and Cancer, 2, p503, 2011.

(3) Bharat B. Aggarwal, Gautam Sethi, Asha Nair, and Haruyo Ichikawa. Nuclear Factor - B: A Holy Grail in Cancer Prevention and Therapy. Current signal Transduction therapy 1, p25,2006.

(4) A. Ikeda, X. Sun, Y. Li et al. P300/CBP – Dependent and Independent Transcriptional Crosstalk Between NF- KB and P53. Mol. Cell Biol. 19, P3458, 1999.

(5) Sergei I. Grivennikov, Florian R. Greten, Michael Karin. Immunity, Inflammation, and Cancer. Cell, 140, p883, 2010.

(6) Aggarwal BB, Shishodia S, Sandur SK, Pandey MK, Sethi G. Inflammation and Cancer: How Hot is the Link? Biochemical Pharmacology. 72, p1605, 2006.

 (7) Erica K. Sloan, Saul J. Priceman, Benjamin F. Cox, Stephanie Yu, Matthew A. Pimentel, Veera Tangkanangnukul, Jesusa M.G. Arevalo, Kouki Morizono, Breanne D.W. Karanikolas, Lily Wu, Anil K. Sood and Steven W. Cole. The Sympathetic Nervous System Induces a Metastatic Switch in Primary Breast Cancer. Cancer Res. 70, p7042, 2010.

(8) Alberto Mantovani, Federica Marchesi, Chiara Porta, Paola Allavena and Antonio Sica. Linking Inflammation Reactions to Cancer: Novel Targets for Therapeutic Strategies. Targeted Therapies in Cancer. 610, p112, 2008.

(9) Tracey KJ. The Inflammation reflex. Nature 420, p853, 2002.

(10) Huston JM, Tracey KJ. The Pulse of Inflammation: Heart Rate Variability, the Cholinergic Anti-inflammatory Pathway and Implications for Therapy. J. of Intern Med. 269, p45, 2011.

(11) Boris Mravec, Yori Gidron and Ivan Hulin. Neurobiology of cancer: Interactions betweennervous, endocrine and immune systems as a base for monitoring and modulating thetumorigenesis by the brain. Seminars in Cancer Biology, 18, p150, 2008.

   

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癌症防治新方法 – 生物神經法

   

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楊維邦 博士 2011/8

我們必須先介紹兩位生物神經法的主角，即細胞核轉錄因子(Nuclear Factor - Kappa B，簡稱
NF-KB)，及腫瘤抑制蛋白(Protein 53，簡稱P53)。NF-KB 是造成身體發炎的主要調節物質，而P53則是抑制腫瘤產生的主要物質。這兩種物質相互影響而造成身體發炎的一連串事件，也是癌症形成的重要因素。

先來說說NF-KB，它是一蛋白的複合體，在很多動物(包括人類)的細胞裏都存在著。平常都
很安靜地躲在細胞質裏，但當其被激發而被喚醒後(如何被激發喚醒，後有詳細說明)，會立刻跑到細胞核及粒腺體裏面。細胞核及粒腺體裏面有著生物的整個基因體，因此NF-KB 便會使得個別基因體產生免疫效果的基因表現出來，同時那些會保護細胞不致於死亡的基因也會表現出來，更甚者那些使細胞增殖的基因亦被表現出來。這原本是件好事，是我們身體為了對抗受傷或是被外界入侵的一種自我保護措施。這種NF-KB 所造成身體局部的反應便是所謂發炎的現象。但問題是：如果NF-KB 這些動作一直被激發著，則細胞都將變成快速增殖及抗拒死亡，這就是細胞癌化及癌症進行的模式。所以，NF-KB 長期被激發就會造成慢性發炎現象；也就會形成了癌症。此種進行模式目前已普遍被醫界所接受。

再來看看P53，它是一53 千道頓的蛋白質分子，它被稱為基因體的守護神，也被稱為天使基
因。因為它守護著基因體，使其保持穩定，不被破壞。當細胞要分裂複製時，P53 會先把基因體巡視一遍，如果發覺基因體有被破壞時，則會請基因修補分子對基因體進行修補動作。如果基因體被破壞過大或該細胞已夠老化(分裂50~60 次)，則P53 便會啟動另一程序，使細胞自行死亡，即所謂細胞凋零。所以如果我們身體的P53 都沒有被抑制或被破壞時，則細胞便不能抗拒死亡，所以癌症也就不會產生了。但問題是：NF-KB 和P53 之活化都需要同一種叫做P21 的伙伴。這個P21 伙伴若被NF-KB 搶走，則NF-KB 就被活化，但P53 便因沒有伙伴而會被抑制。反過來如果P53 搶走了P21 伙伴，則P53 會活化而NF-KB 則被抑制。

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NFkB/p53 crosstalk - a promising new therapeutic target

   

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Gunter Schneider, Oliver H. Kramer

Abstract

The transcription factors p53 and NFkB determine cellular fate and are involved in the pathogenesis of most-if not all-cancers. The crosstalk between these transcription factors becomes increasingly appreciated as an important mechanism operative during all stages of tumorigenesis, metastasis, and immunological surveillance. In this review, we summarize molecular mechanisms resulating cross-signaling between p53 and NFkB proteins and how dysregulated interactions between p53 and NFkB family members contribute to oncogenesis. We furthermore analyze how such signaling modules represent targets for the design of novel intervention strategies using established compounds and powerful combination therapies.


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The Developing Brain and Cancer

   

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The GW Institute for Neuroscience hosts annual symposium.

By Anna Miller
April 28, 2011

Just a few decades ago, the connection between neurobiology and cancer biology was suspected but unspoken.

“Today, it represents one of the most robust interfaces between basic neuroscience and clinical medicine,” said Anthony-Samuel LaMantia, professor of pharmacology and physiology in the GW School of Medicine and Health Sciences (SMHS) and founding director of the GW Institute for Neuroscience (GWIN), at the first annual Neuroscience Symposium on Wednesday.

The symposium featured four leading researchers who highlighted the latest advances in the field of neuroscience that contribute to the understanding of how the brain develops and how cancer can compromise the developing brain.

Held at the Marvin Center, the daylong event brought together close to 80 researchers, graduate students and scientists and was sponsored by SMHS, the Office of the Vice President for Research and the Columbian College of Arts and Sciences — the three entities that support GWIN.

Sally Moody, professor of anatomy and regenerative biology in SMHS, delivered the first keynote address, which highlighted the earliest stages of nervous system development.

“In all vertebrates, we have several steps that take you from the initiation of embryonic cells becoming neural to when you get actual, independent, specified kinds of neurons,” she said.

Using her work with frog embryos as a guide, Dr. Moody hypothesized that the expression of FoxD4/5, one of the earliest genes in the network, plays a key role in neural stem cell fate, particularly through its activation of a group of genes called Sox.

The second keynote speaker was Michael Dyer, a member of St. Jude Children’s Research Hospital in the Department of Developmental Neurobiology and co-leader of the Developmental Therapeutics for Solid Malignancies Program. Dr. Dyer discussed how his work studying retinoblastoma, a childhood cancer of the eye, has helped bridge the gap between developmental neurobiology and cancer genetics.

Among many influential discoveries, Dr. Dyer explained how his lab’s approach to studying tumor cells led to the unpredictable finding that adult neurons can divide without losing their distinctive features.

“What we’ve shown is that everybody was right over the years: These tumors have properties of different cell types. It’s just that nobody considered the possibility that they were all the same cell,” Dr. Dyer said.

Vittorio Gallo, professor of neuroscience at SMHS, director and Wolf-Pack Chair in Neuroscience at Children’s National Medical Center’s Center for Neuroscience Research, presented the third keynote address.

Dr. Gallo discussed how certain signaling pathways help to maintain the balance between specific types of neurons developed in the brain that are critical under both normal conditions and after injury. These pathways contribute to the growth and development of neural progenitor cells, one of the groups of neurons. Because neural progenitor cells and these pathways may influence the formation of brain tumors, they are important to understand for potential clinical applications, Dr. Gallo said.

Scott Loren Pomeroy, Bronson Crothers Professor of Neurology at Harvard Medical School and
Neurologist-in-Chief at Children's Hospital Boston, delivered the final keynote address about medulloblastoma, the most common type of malignant brain tumor in children.

Dr. Pomeroy explained how the reclassification of medulloblastoma into various subtypes is leading to the creation of better targeted therapies. These therapies, he said, may not only improve survival, but they may also help to mitigate the harsh side effects seen with current therapies that treat all medulloblastomas as equals.

“We hope to find common pathways that we will be able to block with a reasonable small number of drugs that don’t have horrible side effects and fundamentally change how we treat the tumors,” said Dr. Pomeroy. “I would say we are much closer to that today than we were 10 years ago.”

Paaqua Grant, Amanda Mathews, Mathew Raymond and Carrie House, graduate students from SMHS’s Institute of Biomedical Sciences, also delivered presentations on their research projects.

The day concluded with a panel hosted by the GW Cancer Institute and moderated by its executive director, Steven Patierno, professor of pharmacology and physiology at SMHS. Panelists included Drs. LaMantia, Dyer and Pomeroy; Javad Nazarian, assistant professor of integrative systems biology at SMHS; Norman Lee, professor in the Department of Pharmacology and Physiology at SMHS; and Weiqun Peng, associate professor of physics in the Columbian College of Arts and Sciences.

The panelists discussed the future challenges and possibilities in the realm of neuroscience research. Dr. Nazarian spoke about the promise of using cerebrospinal fluid as a way to detect and target tumors that cannot be isolated. Other panelists addressed the possibility of the existence of cancer stem cells and raised concerns about computational barriers.

“I still feel like there’s a lot hidden in our data,” said Dr. Dyer. “And I don’t know where it’s going to come from, but I feel there’s going to be a really smart person out there that’s going to figure out a totally out-ofthe-box way to look at this, and it’s going to revolutionize the way we look at all this data.”

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Why Cancer and Inflammation?

   

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Seth Rakoff-Nahoum

Abstract

Central to the development of cancer are genetic changes that endow these “cancer cells” with many of the hallmarks of cancer, such as self-sufficient growth and resistance to antigrowth and pro-death signals. However, while the genetic changes that occur within cancer cells  themselves, such as activated oncogenes or dysfunctional tumor suppressors, are responsible for many aspects of cancer development, they are not sufficient. Tumor promotion and  progression are dependent on ancillary processes provided by cells of the tumor environment
but that are not necessarily cancerous themselves. Inflammation has long been associated with the development of cancer. This review will discuss the reflexive relationship between cancer and inflammation with particular focus on how considering the role of inflammation in physiologic processes such as the maintenance of tissue homeostasis and repair may provide a logical framework for understanding the connection between the inflammatory response and cancer.

中文摘要：
癌症之發生主要源自於基因之改變，這些改變是癌症細胞擁有好幾個特徵，即自主生長，能抗拒抑制生長和摧毀凋零之訊息。雖然，引起癌化之基因改變是發生在細胞裡面；諸如癌化基因之啟動或抑制癌化基因之因子失去功能，這些都能引起癌症，但是只有這些是不夠的。腫瘤之進展需要一些由周邊正常細胞所提供之輔助環境條件。發炎很早便被認定與癌症發展有關。本論文會討論癌症和發炎的反射反應關係，特別從發炎之生理過程及其維持生理系統平衡和修補來了解發炎及癌症之因果關係。


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Inflammation and cancer: How hot is the link?

   

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王群光自然診所：台北市羅斯福路三段271號10樓

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Bharat B. Aggarwal , Shishir Shishodia , Santosh K. Sandur , Manoj K. Pandey , Gautam Sethi

Abstract

Although inflammation has long been known as a localized protective reaction of tissue to irritation, injury, or infection, characterized by pain, redness, swelling, and sometimes loss of function, there has been a new realization about its role in a wide variety of diseases, including cancer. While acute inflammation is a part of the defense response, chronic inflammation can lead to cancer, diabetes, cardiovascular, pulmonary, and neurological diseases. Several pro-inflammatory gene products have been identified that mediate a critical role in suppression of apoptosis, proliferation, angiogenesis, invasion, and metastasis. Among these gene products are TNF and members of its superfamily, IL-1a, IL-1b, IL-6, IL-8, IL-18, chemokines, MMP-9, VEGF, COX-2, and 5-LOX. The expression of all these genes are mainly regulated by the transcription factor NF-kB, which is constitutively active in most tumors and is induced by carcinogens (such as cigarette smoke), tumor promoters, carcinogenic viral proteins (HIV-tat, HIV-nef, HIV-vpr, KHSV, EBV-LMP1, HTLV1-tax, HPV, HCV, and HBV), chemotherapeutic agents, and g-irradiation. These observations imply that antiinflammatory agents that suppress NF-kB or NF-kB-regulated products should have a potential in both the prevention and treatment of cancer. The current review describes in detail the critical link between inflammation and cancer.

中文摘要：
雖然，我們很早便知道發炎是一個為保護受傷、感染、刺激而產生之局部地區之過程，跟而引起之疼痛、紅腫及一些身體之功能消失；現在我們更清楚，發炎其實在很多疾病上扮演著很多種功能，包括癌症。急性發炎是自衛免疫的一部分，但慢性發炎卻會英氣癌症、糖尿病、心血管疾病、肺病及神經性疾病。有數個發炎基因所產生之化學分子已被認出，它們會在抵抗凋零、擴散、血管增生、侵犯、轉移的過程中，扮演主要的角色。這些基因化學分子便是TNF，及一個超級家庭中之IL-1α，IL-1β，IL-6，IL-8，IL-18，化學激素如MMP-9，VEGF，COX-2及5-LOX都在其中。這些基因之表現，是由一個叫NF-Kβ錄制因子所調控，而該錄制因子在腫瘤中非常活躍，且是有致癌物質（如抽煙）、腫瘤催化劑、致癌病毒蛋白質（如HIV-tat、HIV-vpr、HIV-nef、KHSV、EBV-LMP1、HTLV1-tax、HPV、HOV與HBV），化學治療之藥物，及γ-輻射所啟動。這些事實表示抗發炎因素可以經過壓制NF-Kβ或是NF-Kβ之產生化學物來進行癌症之預防及治療。

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Y. 未分類

   

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王群光自然診所：台北市羅斯福路三段271號10樓

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LINE ID：0919730053

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Y1 神經免疫控制
Neural Control of Immunity【資料來源：Bio-Inspired Technology (2011)】

Y2 NFkB/p53 crosstalk - 一種新的治療指標
NFkB/p53 crosstalk - a promising new therapeutic target【資料來源：Biochimica et Biophysica Acta (2011)】