昨天很多人開始詢問,到底甚麼是免疫療法。從各方湧入的問題,我也了解到這四個中文字似乎每個人都有不同的解讀。因此寫這篇希望大家能夠簡單的認識免疫療法。

文章會很長,但請大家務必耐心看一下。

免疫療法包括了【免疫藥物治療】以及【免疫細胞治療】兩種。

【免疫藥物治療】就是我們熟悉的藥物形式,都是國際大藥廠研發出的新藥,進行各種癌別的治療,例如 Keytruda 和 nivolumab。目前看到這類免疫藥物,對黑色素瘤的效果很好,都有超過50%以上的良好反應率。對其他癌別的效果則還要看更多臨床的統計數據判定會比較準。這類藥物,只要台灣的衛福部有核准癌症病患就可使用,只是他的藥費非常貴,是以病人體重去計算施打的劑量,一個月初估都會在一百萬左右,若有效,醫師通常都會建議持續施打。

【免疫細胞治療】我都分享我從日本醫生就診詢問得知的資訊分享給各位,【免疫細胞治療】是抽取病患自身的血液、癌細胞切片(部分療程需要)後,透過體外培養的方式,去培養免疫細胞,然後將大量的免疫細胞回輸到癌症病患體內,讓免疫細胞去攻擊癌細胞。但是這邊有個需要特別被重視的問題是: 到底是培養了那些免疫細胞,然後回輸到癌症病患的體內呢? 主要培養是以下三種免疫細胞後回輸體內:

1. NK細胞(自然殺手細胞)

2. DC細胞(樹狀細胞)>>>>>>>>>>>進行這項細胞治療,通常都會需要切取到癌細胞的組織

3. T細胞

除了以上三種免疫細胞,還有胜肽疫苗的免疫細胞治療方式,這種方式也是抽取病患的血液檢測HLA類型,然後配對胜肽輸體內。原理是透過胜肽去刺激免疫細胞快速增長,然後讓免疫細胞去攻擊癌細胞。我目前進行的久留米大學醫院的實驗計畫,就是屬於這種。

我的日本醫生說,日本醫界目前認為,單獨施打NK細胞,不管標榜其濃度有多高、多精純,對於殺死癌細胞其實是沒有幫助的,只能提升免疫力。

而我在千葉大學醫院做的免疫細胞治療,則有施打前述的自然殺手細胞、DC細胞跟T細胞 (我被同時輸入三種免疫細胞)

這樣的治療在這次的提案中,衛福部回應中承諾,明年2月就會修訂人體實驗管理辦法,讓台灣的癌友可以快速地享有這樣的治療。若實驗有超過名額,超過名額部分可以自費進行治療,詳細辦法我們還要再繼續監督。

所以說到這邊,在明年2016年辦法實施後,我相信有能力提出實驗計畫的,一定都是台灣值得信任的【教學醫院】的醫生,例如:台大、北榮、高醫、北醫、成大、北醫、長庚等等,絕對不會是一般的民間診所。所以反過來思考,若現在在台灣,有任何民間診所跟您說可以收費進行【免疫細胞治療】,那絕對是違法的。違法對我代表的意義是: 沒有辦法確認打進我體內的是甚麼東西,所以我不會做這樣的治療。

第二就是各位一定要問,做【免疫細胞治療】,培養細胞的實驗室是不是有符合國際GMP的規範。因為這樣才能確保免疫細胞的培養品質。據衛福部表示,目前台灣有符合GMP規範的實驗室有三座,分別在北醫、北榮跟高醫。

接下來是治療選擇的問題。我該何時選擇免疫治療? 我自己的經驗是我經歷了33次放射線,7次化療(每次化療連打五天鉑金、5FU等藥物),都無效,在台灣,我還試過硼中子放射線的實驗,因我自己體質問題無法接受治療,才自己陰錯陽差尋找到免疫療法。

也有人問我,若時光倒轉,我在第一時間會選擇先做放化療,還是【免疫細胞療法】?我會很篤定的說,我還是必須要選擇放射線治療跟化療。原因是:

放射線跟化療,是已經很明確的有統計數據跟我說,他的效果會有60%、70%的有效率,雖然有很多副作用,但要拚,也要從有效率高的開始拚吧~~~因為治療的時間對我來說也很重要,所以我還是會要選擇放化療。即使到今天,假設,【免疫細胞療法】對我沒效了,我還是必須要選化療。

在此只有一個選擇的邏輯,就是: 要拚,先從反應率高的、比較有把握的開始拚吧!

我也必須承認,我是一位幸運的人。因為【免疫細胞療法】我看到的反應率數據,會讓腫瘤縮小的機率約10%~15%,會讓腫瘤維持不變(沒變大也沒變小)的機率是25%~30%,反應率是低於化療的。因此我的訴求一項都是,這項治療是給癌末病患多一個機會跟選擇,但我不希望很多病友因為對效果有過度的期待,甚至神化了【免疫細胞治療】,而延後原本該做的正規治療,實在非我樂見。

最後彙整一下最近很多病友來信問我的兩個問題,如下:

1. 我看到有廣告說,在健康的時候先儲存細胞,等到我得癌的時候就可以培養好的免疫細胞去攻擊癌細胞,這會有用嗎?

2. 有公司可以讓我去日本或大陸的民間診所去進行治療,我該去嗎?

針對第一題,我有問過我的日本醫生(千葉大學跟久留米大學的醫生),他們的回答如下:

這樣的方式在日本並不風行,同時目前的研究,是沒有辦法證實這樣的方式有效。而他們很懷疑的是,就他們的認知,目前世界上還沒有儀器可以儲存細胞那麼久,並且維持細胞活性。同時健康時抽取細胞儲存,這時體內並沒有癌細胞,就算培養出免疫細胞回輸體內,免疫細胞也很難去辨識癌細胞進而去攻擊癌細胞,因此目前日本醫界沒有朝這方面進行研究。>>>>>>>>>我相信我的日本醫師,所以我對這個問題的回答都是,我不建議。

針對第二題,我也問過我的日本醫生,我問:日本也有很多民間診所可以進行免疫療法,我們該選擇這樣的醫院嗎?我的日本醫生回覆:

這類的醫院他們並不清楚它們培養細胞的實驗室,在不清楚的狀況下,他們不會推薦我們去。同時日本也是有發生過民間診所以【免疫細胞治療】的詐騙事件,因此勸我們前往這類診所前請務必三思。我還是選擇相信我的日本醫生,所以,即使是日本民間的【免疫細胞治療診所】,我也不會前往治療。

有病友接著問,他們病況很緊急,真的需要前往治療,我會分享我找到的資訊如下:

我看到日本民間診所的【免疫細胞治療】,最貴最貴的一個療程(施打六針免疫細胞),醫療費的價格是300萬日幣 (約台幣75萬~80萬),我會建議他自己跟這家醫院聯絡,同時找日本當地的翻譯前往治療(我再重申,這是最下下下策),費用會是最合理的,而不要透過某些公司的仲介。

接下來再提一下CAR-T,這是屬於【免疫細胞治療】的一種,這項治療是培養T細胞,同時再透過改變基因排序的方式與T細胞結合後,再回輸人體體內。這是今年下半年才有研究成果發表的【免疫細胞治療】,因此非常新,也結合了改造基因跟免疫細胞兩個領域。目前研究的成果發現,對血癌、淋巴癌、肉瘤類的癌症,效果出奇的好,但部分受試者的副作用非常大。這項療法,也會是這次衛福部修法的重點,因為牽涉基因排序的改變,若不修法,台灣永遠無法引進這項治療。

最後希望大家早日恢復健康。

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  • 訪客
  • 一直很關注你的訊息與免疫療法的分享與活動 加油 加油!!!
  • Gary YC LIN
  • 謝謝卡斯柏的分享
  • 訪客
  • 請問台灣是否有針對胰臟癌肝轉移的患者有進行免疫療法?
  • 抱歉,目前我沒有看到台灣有針對胰臟癌有人體實驗計畫。

    卡斯柏 於 2015/12/16 09:20 回覆

  • David
  • 卡斯柏這篇是經典之作 相信許多人能夠受惠 給你一個讚
  • 謝謝david常關心,你也常提供很多有用的資訊

    卡斯柏 於 2015/12/16 19:25 回覆

  • Sora
  • 您好,我閱覽您的文章後,初步與久留米大學取得聯繫了。大學回覆我,他們是使用尚未被認可的藥進行投藥,然後邊研究效果與副作用。然後全額必須自費,因為我記得有看到文章寫到有補助問題,所以想請教。另,他們有提到這個治療無法完全消滅癌症,也無法取代放射及抗癌藥劑,故也不能期待腫瘤會縮小等。所以想請問這是同一個療法嗎?因為感覺上不太一樣。
  • 確實是阿,因為這個是實驗計劃,所以是尚未被核可的細胞治療。全額自費也沒有說錯,久留米針對參加這個實驗計劃會收取72到92萬日幣(一整個療程)的費用,他們申請書內都有寫的。

    卡斯柏 於 2015/12/16 11:16 回覆

  • David
  • 今天的蘋果日報有報導說衛福部打算近期開放"免疫療法"了

    2015年12月14日12:40


    美國前總統卡特罹患腦癌,接受免疫療法後腫瘤消失,讓國內癌患看見治療希望,但礙於國內目前的細胞免疫療法人體試驗,僅限於被收案的癌患才能接受治療,鼻咽癌末期患者王先生在國內歷經33次放療、7次化療效果不好,2年前遠赴日本接受細胞免疫療法,他今公開要求政府應全面開放癌症細胞免疫療法,給癌患一條生路。衛福部回應,將儘速修訂「人體試驗管理辦法」,最快明年2月底前公告實施,讓癌症免疫細胞療法不限收案對象,擴及其他癌患也能自費治療。

    王先生在2012年確診末期鼻咽癌,因腫瘤包覆頸動脈無法手術,在國內接受33次放療、7次化療,效果均不理想,醫師告知若繼續放療或化療,恐因頸動脈破裂變植物人,隔年他轉赴日本千葉大學尋求細胞免疫療法,治療7個月後腫瘤縮小30%,今下午將再度前往福岡久留米大學接受免疫療法。

    高雄醫學大學附設醫院細胞及免疫治療研究室主任林成龍說,細胞免疫療法是取出癌患的自體免疫細胞,經實驗室培養增強其抗癌能力後,再輸回癌患體內,優點是不會產生如化療的掉髮、噁心嘔吐等副作用。他強調,許多國內癌患受限法規,被迫前往日本治療,國內的免疫細胞療法已具水準,但法規限制對癌末患者太殘忍。

    衛福部食藥署副署長吳秀英說,目前正加速修訂「人體試驗管理辦法」,制定人體試驗附屬治療計畫,因非母法修訂不需送立院,癌症患者須符合「危及生命或嚴重失能」且「國內尚無適當藥物或替代療法」兩條件,醫師可在人體試驗階段,另訂附屬治療計畫,經該署評估安全無虞後,讓癌症患者可自費接受治療,放寬細胞免疫療法的對象。

    她說,醫師向該署申請的人體試驗附屬治療計畫,其治療對象、收費標準,均須由該署專家會議討論後核定,並非由醫院決定收多少費用,修法目的是確保患者權益及安全無虞下,讓無法被收進人體試驗的癌患,也有機會接受免疫細胞療法。

    衛福部醫事司長王宗曦補充,今早召開第二次專家諮議會,會議對修法有共識,若預告後沒有太多反對意見,「人體試驗管理辦法」修法預定明年2月底前公告實施。(蔡明樺/台北報導)
  • 安
  • 放丶化療反應率雖高,但副作用對老年人實在有不可承受之重,
    所以父親當初才會選擇反應率20%的免疫療法。希望日後的治療
    反應率能提升,讓治療過程不在那麼痛苦。免疫療法在爸爸身上
    真的幾乎沒什麼副作用。大家加油
  • 完全理解。所以我一直訴求,多個治療選擇是台灣癌症患者之福。

    卡斯柏 於 2015/12/16 19:23 回覆

  • 訪客
  • 請問要如何得知國內有進行免疫療法的醫院?看到您對高醫 林成龍醫師介紹的那篇文章,是否可以帶著目前的檢查報告直接到高醫掛號?
  • 您好,可以的阿,請掛高醫癌病中心林醫師門診,健保給付的門診

    卡斯柏 於 2015/12/18 09:30 回覆

  • David
  • After 9th infusion (of Keytruda), My dad's status update

    There is no sign of disease progression.
    One third of the tumor site has been replaced with fresh normal tissue.
    The tumor site also appear enclosed by normal tissue, suggesting the T cells are slowly eatting up the tumors.
    There is no doubt there are anti tumor response, even with my dad's age: 83.
    My dad also has new skin on his face and scalp. New skin replacing some of his old skin. He has a 大花臉 now.
    That is the most visible thing of Keytruda's effect.
    He experience no fatigue, no fever, nothing unusual.
    The UCLA doctor will continue Keytruda infusion.
  • David
  • Keytruda: 10th infusion

    My dad started Keytruda infusion in March, 2015. He has 10 infusions so far.
    Because he is on patience assistance program, so finance is not a concern.
    The doctor keeps the infusion going so far.

    The UCLA doctor was the one that did Keytruda clinical trial so he knows what he's doing. The medicine halted the disease progression early on. And it stayed that way for a long time. I thought my Dad had no response, but was glad that Keytruda halted the disease.

    It is strange that we rarely talk about his disease any more ever since he started the infusion... as if... he is cured. The subsequent CT-scans and MRI did not disappoint us.

    We become more concerned with his memory loss. My sister and I even thought the cancer somehow get into his brain. But MRI is negative. (Brain tumor has to be BIG to affect memory)

    Finally, the recent reports show part of the tumors are eaten up by T-cells.
    My dad also has new skin on his scalp and face. New skin like baby's.
    Nurse said that is the response. She saw it on other patients too.

    I could not figure out why. But there are many things I don't know and God has not revealed to me. But I do try my best to pass on the secret that God revealed to me to those who need it the most.

    I am sure my dad can live to the 90's.
  • 悄悄話
  • Gary YC LIN
  • 恭禧 David,知道令尊的治療有不錯的成效,真是替你高興。相反的,家父是前列腺癌的患者,目前的研究顯示,PD1/CTLA4 等治療,在此種癌症上無明顯的效果。看樣子,若沒更好的選擇,只有回頭去做化療了。
  • David
  • Just want to share some of the things I've learned over the past two years.

    CTLA-4 pathway blocks the immune system from starting an immune response against cancer. How tumor employ this mechanism to block anti tumor response is still not completely known. What the scientists do know is when the dendritic cells present tumor antigens to an naive T-cell (a T cell which never been activated), it fails to activate the T-cell.

    PD-1 is more direct. Most cancer types use this mechanism to fend of T cell attack. PD-1 is a receptor on the T cells. It stands for Programmed Death-1. When attached by PDL1, the T cell become deactivated, and will die over a period of time. When cancer cells are under T cells attack, dying cancer cells secret substances to alert cancer cells nearby. These cancer cells will respond to the signal by presenting PDL1 on their cell surface. When T cells attack these cancer cells, T cells will become deactived and die gradually. This is why T cell therapy, DC cell therapy and cancer vaccine maybe only effective for a short time.

    My observation is anti PD1 is effective in preventing the disease from spreading.
    This is logical because T cells are based in lymph nodes and lymph nodes are body's check point for intruders**. Lymph system are interconnected to blood vessel system to form a complex network. All substances (virus, bacteria, cancer cells) flowing in the blood vessel are subject to examination of the T-cells (a white blood cell). In my opinion, it is easier to eliminate free flowing cancer cells. And this observation is back by medical data. In a recent Nivolumab clinical trial, Hodgkin lymphoma achieved a high response rate 87% (20/23).

    Solid tumors are harder to attack. Still using anti PD1 to treat various cancers, we still see an average of 20% response rate, which is remarkable in my opinion.

    Solid tumors are cluster of cancer cells. 1 cm of tumor packed with 1 billion cancer cells.
    Solid tumors have several defense mechanism to fend off immune system attack.
    1) thick wall called vasculature.
    2) regulatory T cells and Dentritic cells, macrophage, MSDC in the tumor micro environment, which can turn off anti tumor immune response. (All of above use PDL1 to turn off immune response, that is why anti PD1 is so critical in the fight with cancer).
    3) PDL1 on cancer cells.

    Even armed with anti PD1, a T cell works on one cancer cell at a time. Patients who previously treated with chemo therapy generally have weaker anti tumor immune response. These could mean less number of cytotoxic T cells. If tumor grows faster than the T cells are able to eliminate them, the tumor may appear to be growing. Thus, anti PD1 works best when combined with radiotherapy or target therapy or even chemotherapy. Use traditional therapy to destroy as much tumors as possible, then start on anti PD1 to chase after remaining cancer population.


    **Many cancer patients have swollen lymph nodes, which indicates their immune system detected tumor cells and have activated immune response. These patients should try Anti PD1. On the other hand, if the cancer cells can sneak pass lymph nodes without being recognized, the immune system may not be able to recognize the cancer cells, thus, Anti PD1 may not be effective. The rule of thumb is the more mutation the cancer cells have, the easier the immune system is able to recognize and eliminate them.
  • David
  • Gary, there are currently seven prostate cancer anti PD1/CTLA4 clinical trials going on in the US. Judging by the number of clinical trials, I think the researchers and drug companies are betting that anti PD1/CTLA4 can treat prostate cancer patients.

    Source:
    http://www.cancerresearch.org/prostate-cancer
  • David
  • The following excerpt explains why some patients have no Tumor reactive T cells. Conventional therapies (radiotherapy/chemo/target/surgery) are needed to remove as much tumor burden as possible before starting anti PD1 therapy.

    http://www.sciencedirect.com/science/article/pii/S1074761313002896

    Generation of Tumor-Reactive T Cells

    Dendritic cells (DCs) are extremely important for the coordination of an anti-tumor immune response. As professional APCs, they present tumor antigens to both B cells and T cells, generating an antigen-specific antitumor response. Tumors have a profound effect on the functions of dendritic cells (Gabrilovich, 2004). Defective dendritic cell function is often combined with deregulation of DC maturation, and in humans as well as in mice, tumor-infiltrating cells expressing DC markers also express markers of macrophages and immature monocytes, indicating recruitment of myeloid precursors with incomplete differentiation (Conejo-Garcia et al., 2004). Dendritic cells can have significant heterogeneity both in vitro and in vivo (Hashimoto et al., 2011), and they include resident and bone-marrow-derived myeloid dendritic cells and plasmacytoid dendritic cells. These cells have different functional properties, and they might contribute differently to tumor tolerance or rejection (Kim et al., 2007). For example, although DCs are important APCs, depletion of CD11c+ cells (primarily DCs) can actually inhibit tumor growth (Huarte et al., 2008), an effect that reflects the role of tumor-coopted tolerogenic dendritic cells in establishing tumor tolerance and dissemination (Labidi-Galy et al., 2011 and Sawant et al., 2012).

    Most tumor myeloid DCs present a phenotype of partially mature DCs expressing intermediate amounts of MHC class I and II and costimulatory molecules, as well as high amounts of coinhibitory molecules and immunosuppressive cytokines. In the mouse, such cells are unable to elicit antigen-specific effector T cells (Conejo-Garcia et al., 2004). Human DCs isolated from breast, neck and/or head, and lung cancer patients were also functionally impaired in a mixed leukocyte reaction, and this functional impairment corresponded to a more severe (higher stage) cancer diagnosis (Almand et al., 2000). Immature or incompletely matured DCs might mediate tumor tolerance, inducing anergy of effector T cells and/or expansion of Treg cells in the lymph nodes or at tumor sites (Lutz and Schuler, 2002 and Mahnke et al., 2002).



    Gabrilovich and colleagues were the first to identify vascular endothelial growth factor (VEGF) as a tumor factor capable of impairing both dendritic cell function and maturation from CD34+ hematopoietic precursors (Gabrilovich et al., 1996). Similar observations of defective DCs have since been made in association with VEGF in cancer patients (Della Porta et al., 2005 and Takahashi et al., 2004). VEGF is an important regulator of hematopoiesis, and its artificial overexpression has led to widespread changes in the differentiation of multiple hematopoietic lineages. In patients, treatment with the VEGF-blocking antibody bevacizumab has been shown to reverse DC maturation defects (Almand et al., 2000, Fricke et al., 2007 and Osada et al., 2008). Defective DC maturation that is reversible with VEGF blockade was also found in mouse models (Gabrilovich et al., 1999, Nair et al., 2003, Roland et al., 2009 and Ishida et al., 1998). VEGF most likely exerts effects on dendritic cells beyond its role in the suppression of normal hematopoiesis. Programmed death ligand 1 (PD-L1) is a major negative regulatory ligand of the B7 family that engages the cognate programmed death-1 (PD-1) receptor that is expressed on activated T cells and which transduces a signal that inhibits T cell proliferation, cytokine production, and cytolytic function (Riley, 2009). PD-L1 is expressed on tumor cells, but it is also highly expressed on tumor-associated myeloid DCs in ovarian cancer patients (Curiel et al., 2003). Incubation of blood myeloid DCs with VEGF induced robust expression of PD-L1 on the cell surface, offering a potential mechanism by which VEGF might affect DC function (Curiel et al., 2003).

    A number of other tumor-derived soluble mediators can also disrupt DC function and play critical roles in defining the semi-mature, tolerogenic phenotype of tumor DCs. Such mediators include transforming growth factor β (TGFβ) (Geissmann et al., 1999), interleukin 10 (IL-10) (Steinbrink et al., 1999), macrophage colony-stimulating factor (M-CSF), and IL-6 (Menetrier-Caux et al., 1998). IL-10 also induces PD-L1 expression on DCs (Curiel et al., 2003). Additional mechanisms can contribute to a tolerogenic phenotype for DCs. Physiological stimuli such as hypoxia (Elia et al., 2008) and lactic acid (Gottfried et al., 2006) in the tumor microenvironment can also influence DC phenotype and function. In vitro, DCs differentiated under these exposures tend to have a less mature phenotype, express immunosuppressive molecules such as indoleamine 2,3-dioxygenase (IDO) and prostaglandin E2 (PGE2), and fail to stimulate T cells efficiently (Elia et al., 2008, Gabrilovich et al., 2012 and Gottfried et al., 2006). In particular, PGE2 signaling on DCs can induce the expression of immunosuppressive molecules such as IL-10 (Kaliński et al., 1997) and IDO (Braun et al., 2005), suppress IL-12 production (Watchmaker et al., 2010), and inhibit chemokine expression (Muthuswamy et al., 2010).

    Thus, it is not surprising that in many patients there are no detectable tumor-reactive T cells. For example, in ovarian cancer, tumor-reactive T cells were detected in the peripheral blood of only half the patients tested (Schlienger et al., 2003). The defective phenotype of DCs might contribute further to deregulation of the T cell tumor attack; properly mature DCs that express costimulatory ligands might be required in the periphery at the inflammatory site to maintain an effective effector CD8+ T cell response (Dolfi et al., 2011), and these are typically absent in the tumor microenvironment. Finally, defective DCs fail to secrete appropriate chemokines that play a critical role in recruiting effector cells to tumors (Muthuswamy et al., 2012). As described above, disruption of normal DC function is an essential component of tumor-mediated immune suppression that leads to tumor immune tolerance, and strategies aimed at relieving this immune suppression or generating potent DC-vaccines ex vivo are an active area of research that has already enjoyed some early success.
  • David
  • 上面的醫學報告 相信很難懂 簡單的說就是
    在腫瘤附近的樹突細胞(myeloid DCs)都是抑制免疫反應的
    腫瘤會分泌介白素M-CSF TGFβ IL-10 IL-6 影響腫瘤附近的樹突細胞的成熟
    讓它們不但不能起動免疫反應 反而抑制免疫反應
    你能夠想像這些樹型細胞表面長出PDL1嗎?
    真的是異型! 造成免疫系統對癌症識而不見
    有50%的卵巢癌患者測不出有抗癌的T細胞
    原因就是腫瘤收買了樹突細胞
    所以腫瘤都是抑制免疫反應的
    若是病人沒有抗癌的免疫反應
    第一步就是要用放化療標靶摧毀或縮小腫瘤
    再用Anti PD1會比較能看到 效果
    卡特總統 的 腦瘤是用放療除去的
    Anti PD1幫助卡特總統 的免疫系統清除剩餘的癌細胞
  • 阿城
  • 衛福部在限制什麼?
    這麼好的免疫療法.連英美日等先進國家已列入癌症治療重要一環.甚至將它SOP化.
    連大陸醫療品質差台灣一節的.都已經在想辦法.積極投入這領域.
    衛福部官員到底在顧忌什麼
    真的搞不懂------------------------------------------------
  • 訪客
  • 卡斯伯雖然離開,卻留下如此豐富資訊,非常感謝。有可能長期化療,造成卡斯伯血管壁變薄。如果早在化療初期同步實施免疫療法,那時身體免疫力還很高,也許就不一樣結果。誠如阿城的意思,衛福部要有擔當,過去細菌病毒的疫苗也非一開始就成功,所以不要有太過保守,希望我們正奮鬥的,繼續努力推動免疫療法早日立案成功,這是對卡斯伯最好的願望之一。
  • 是的,革命尚未成果,同志仍需努力,我們會一直努力不懈的!~Karen

    卡斯柏 於 2016/04/07 09:33 回覆

  • 悄悄話
  • Martin Chen
  • 可以給我你及日本醫師的電話及email 嗎?
    已經到無路可走的地步
    希望能看到一一線曙光

    我的電話0960035868. email : maotingchengmail .com
  • 不好意思回覆晚了,您可以跟聯絡lazarsfeldgmail .com, 感謝您

    卡斯柏 於 2016/08/04 22:25 回覆

  • sonyjapan371
  • 您好。
    請問台北榮總也有可以咨詢免疫療法的窗口或是門診嗎?
  • 您好, 台北榮總目前若有免疫療法應會公告在台灣藥物臨床試驗資訊網:http://www1.cde.org.tw/ct_taiwan/archive1.html, 可以用關鍵字搜尋看看, 日後有任何問題也請至台灣癌症免疫細胞協會粉絲頁私訊詢問~感謝您

    卡斯柏 於 2018/03/19 13:36 回覆

  • 悄悄話