這幾天Cincia電訪一位肺腺癌四期抗癌成功的戰友 - 藍媽媽,她的聯絡方式是一位熱心的鄭姐所提供給我,也曾在戰友見面會分享過自身的案例,激勵了許多正在奮戰中的癌友。電話接通後,另一頭傳來的是元氣十足的聲音,讓Cincia完全想不到藍媽媽已經71歲了,還"曾經"是癌症四期的病患。

是的,藍媽媽早已經痊癒了,目前僅每三個月回台大拿慢性病(高血壓)的藥物,而癌症方面,醫師安排每六個月的胸腔和腦部CT檢查追蹤。肺腺癌四期能夠痊癒,又是個振奮人心的真實案例啊!

hope_by_burythereckless-d6vz97y


抗癌鬥士:藍媽媽(現年71歲)

抗癌資歷:11年前確診,當時60歲

病情概述:

馬偕健檢時照出乳房和肺部有陰影,原以為自己罹患乳癌,因更年期吃荷爾蒙藥物,罹患乳癌風險提高。更進一步檢查後,乳房的陰影僅是水泡,反倒是胸腔斷層照出左右肺各有一顆腫瘤(左肺0.7cm & 右肺3.6cm)。

右肺腫瘤穿刺切片,確診為肺腺癌,左肺小顆腫瘤也用內視鏡切除,病理分析結果兩邊腫瘤細胞一樣,表示癌細胞已經移轉到對側肺葉,判定為第四期。

身體完全沒有任何不舒服症狀,咳嗽、胸痛通通沒有。

治療院所:台大 / 余忠仁 主任(手術:胸外李元祺主任)

治療歷程:標靶+手術

當時健保給付的第一線治療僅化療,若要採用標靶治療得自費。當時數據資料,化療對30~50%病患有效,而標靶僅15~30%。

余主任告訴藍媽媽,可能只剩下3~6個月的時間,家人為了不讓藍媽媽承受化療的痛苦,決定自費吃標靶藥物(艾瑞莎,要價一仟多元/顆,一天一顆)。當時也沒有檢驗是否為EGFR突變,真的好像站在命運的十字路口讓你自己選擇。幸運的是,正當藍媽媽和家人決定自費吃艾瑞莎時,恰好艾瑞莎剛好有臨床試驗的計畫,於是藍媽媽開始當起了白老鼠。

艾瑞莎效果很好,藍媽媽的腫瘤短期內就明顯縮小了,可想而知她的心情是雀躍不已的。

沒想到吃了兩周後,藍媽媽的肝指數飆高到200U/L多,差點要被退出研究計畫,幸而藥廠後來允許她改變劑量,由每天服用一顆改成兩天服用一顆,加上余醫師開立保肝錠給她吃,雙管齊下的做法,肝指數終於降到70U/L。

罹癌本身從沒有讓藍媽媽感到不舒服,反而是藥物副作用讓她吃足了苦頭。黑色素沉澱讓她的外表看起來像中毒的人,背部長滿整片痘痘,因抓癢常導致襯衫血跡斑斑,還不時有便祕和腹瀉輪替著。

吃艾瑞莎快2年,腫瘤由3.6cm縮小至1.2cm,之後就穩定不再縮小。這時藍媽媽向主治醫師詢問是否可開刀切除剩下1.2cm的腫瘤,雖然余主任表示不贊同,但也建議她可以去諮詢胸腔外科的意見,於是藍媽媽去找了李元祺主任。李主任評估後認為可以手術,於是藍媽媽便手術切除了剩下那顆1.2cm的腫瘤。

術後藍媽媽繼續吃艾瑞莎。共吃了3年多(or 4年?藍媽媽有點忘了),她覺得每個月回診有點麻煩,再加上覺得自己已經被醫治了,故主動向醫師提出停吃藥物的要求。停吃藥物意味著退出研究計畫,以後如果要再吃艾瑞莎就得自費了,但她還是決心停藥。

迄今癌症再也沒有復發過,當時副作用所留下的黑色素沉澱也恢復得差不多了。

<抗癌心得>

藍媽媽覺得自己在花甲之年罹癌算幸運,因為自己已經退休,沒有工作上壓力,加上孩子已經成家,自己煩惱相對少很多。統計上每四個人就會有一人罹癌,家裡人口四人(丈夫、兩個女兒),依比例是會有一人罹癌,藍媽媽表示其他家人罹癌她都很難接受,所以她以感恩的心去看待自己罹癌的事情。

放寬心、樂觀的心很重要。

『喜樂的心乃是良藥;憂傷的靈使骨枯乾。』(聖經-箴言17:22)

<飲食方面>

沒忌口,甜點也照吃,但有少油、少鹽、少醃製食品,吃新鮮食物。

保健食品幾乎都沒有吃,只有一開始喝過2、3箱安素,但太甜後來也放棄了。

<生活作息/運動>

因藍媽媽腿部不方便運動,故以甩手功和伸展操等緩和運動為主。


這個案例和之前林大哥、于鴨鴨的例子都有個共通點,腫瘤都屬於大顆但個數少的型態;果然總蔡主任說的沒錯,瀰漫型(滿天星)的腫瘤型態真的是比較棘手,目前還沒有痊癒的案例,最佳的狀況就是與之和平共處,好吧!革命尚未成功,同志我們繼續努力吧!!

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創作者介紹

星希亞的抗癌日誌

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  • FA0500
  • 真的很開心看到這個消息, 祝福藍媽媽, 星希亞, 及所有仍在努力的癌友
    加油!!
  • 對阿! 我每次聽到四期可以痊癒都覺得很振奮!! :)

    Cincia 於 2016/08/05 09:10 回覆

  • 胃出血
  • 個人容易因為某些小事或過去的事鬱鬱寡歡..喜樂的心..恩~~~向藍媽媽跟星希亞看齊..星希亞面對驚滔駭浪的心猶如航空母艦..馬上來去書櫃拿本卡內基來複習一下
  • David
  • Cincia 加油 妳的癌細胞穩定(至今無抗藥性) 只要想辦法讓藥進腦
    妳也會痊癒的
  • David
  • 如果當初藍媽媽的家人相信應該用反應率高的化療
    藍媽媽後來會怎樣呢?

    化療反應率高卻極其傷身 病人越化療 免疫力越差
    最後許多人因感染而離開的

    可以做手術 放療 標靶 免疫
    唯獨化療 要考慮清楚
    一旦開始化療 你的身體會越來越虛弱 癌症也會越來越猖狂
  • David
  • PS. 醫師只會告訴病人化療反應率高 比較有效
    有多少醫師告訴病人 一旦開始化療
    病人的身體會越來越虛弱 癌症也會越來越猖狂?


  • 其實也不一定啦! Kim姊就一直是採用化療,已經超過5年了。
    因為她也沒有基因突變,所以過去也沒有其他治療方式,不過她最近很幸運開始打PD-1,希望她會是那個有效果的病患。

    Cincia 於 2016/08/05 10:00 回覆

  • David
  • The Sad And Shocking Truth About Chemotherapy

    http://www.sarahbesthealth.com/shocking-truth-about-chemotherapy/

    Someone who has been a part of my life for the last 15 years died today, at the age of just 66.

    Not wishing to invade his family’s privacy, I will refer to him only as G.

    G was diagnosed with cancer a year ago and was “treated” with repeated bouts of chemo.

    I feel incredibly sad and angry right now, knowing that G put his faith in orthodox medicine and continued to trust he was getting the best “treatment” available as he was pumped full of deadly poison day after day – with precisely nothing done, at any time, to actually support the health of his body.

    I’m not saying his cancer could have been cured. I don’t know whether it could have. But the best modern medicine had to offer him (in common with so many patients) was intravenous administration of extremely hazardous substances (more on that below) and that, to me, is a travesty.

    Chemotherapy. Chemo“therapy”? The term itself is rather a confusing misnomer.

    It’s not therapy – a word whose dictionary definition is “a treatment intended to relieve or heal a condition”.

    Poison can’t heal. Can it relieve?

    Chemo is capable of killing cancer cells, so it can shrink tumours – though often only in the short term.

    But it also kills healthy cells so it can (and often does) destroy the immune system (many who die during chemo die of relatively minor infections their body could not fight), and cause organ failure, internal bleeding and death (to name just a few of its common side effects).

    In G’s case, initial scans showed the tumour shrinking, but within a few months the cancer had spread like wildfire, as happens so often, and as I wrote about here.

    For several reasons, this outcome is not in the least surprising.

    First, chemo drugs are such toxic and dangerous substances that if a spill occurs in a hospital, it is considered a major biohazard.

    No member of hospital staff must go near the spill unless they’re wearing full protective clothing, and the incident must be reported.

    In fact, to illustrate just what a big deal a chemo spill is, here is the University of Toledo’s “Hazardous Materials Spill Procedures” document. On pages 3 and 4 you can read its elaborate 18-point procedure for dealing with a spill of “chemotherapeutic hazardous materials”.

    Sorry if I’m nit-picking here, but “therapeutic hazardous”? Isn’t that a rather obvious oxymoron?

    One reason chemo agents are treated as biohazards is that they cause serious burns if spilled onto skin.

    Anyway. The toxic, hazardous substance that is the subject of the 18-point emergency health and safety protocol linked to above is the same substance that is injected into the veins of sick patients.

    I’ll leave you to ponder how logical that is, how likely it is to be in the best interests of the patient, and how in keeping it is with the Hippocratic Oath “First, do no harm”.

    I’ll tell you what I think.

    As chemo is so widely administered to cancer patients, yet also so deadly, it is my belief that more people die of chemo than of cancer itself.

    Here is another reason I believe that.

    Recent research identified a compound in chemo drugs that fuels cancer growth.

    Yes, really.

    It found, specifically, that repeated bouts of chemo can cause healthy cells to secrete a protein – WNT16B – that helps cancer cells to grow, invade surrounding tissue and resist chemo treatment.

    In lab tests, scientists observed an up to 30-fold increase in WNT16B production in response to chemotherapy.

    So now we know that when cancer suddenly starts growing and spreading more aggressively after chemo – as so often happens – that is not only due to chemo’s ability to quickly ravage the immune system, but also because chemo causes healthy cells to start churning out a chemical that accelerates cancer growth.

    This research was published in August and you’d hope that it would lead to chemo being used a lot more judiciously.

    But in fact that should have happened at least 20 years ago.

    That was the time at which a landmark review of the evidence around chemotherapy for advanced cancer, conducted by a leading epidemiologist and biostatistician, showed it to be a useless treatment in the majority of cases.

    In the late 1980s Ulrich Abel contacted 350 medical centres around the world and asked them to send him anything they had ever published regarding chemotherapy for advanced cancer, and also reviewed and analysed thousands of articles published in medical journals.

    In a 1990 interview in German magazine Der Spiegel, Abel commented that chemotherapy for advanced cancer is “a scientific wasteland” and its overall success rate “appalling”.

    His paper, Chemotherapy of advanced epithelial cancer – a critical review was published in 1992. In it, Abel concluded that “there is no direct evidence that chemotherapy prolongs survival in patients with advanced carcinoma” (cancer). (Note: the term “epithelial” encompasses all of the most common cancers, which account for at least 80% of cancer cases.)

    He wrote that: “Many oncologists take it for granted that response to therapy [i.e. initial tumour shrinkage] prolongs survival, an opinion which is based on a fallacy and which is not supported by clinical studies”.

    If you’re reading this because you or a loved one is trying to decide whether to have chemotherapy, my advice would be, do your research.

    Cancer patients are often made to feel by their doctors that if they refuse the chemo recommended to them, they are taking a big risk with their health.

    But they are often not told enough about the big risk they are taking by having it.

    There are cases where chemo is indicated; please don’t think I’m saying otherwise.

    But (1) it is overused, and (2) regardless of whether chemo is or isn’t indicated, all cancer patients need to be on a diet and lifestyle regime which supports their overall health and immunity, yet that’s something else you’re unlikely to hear from your doctor.

    Ben Goldacre’s new book Bad Pharma – which I reviewed here – is about the worrying influence of pharmaceutical corporations on medical research and practice.

    The book shows that “evidence-based medicine” is not in fact reliably “evidence based”. Other interests are coming first and large numbers of patients will continue to suffer and die needlessly until it stops.

    G was wealthy enough to afford the best treatment money can buy, and I find it indescribably sad that he died believing he’d had that, when he’d in fact had nothing of the kind.

    Like so many before him, he did what his doctors told him to because he believed that they knew best and that if there was anything that could be done for him, they would be doing it.

    The whole thing is tragic beyond words.
  • 訪客
  • 謝謝Cincia為大家收集正面的例子,打強心針,這真是好重要

    但這裡有點小小的困惑.....
    關於(腫瘤都屬於大顆但個數少的型態;果然榮總蔡主任說的沒錯,瀰漫型(滿天星)的腫瘤型態真的是比較棘手..............................................)

    應該是說在手術可行性上,腫瘤個數少,比較有施作的可能!..另外應該和大小,位置也有關係吧! 所以應該是在鏢鈀和化療外多一種選擇,而非比較簡單.
    另外...那對化療 和 鏢鈀 反應不好的來說.腫瘤數量少也是挺麻煩的,不就也只能一搏手術嗎...?

    另外,現在是不是所有的有效療法..都連結到基因.基因天註定,那真是不太可逆.只能找出更多的潛在基因吧!


  • 訪客
  • 看目前分享的五個案例,化療+標鈀是共同點,所以正規治療,放下對副作用的恐懼.是很重要的
  • 不管用什麼方式治療,這些案例最大的共通點都是"病患本身是很樂觀的",所以想要戰勝癌症,正面的心態絕對是第一步。

    Cincia 於 2016/08/05 16:05 回覆

  • 訪客
  • 不是很明白,為何持續標靶仍轉移腦也不算是抗藥?除了是腦屏障問題,還有其他理據嗎?
  • 因為對原位癌還是控制得很好啊! 腦部就像你講的,我的藥物因為血腦屏障的關係進不去大腦(正確說法是進入的比例很低),所以大腦的腫瘤才會一直長。
    但如果是移轉到其他部位去,就算出現抗藥性了。

    Cincia 於 2016/08/05 16:02 回覆

  • 黃媽媽
  • 請問妳之前做全腦放射期間 是否同時有吃實驗的藥?
    還是暫停 等結束放射治療後再吃
    家人有相同情況 請解惑 謝謝
  • 計畫規定放療中和前後都要暫停喔!

    Cincia 於 2016/08/05 15:59 回覆

  • Gary YC LIN
  • 真的好希望 星希亞 Lynn姐 Kim姐 彭彭 田田… 大家都能像這位藍媽媽一樣,邁向痊癒之路,大家繼續當一輩子的好朋友。 一起加油喔! ^_____^
  • 沒錯,我們要當很久很久的朋友。:)

    Cincia 於 2016/08/12 14:26 回覆

  • 唉
  • 給五樓。
    正因為Kim姊已經接受了化療,即使目前她現在用兩種PD-1藥物正在搶救她的肺腺癌轉移腦部的腫瘤,也是沒用的,因為受過化療的人體免疫系統與沒接受過化療的免疫系統是差很大的,也就是PD-1的效果會差很多。因此Kim姊的勝算是很低的。從她目前反應的頭痛現象就可以觀察出,因為PD-1的副作用並不會造成腫瘤部位的疼痛,很明顯她的頭部疼痛是腫瘤的擴散與變大造成。簡單講化療就是飲鳩止渴,短期內雖然腫瘤抑制住但最終仍會反撲。
  • Kim姊有蔡主任照顧,我們樂見她的PD-1治療成功,一起為她加油和禱告吧!:)

    Cincia 於 2016/08/12 14:27 回覆

  • David
  • 唉先生 在Cincia這裡討論別人病情是不尊重人的行為
    請自重
  • 唉
  • 給13樓
    Kim姊的病情是她部落格自己公開給大家看的,若她不想讓陌生人看到或討論,大可設定為只限好友可看。討論病情是希望能有其他能人願意出手提供救命之方,若這裡只能討論參加誰的告別式的話,那部落格也可以關了。
  • Mimi792
  • 這一篇不是想要鼓舞士氣的嗎?別忘了雁行應該是互相鼓勵扶持的精神。Kim姐格子裡灑脫樂觀的態度鼓舞了無數的病人和家屬,我由衷的欽佩和祝福她。
  • me too, 被Kim姊鼓舞到了~繼續往前飛~

    Cincia 於 2016/08/12 14:29 回覆

  • 訪客
  • 我覺得暱稱會取 " 唉 " 的,應該是個悲觀的人.別理他
  • 唉
  • 給16樓的訪客。本來我想保留不想說太多了,怕大家太難過。既然你說我悲觀。哈~那我就直說不忌諱了。Kim姊因頭痛的關係用了大量的類固醇,但用大劑量的類固醇時,就會抑制身體的免疫功能,與她使用的兩種PD-1免疫藥物形成了相剋作用,故進入了死胡同。她自己也應該直覺感到大限已近,所以把握時間回顧了她的人生。我說的是事實,既然妳認為我悲觀不用理我也無妨啦,你可以再樂觀一點沒關係~有時候無知反而是一種幸福~
  • 我們都不是醫生,我相信蔡主任會給Kim姊最合適的治療,我們衷心期盼PD-1對她產生效果。:)

    Cincia 於 2016/08/12 16:57 回覆

  • Andrew Chen
  • 目前免疫療法還有很多未知的領域需要再進一步研究, 一些最新的研究結果, 跟我們既有的觀念完全不同:

    * 化療後數週, 有更多的T細胞在腫瘤的微環境中 => 利用化療或立體放射治療破壞癌細胞, 吸引T細胞, 增加免疫檢查點阻斷劑的效果:
    https://www.statnews.com/2016/08/04/combination-cancer-treatments/
    Biologists in England recently got an inkling of that. Researchers led by Frances Balkwill of Queen Mary University of London compared 54 women with serious ovarian cancer who received standard chemotherapy (carboplatin or paclitaxel) before surgery to six who did not. In the women treated with chemo, there was significantly more activation of the kind of T cells that attack cancer cells than in the other six, the scientists reported in June in Clinical Cancer Research. “There is a belief that chemotherapy suppresses the immune system, but weeks after treatment, we found lots of T cells in the tumor environment,” Balkwill said.

    * 服用類固醇對免疫治療的效果影響不大:
    http://www.uptodate.com/contents/toxicities-associated-with-checkpoint-inhibitor-immunotherapy?source=search_result&search=nivolumab&selectedTitle=5~38
    Impact of immunosuppression on efficacy — The need for immunosuppressive therapy to manage irAEs does not appear to affect the response to checkpoint inhibition.
    The most extensive data come from a study in patients treated with ipilimumab for advanced melanoma. A single-institution experience analyzed the incidence of irAEs and treatment outcomes in 298 patients treated with ipilimumab (3 mg/kg) outside of a clinical trial setting [3].
    ●IrAEs were seen in 254 patients (85 percent), and 103 patients (35 percent) required corticosteroids. Anti-tumor necrosis factor-alpha therapy was used in 29 cases (10 percent) who did not respond promptly to corticosteroids.
    ●The median overall survival was 16.5 months, and the estimated two-year survival rate was 39 percent for the entire cohort. Overall survival was the same in patients who had an irAE compared with those without an irAE, and there was no difference between those requiring corticosteroids and those not requiring immunosuppressive therapy.
    ●The time to treatment failure, defined as the need for alternative therapy or death, was 5.7 months for the entire cohort. As with overall survival, there were no significant differences between those with and without an irAE or between those treated with corticosteroids and those not receiving corticosteroids.
    IrAEs are significantly less frequent with the anti-PD-1 antibodies. Any possible correlation between PD-1 blockade efficacy and treatment of irAEs may be harder to establish. Nonetheless, it does not appear that immunosuppression to treat PD-1 blockade toxicity affects outcomes. In a study of 576 patients with melanoma pooled from nivolumab clinical trials, the objective response rate in patients treated with immunosuppression was 28.8 percent (median duration of response was not reached), and the response rate in patients who did not receive immunosuppression to treat a side effect was 32.3 percent (median duration of response was 22.0 months) [4].
  • 安
  • 給17樓的,人要有人性、慈悲心,才有資格當人。
  • 訪客
  • 醫學上這不叫相剋,是擇優.免疫藥物的作用即使在美國這,目前也是且戰且走,未知領域還很多,不走進死胡同,就不會找到出路.
    在這裡如果你未獲得允許,公開(或引用)討論某人的病情,更別說是揣謀推測某病患的心情與想法,那是非常嚴重的罪.
    說風涼話並不灑脫,無知是一種幸福always,樂觀是最好的處方,對重症病患,樂觀代表他對他的人生與家人的愛.
  • 訪客
  • 給,唉,你以為你是神,上帝嗎?沒人能知道自己跟別人生命的長度,你這種人……滚
  • 唉
  • 給19樓。有時候有慈悲心的人反ˊ而被當作沒慈悲心。無知的人卻被當作有慈悲心。有人游泳快淹死了卻沒人看到,有人指出來有人將淹死了,眾人卻將指出的那人當作沒慈悲心。在岸上搖旗吶喊加油的人卻被當作有慈悲心。我若沒有動了惻隱之心,犯不著浪費時間回應。算了,世道炎涼,劣幣驅逐良幣,我不想在這裡再發言了。最後留個訊息給 Kim姐當祝福吧。請自行GOOGLE:
    adverse events with immune checkpoint
    不是我不幫妳,這世界有太多的阻力需時間解決~
  • Andrew Chen
  • 免疫療法還是有很多未知的地方需要進一步研究, 一些最新的研究結果跟既有的認知不同:

    * 化療後數週, 有更多的T細胞在腫瘤的微環境中:
    www.statnews.com/2016/08/04/combination-cancer-treatments/
    Biologists in England recently got an inkling of that. Researchers led by Frances Balkwill of Queen Mary University of London compared 54 women with serious ovarian cancer who received standard chemotherapy (carboplatin or paclitaxel) before surgery to six who did not. In the women treated with chemo, there was significantly more activation of the kind of T cells that attack cancer cells than in the other six, the scientists reported in June in Clinical Cancer Research. “There is a belief that chemotherapy suppresses the immune system, but weeks after treatment, we found lots of T cells in the tumor environment,” Balkwill said.

    * 類固醇可以降低免疫的副作用, 對免疫治療的效果影響不大
    www.uptodate.com/contents/toxicities-associated-with-checkpoint-inhibitor-immunotherapy?source=search_result&search=nivolumab&selectedTitle=5~38
    Impact of immunosuppression on efficacy — The need for immunosuppressive therapy to manage irAEs does not appear to affect the response to checkpoint inhibition.
    The most extensive data come from a study in patients treated with ipilimumab for advanced melanoma. A single-institution experience analyzed the incidence of irAEs and treatment outcomes in 298 patients treated with ipilimumab (3 mg/kg) outside of a clinical trial setting [3].
    ●IrAEs were seen in 254 patients (85 percent), and 103 patients (35 percent) required corticosteroids. Anti-tumor necrosis factor-alpha therapy was used in 29 cases (10 percent) who did not respond promptly to corticosteroids.
    ●The median overall survival was 16.5 months, and the estimated two-year survival rate was 39 percent for the entire cohort. Overall survival was the same in patients who had an irAE compared with those without an irAE, and there was no difference between those requiring corticosteroids and those not requiring immunosuppressive therapy.
    ●The time to treatment failure, defined as the need for alternative therapy or death, was 5.7 months for the entire cohort. As with overall survival, there were no significant differences between those with and without an irAE or between those treated with corticosteroids and those not receiving corticosteroids.
    IrAEs are significantly less frequent with the anti-PD-1 antibodies. Any possible correlation between PD-1 blockade efficacy and treatment of irAEs may be harder to establish. Nonetheless, it does not appear that immunosuppression to treat PD-1 blockade toxicity affects outcomes. In a study of 576 patients with melanoma pooled from nivolumab clinical trials, the objective response rate in patients treated with immunosuppression was 28.8 percent (median duration of response was not reached), and the response rate in patients who did not receive immunosuppression to treat a side effect was 32.3 percent (median duration of response was 22.0 months) [4].
  • Andrew哥讚啦!!:)

    Cincia 於 2016/08/12 16:58 回覆

  • 訪客
  • 唉 - 在我們的lab中,最忌諱自以為是,那會阻礙創新,在死胡同中鑽不出來.所以對新的領域,我們都不會僅以過去的經驗(學識)來評斷.
    你講的大家都懂(也不必勞煩谷歌了),問題是以現今的醫療技術,你有別的建議嗎?
    相信你不是台灣的醫療人員,台灣的醫學倫理(Medicine ethics)課程也沒哪麼差啊!
    應該不會這樣來評斷病患病情的!!!!
    傳統上認知類固醇會降低免疫反應,但它與近年來分子免疫藥物間會有何交互作用,這沒定論(不同器官vs不同免疫療法),現在我們由臨床實驗中第一線醫師的用藥處置反饋中,去逐漸建立模式,"前人種樹,後人乘涼".
    人體是奧妙的,很多新藥與療法,常是試驗(治療)過程中無意發現的.如果我說樂觀的心情會誘發免疫反應,你相信嗎?
  • 十分中肯的言論!!推~

    Cincia 於 2016/08/16 18:15 回覆

  • 胃出血
  • 推19..22.23樓對自以為是的人的回應..看到IQEQ....生活與倫理..公民與道德..是國小課本捏..怎麼那麼多人不懂
  • 我們不要為了少數奇怪的人壞了自己的好心情,正面的態度是抗癌的第一要務,繼續開心過日子吧!

    Cincia 於 2016/08/16 18:14 回覆

  • David
  • Andrew 關於化療會引發新的免疫反應
    我以前也有看過類似報告 也在Cincia這裡報導過
    http://www.cell.com/trends/cancer/pdf/S2405-8033(15)00009-6.pdf
    不只化療 任何破壞腫瘤微環境的治療 放療 冷凍療法 都有類似作用
    然而這些T細胞最終會被腫瘤附近的調節型T細胞, MDSC, Tumor associated Macrophage, Tumer associated DC cells 所抑制
    而這些抑制型的免疫細胞 共同特色是都有PDL1
    若是在放療化療後能輔以anti PD1 or anti PDL1治療
    好像好不容易起的火種 給與適時的呵護 將會成為遼原大火
    總節一下
    Anti PD1 anti PDL1免疫治療 需要搭配 放療 化療 或冷凍療法
    先破壞腫瘤微環境 激起免疫反應 會比較有效
  • 感謝David分享。:)

    Cincia 於 2016/08/16 18:10 回覆

  • David
  • 8/5/16 Opdivo 做為一線藥品治療肺線癌實驗未達標 宣告失敗

    我簡單說明這項實驗失敗的意義:

    1) 除非病人驗出是PDL1 positive 不建議使用Anti PD1 anti PDL1做為一線藥品
    2) 對於PDL1 negative 的病人Anti PD1 anti PDL1不適合做為一線藥物
  • 同為Anti PD1藥物,Keytuda可以用作第一線用藥。

    Cincia 於 2016/08/12 17:02 回覆

  • Tiffany
  • 我的母親當初也是第四期肺腺癌併肋膜積水,治療到今年邁入第七年。
    而今年,自己的低劑量電腦斷層也出現0.6公分的東西,等待三個月後的追蹤中。
    想想外公、母親都是肺癌,自己中獎的機率大概八九不離十,但我並不悲觀。
    Cincia提供的這些成功經驗真的是一劑強心針,積極的面對、治療,保持心情愉快,才是成功抗癌的不二法門。
  • 令堂也是抗癌前輩,請教一下目前的治療方式是?還是已經痊癒了啊?
    Tiffany真的很鎮定,三個月後一定不會有問題的,加油!!

    Cincia 於 2016/08/11 13:08 回覆

  • 阿姨
  • 這裡討論是開放的 大家必須尊重他人看法,
    聰明人也要看不同意見,不認同跳過不看就好。
    但這裡怎麼老見到幾個人不爽就圍剿一個人的情況。

    大家都有40,50和60以上年紀,
    我們又不是笨蛋,我們會分辯,
    美化的假像 難道我們看不出來?

    不要當笨蛋,別人塞什麼給你都說對,
    生病了 更要當聰明人," 一定要多看不同說法"。
    人家要賣書 當然有她的做法。
    不要跟著別人猛拍馬屁
    別人活 不代表你也能活。

  • 1. 阿姨可能沒搞清楚,Blog是個人的網路空間,就跟FB個人頁面網頁相同,都是屬於私人所有,並不是開放的討論版面。
    2. 大家都有40,50和60以上年紀-->阿姨年紀較長,Cincia還沒40歲,不要把我變老啦!
    3. 什麼美化的假象阿?這點我真的不懂,如果是說上面的抗癌成功個案,那是該病友親自口述,Cincia打成文字而已,完全沒有美化喔!我可以請當事人出來見證。
    4. 我同意你說的,一定要多看多聽不同的看法,但最重要的,自己本身要有足夠的智慧來判斷。
    5. 人家要賣書 當然有她的做法-->我的做法是什麼啊?
    跟我熟識的朋友都知道,Cincia出書不是為了賣書賺錢,我有一份穩定且收入不錯的工作,不需要靠賣書來賺錢,事實上賣書也賺不到多少錢,就幾萬塊吧!我只是單純想要完成自己的心願清單,鼓勵更多的癌友正面看待罹癌這件事,所以我也不在乎銷售量(只希望出版社不要賠錢就好)。

    最後,可以請你不要再來留言了,我日後看到就會直接刪掉,以免影響我和其他人的好心情。

    Cincia 於 2016/08/11 10:47 回覆

  • 胃出血
  • 不是圍剿一個人..是圍剿你..其他人也應該知道你一直換名一直亂..前幾篇就有啦..我想星希亞是不會被你影響的..但是我生氣了..有沒有勇氣挑戰我啊..阿姨唸快一點就是唉
  • 你好聰明喔!我都沒發現"阿姨"念快一點跟"唉"很像耶!
    厲害厲害~
    我還想說什麼時候又出現一個阿姨?哈哈!!

    Cincia 於 2016/08/11 09:58 回覆

  • TK
  • TK是新viewer, 我去年四月腦開爐把right frontal tumor 3.6cm 割除, 現又長0.5CM
    brain meta 是2013 發現. 在 左枕葉 0.5-0.7-1.1cm後 沒長 但現似乎長一點
    2011 肺腺癌術後只吃2個月友復, 從未有放/化療, Cincia 有質子治療資訊嗎? 在考慮長庚 謝謝你提共分享
  • 我有去長庚放射科找王俊傑醫師諮詢過,他是說單顆大顆的腫瘤比較適合質子治療,建議你還是將影響資料帶去給醫師看最準。

    Cincia 於 2016/08/16 17:48 回覆

  • 阿姨
  • 我跟這位"唉"是不同人。

    我是年紀50的癌病友。
    留言是說出多年抗癌看法,
    沒想汙衊別人或拍馬屁或講假話。
    一把年紀了,幹麻改暱稱。

    小朋友們,得癌和抗癌,
    切記,切記,
    一定要多了解不同看法,不要只想聽好話,
    壞的消息 其實智慧就在裡面。
    (阿姨不想迎合版主
    又不想拍版主小姑娘馬屁 她可能會把我刪了)
    大家平安。平安。


  • 阿姨不想迎合版主又不想拍版主小姑娘馬屁-->我也沒有期望大家這樣做啊!
    真的不知道你哪來這樣的認知,年齡和智慧果然不一定成正比啊!XDDD

    Cincia 於 2016/08/12 14:25 回覆

  • yayadragon
  • 我媽媽也吃了六個月的妥復克
    目前腫瘤大小控制在一公分以下
    而且只有右肺有腫瘤
    如果狀況穩定,可不可以去要求台大的廖醫師
    讓我媽媽用手術摘除右肺的腫瘤呢
    可是這樣問醫師,他會不會回說
    這是聽誰說的
  • 哈哈~廖醫師確實有可能這樣問,你就說聽癌友分享的就好啦!

    Cincia 於 2016/08/12 14:20 回覆

  • 阿罵
  • 負面的,病友與家屬都清楚,不是不想聽,是不需要.
  • 放寬心吧~我們一起加油!:)

    Cincia 於 2016/08/16 17:45 回覆

  • 紫藍
  • 星妹妹你好,我是紫藍,一年前有過來留言。我很謝謝妳,光只是看看妳的文章,知道一些訊息,給我很大的鼓勵。真的很感恩!就像iherb買保健品也是從妳這邊學到的。在生病這段過程中,經歷很多很多,我已經快2年了(9月確診的)。正面的訊息與力量,是多麼的難得:-)相信大家都有同感妳所帶給大家的!感恩您!
  • 不用這麼客氣啦!癌友當然要彼此分享資訊阿!一起飛才能飛得更好更遠....大家一起加油!:)

    Cincia 於 2016/08/16 17:41 回覆

  • 訪客
  • To: yayadragon
    建議直接徵詢胸腔外科,如以上病例:內科余主任表示不贊同開刀切除, 胸腔外科李元祺主任評估後認為可以手術,內外科醫師意見可能不同。不過李主任已經過世,請諮詢其他胸外醫師
  • 建議可以找胸外的陳晉興主任諮詢看看喔!

    Cincia 於 2016/08/16 18:03 回覆

  • Gary YC LIN
  • 為星希亞鼓鼓掌,義正嚴辭,回覆得好啊! ^_____^

    說得沒錯:Blog是個人的網路空間,是屬於私人所有,並不是開放的討論版面。有些來亂的,不懂得為客之道,請你們不要再來啦!
  • 謝謝Gary大哥的支持,最近都有一些奇怪的人來亂,我要去廟裡拜拜了。

    Cincia 於 2016/08/16 17:37 回覆

  • 路人K
  • 星希亞我很欣賞妳在逆境中的正向心情,那是不容易的,很多人經歷多次治療,都會對副作用恐懼焦慮,但妳卻一直正向,我是妳的忠實讀者,我只希望妳能一直寫布落格,我也很喜歡看第四期抗癌成功的例子,我知道藍媽媽有辦一場小型演講也有邀妳參加!
  • 感謝路人K的鼓勵,我會再繼續收集案例的,也希望版友如果有認識四期抗癌成功人士,可以分享給Cincia,讓我可以去聯絡採訪他/她。

    Cincia 於 2016/08/16 17:31 回覆

  • 胃出血
  • 神啊~~請您輕拂那治癒之手
  • 治癒我們吧!Please~

    Cincia 於 2016/08/16 18:03 回覆

  • David
  • #32 yayadragon 腫瘤都都是抑制免疫反應的 放在身上是個禍害 能除就除
    如果可以 用電腦刀除去更好 免去開刀的危險
  • 如果腫瘤只是一兩顆的話,我應該也會考慮除掉吧!

    Cincia 於 2016/08/16 18:04 回覆

  • David
  • Annals of Oncology

    Nov 2015

    Successful treatment with an anti-PD1 antibody for progressive brain metastases in renal cell cancer

    We present the case of a woman age 54 with clear-cell renal cell cancer, who developed metastases in multiple organs including one brain metastasis. She was treated with pazopanib and the solitary brain metastasis was irradiated with 30 Gy in July 2013. In February 2014, after 8 month treatment with pazopanib, this metastasis increased in size and two new brain metastases were detected. Whole brain radiotherapy was performed leading to a cumulative dose of 52.5 Gy at the site of the gyrus cingula metastasis.

    The patient was subsequently treated with bevaciumab for progressive cerebral oedema interpreted as radiation-induced brain necrosis. Upon systemic and central nervous system (CNS) progression 5 months later, treatment with axitinib was started – achieving partial response. However, after 4 months, in March 2015, further systemic and CNS progression was documented.

    Treatment with pembrolizumab (Keytruda) was initiated. Pembrolizumab was chosen due to off label availability at a time when no anti PD1 or anti PDL1 antibody was licenced in Europe. After four infusions, the patient experienced complete resolution of lung metastases, stabilization of other metastases. Importantly, regression of all brain metastases was documented on MRI. This excellent response was seen despite continued steroid use of 4 mg dexamethasone/day and is still ongoing after 7 months of treatment.

    http://annonc.oxfordjournals.org/content/early/2015/12/24/annonc.mdv581.extract
  • 小芳
  • 提供個人經驗:
    5年前健檢發現左上肺有1個2公分的腫瘤(有切片確認是肺腺癌)
    右中肺1個0.5的腫瘤左下肺有很多陰影
    醫生斷定是四期
    打了5次化療,吃了4年的艾瑞莎
    後主治建議我開刀
    但諮詢了同院的外科主任,得到的是不贊同的意見
    他說為什麼四年前不開現在要開
    再諮詢了他院2位胸腔外科醫生,均說可以開
    胸腔鏡,只開了一個5至6公分的口
    開刀後檢驗我左上肺那一顆腫瘤是1B
    右上與右中的小節結追蹤觀察就好,若有變大再開刀
    至今已經7個多月了,期間沒有再做任何治療
    應該是健保不給付1B者吃吧

    以個人的經歷建議
    多諮詢幾個醫生,能開刀一定要開刀
  • 感謝小芳的分享,也祝福妳從此不用再治療。:)

    Cincia 於 2016/08/16 17:28 回覆

  • 過來人
  • 小芳若五年前就手術了 很有可能手術後無需化療與標靶
    若有多顆 需先分辨是多發或是轉移 前者是第一期只需手術 後者是第四期 天地之差 所以建議多顆的病友先看外科
  • 小芳確實有可能兩邊腫瘤都是原生的,並非轉移,當初醫師有兩邊都切片化驗嗎?

    Cincia 於 2016/08/17 12:20 回覆

  • David
  • NSCLC 用Anti-PD1? 還是化療?

    The U.S. Food and Drug Administration (FDA) has approved anti-PD-1 drugs for melanoma (nivolumab and pembrolizumab) and squamous non-small cell lung cancer (NSCLC—nivolumab). Along with the PD-L1 antibody atezolizumab, these drugs are expected to be FDA approved for some other cancers fairly soon. These treatments are superior to chemotherapy, but still, they do not work for all patients.

    Expression of the protein PD-L1 on tumors has been thought to be a good predictor of a patient’s response. However, none of the three FDA approvals mention expression of PD-L1 as a prerequisite for prescribing these drugs. Attempts to figure out the prognostic significance of PD-L1 are at their peak, though it is not yet clear what lies beyond. Nonetheless, it is of obvious importance: there is no compelling reason to give these very expensive drugs to patients who are not likely to benefit from them.

    Here is a very brief history of this complicated connection: in 2012, the very first sensational publication reported on the activity of nivolumab in three different cancers. The study looked at PD-L1 expression in about 15% of patients who participated in the clinical trial. Of 17 patients with PD-L1-negative (no PD-L1 detected) tumors, none had a measurable response, whereas 9 of 25 patients (36%) with PD-L1-positive tumors responded. This report certainly put PD-L1 at the center stage of anti-PD-1 development, but it was only the beginning.

    Numerous following trials have reported that the efficacies of pembrolizumab (Keytruda) and nivolumab (Opdivo) indeed correlate with expression of PD-L1, but only to a degree. For example, in the KEYNOTE-001 trial, patients whose lung tumors had high levels of the PD-L1 protein had a response rate of 45%, but 10% patients whose tumors tested negative for PD-L1 also responded.

    Even the anti-PD-L1 drugs in development, atezolizumab (previously known as MPDL3280A) and durvalumab (MEDI4736), do not show a strict dependence on the presence of their target PD-L1 in tumors, as would have been expected. Across several tumor types, responses to these drugs have been observed more often in PD-L1-positive tumors, but also in a lower proportion of PD-L1-negative ones.

    Three years later, there is still no consensus regarding the value of PD-L1 expression in NSCLC as a predictive marker of response. Across the board, positivity for PD-L1, while predictive of response, does not always guarantee it, and lack of PD-L1 does not exclude response. Obviously, one must conclude that PD-L1 is just one of several (many?) factors that determine the likelihood of response. To compound the PD-L1 problem, there is a lack of defined criteria about what ‘PD-L1-positive tumor’ really means:

    The criteria used to define the PD-L1 status of a tumor biopsy differ vastly. In trials of nivolumab, the cutoff used is 1% to 5% of positive cells in a biopsy. For pembrolizumab, the cutoff is 1% to 50%! And for atezolizumab it is 1% to 10%.
    Different companies in the checkpoint drug business use PD-L1 reagents from different commercial sources to measure its levels and, without doubt, these different reagents have different sensitivities.
    Possibly the most confounding factor is that PD-L1 expression in tumors is not stable: not only can it be confined to different parts of tumors, but it can appear and disappear, depending on treatments and other poorly understood influences.
    Leading clinicians agree that they would give anti-PD-1 drugs to patients with metastatic lung cancer or melanoma regardless of PD-L1 status, according to FDA guidelines. At the same time, many ongoing clinical trials testing these drugs group patients based on PD-L1 expression, or simply exclude patients without PD-L1 expression in their tumors.

    Right now, PD-L1 is just not a good enough biomarker to exclude patients from receiving an anti-PD-1 drug, because even PD-L1-negative patients derive more benefit from PD-1 blockade than from docetaxel (a standard chemotherapy drug). If patients with PD-L1-negative NSCLC have a 10% to 12% chance of a meaningful response, they may be strongly inclined to receive a PD-1 or a PD-L1 blocker rather than going for a harsh conventional chemotherapy that may provide only a short-lived response.

    One more problem is that most trials with checkpoint blockers only accept PD-L1-positive patients. This not only deprives patients from potentially life-prolonging treatment, but precludes a meaningful analysis of what determines the possibility of response in patients with PD-L1-negative tumors.

    A recent study conducted a meta-analysis of 20 trials (1,475 patients) with nivolumab, pembrolizumab, and atezolizumab in NSCLC, melanoma, and genitourinary cancers. It looked at correlations between the presence of PD-L1 on tumors and patients’ responses. Significant differences were seen in NSCLC and melanoma, but not genitourinary cancers. Ignoring the different cutoffs for PD-L1 expression in different trials, responses were observed in 34.1% of PD-L1-positive and 19.9% of PD-L1-negative patients who were treated with nivolumab and pembrolizumab. This difference is obviously significant, but not tremendous.

    Excluding PD-L1-negative patients from trials of immune checkpoint inhibitors appears to be a fallacy. Ignoring many other possibilities, it is entirely probable that because of the shortcomings of reagents, and the elusive nature of PD-L1, many PD-L1-negative tumors may be ‘false-negative‘; they really do express enough PD-L1 to respond to immune checkpoint drugs.

    https://www.cancercommons.org/2015/09/09/to-pd-l1-or-not-to-pd-l1-that-is-the-question/
  • David
  • Lung cancer—in particular, non-small cell lung cancer (NSCLC)—in young people is a topic of great interest. It has been made even more so by the recent publication of a study in The Journal of the American Medical Association (JAMA) that analyzed over 2,000 NSCLC patients of all ages and resulted in two major conclusions: First, that younger patients (less than 40 years old) have a higher frequency of targetable mutations. Second, that they have relatively poor survival when compared to older patients, except those older than 70 years.

    所有病人
    EGFR 26%
    ALK 5%
    KRAS 27%

    40歲以下的病人
    EGFR 32%
    ALK 19%
    KRAS 9%

    https://www.cancercommons.org/2016/03/29/lung-cancer-in-younger-patients/
  • David
  • ASCO 2016 highlights

    EGFR-mutant NSCLC

    At the meeting, which took place from June 3–7 in Chicago, a special panel of experts generally agreed that there is not much difference between the first-generation EGFR inhibitor drugs erlotinib (Tarceva), gefitinib (Iressa), and afatinib (Gilotrif). This interchangeability suggests there are several good choices for first-line treatment of EGFR-mutant non-small cell lung cancer (NSCLC).

    Another hot topic was the use of liquid biopsies. The same panel of experts discussed the role of liquid biopsies in diagnosis and treatment follow-up, with a particular focus on EGFR-mutant lung cancer. The U.S. Food and Drug Administration (FDA) had already approved the cobas EGFR mutation liquid biopsy test earlier this month, but the panel was still divided over whether testing tumor DNA isolated from blood is a good enough substitute for a standard tumor biopsy. Obviously, liquid biopsies are no substitute for an initial diagnostic biopsy, but the availability of this technology for follow-up is a great advantage.

    However, the panel had no disagreements about third-generation EGFR inhibitors. Several promising ones are in clinical trials, and trial results presented at the ASCO conference showed these drugs’ activity in tumors with an EGFR T790M mutation (T790M frequently arises as a resistance mutation in the EGFR gene after treatment with erlotinib or other inhibitors). However, newer T790M inhibitors will have a tough time competing with osimertinib (Tagrisso). The FDA approved osimertinb late last year, and it has excellent activity that will be hard to beat. Osimertinib is also active in leptomeningeal disease, a dangerous condition in which metastatic cells grow inside the spinal and meningeal space.

    NSCLC with ALK translocation

    Brigatinib, a second-generation ALK inhibitor, was reported at the meeting to be highly active in ALK-translocated NSCLC. In a clinical trial, 72% of patients who stopped responding to the first FDA-approved ALK inhibitor, crizotinib (Xalkori), had objective responses to brigatinib. The median duration of responses in this group was 14.5 months, and longer in patients who had not received crizotinib previously. Most encouragingly, patients with brain metastases had a similarly high rate of responses to brigatinib (67%).

    https://www.cancercommons.org/2016/06/16/lung-cancer-highlights-from-asco-2016/
  • 小芳
  • 只有左上肺大顆的有切片,其他的太小切片不好切 取樣也不準,
    ,我一直有兩個疑惑,多發與轉移,以目前的醫學能否判斷出來?
    良性與惡性在不切片的情形,能否判斷出來?
    剛開始的斷層顯示左下肺有一堆陰影,後來卻不見了,也不知道那是什麼,主治也沒告訴我,每次回診只針對大顆的情況,告訴我穩定中 沒有變化 持續吃藥,
  • David
  • 癌症要透過血液淋巴結才能遠端擴散
    腫瘤到後期因為缺氧會經由血管淋巴尋找殖民地 
    轉移通常在淋巴結血液可以驗出癌細胞
    期數都是由病理師決定 病理師都是很有經驗的
    良性與惡性不切片無法判定
    左下肺陰影可能是腫瘤引起的慢性發炎

  • 過來人
  • 要手術後病理檢查才可確定分期 所以我會一直建議多顆的病友看外科
    手術取下每個節結與做淋巴結廓清
    1. 病理檢查每個nodule是良性或惡性,若是惡性 每顆種類是否相同,如肺腺癌 (AC)或肺泡癌 (BAC)?基因突變種類是否相同?越是不同越好
    2. 取出淋巴結檢查是否有癌細胞? 若都沒有,應該就沒轉移
  • 23
  • 手術取下每個節結與做淋巴結廓清,在外科手術上不知道做不做的到,畢竟有些很微小,有些靠近主動脈O不過我倒覺得是還好先化療再標靶有發揮清除癌細胞及使腫瘤縮小並局限在肺部,最後再手術拿掉,健檢時發現-運氣好,勇於接受治療-有智慧,遇到好醫生最後願意幫忙開刀-人緣好,天時地利人和,這種CASE不常見,很多人檢查出來想說一期而已,切除只願追蹤,而不願做預防性化療,結果一年後,肺積水,轉移變第四期,癌細胞跑全身就不妙了,這種痊愈的例子不常見,不過如果是我也會選擇這樣的治療
  • 陳琬涒
  • 能請問你吗?我媽媽肺腺癌 因電療 食慾很不好 如果我想弄蔬果汁給他喝 (不是不能吃生食吗?)我該怎弄阿??
  • 有化療嗎?不然是可以吃生食的喔!
    如果有化療,就把蔬菜先川燙過,水果削皮,就沒有問題啦!

    Cincia 於 2016/08/24 22:07 回覆

  • 丫頭
  • 請問,本文能分享到臉書抗癌戰友會嗎?
    謝謝您
  • 當然可以囉!:)

    Cincia 於 2016/08/31 13:11 回覆

  • 丫頭
  • 謝謝!!
  • :)

    Cincia 於 2016/09/04 17:35 回覆