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上個月回診時,原本打算跟廖醫師講要自費多安排一次腦部MRI檢查,沒想到還沒有開口,廖醫師就說:「我幫妳安排增加腦部斷層檢查,我看剛好4月下旬妳要去照胸部&腹部斷層,就一起吧!顯影劑也不用打兩次。

WOW! 這算是心有靈犀嘛?在我還沒有說出要望前,廖醫師竟然已經幫我都處理好了,這不是我的守護天使是什麼呢?

「不過CT不是比較不精準,這樣沒問題嗎?」我問。

「CT當然準確度沒那麼好,但我們的目的只是要確腫瘤有沒有惡化,所以如果連CT都顯示沒有,當然也用不著處理囉!」廖醫師回答。

這樣一說挺有道理的,好像也不一定要用MRI檢查,除了省事還省下了自費檢查的錢,真是一舉兩得啊!

於是,就安排4/25進行頭部+胸部+腹部CT檢查。


4/27回診,一見到廖醫師就知道事情不妙了......

我已經訓練到可以從他臉部的表情來猜測檢查結果,這天是嚴肅的一張臉,果然就不是太好的消息。

「廖醫師,腦部狀況如何?」我問。

「嗯...不大好耶!我們追蹤的那顆腫瘤又長大了。」廖醫師邊打開影像資料邊回答。

「那這次變多大了啊?上次(3月初)你說1cm左右。」我繼續問。

「差不多1.4cm左右。」廖醫師回答。

「不過MRI和CT的片子可以直接這樣比較嗎?」我又問。

「兩個片子都是同一個人判讀的,應該不會有問題」廖醫師說明。

「第三代ALK標靶藥物試驗計畫出來了,今天剛公佈,但妳資格不符合,因為收案條件要1cm以上的腫瘤(腦部除外),你現在肺部的腫瘤根本就快看不到了。」廖醫師又說。

「所以我也不能停吃我現在的標靶,看肺部腫瘤會不會長回來對吧!」我失望地問。然後廖醫師丟給我一個:妳在想什麼的表情!現在的藥明明就把肺部腫瘤控制那麼好,妳想停吃是怎樣?

「不過那個藥副作用挺恐怖的,有人吃了還差點崩潰自殺。」廖醫師說。

天啊!雖然藥物可以進到腦部,但讓人崩潰也太恐怖了吧!

(Andrew哥協助查了這個輝瑞的藥,應為Iorlatinib,代號是PF-06463922)

「所以現在除了放療也沒有其他辦法了對吧!」我無奈地問。

「是啊!只能用電腦刀處理。腫瘤成長速度算快,現在不處理,愈大顆再處理可能產生的副作用更大,妳等一下就過去找許醫師吧!」廖醫師說,語畢立即撥電話給許醫師,告知等會我會過去找他諮詢。

接下來當然我就是出現在放射科門診......


許醫師應該也早就已經看過片子,看到我就說:「所以妳準備好要處理了嗎?」

「好像也沒有別的選擇。」我苦笑著回答。

「那我們會儘快幫妳安排,先要做更精密的MRI檢查(一般追蹤的MRI是5mm切片,放療要切到1mm),然後再來安排電腦刀的時間」許醫師說。

「那劑量是?」我問。

「如果打一次的話差不多要用20Gy,也可以分開打,分三次的話,一次打10Gy,副作用會比較小」許醫師解釋。

「副作用會像上次全腦放療一樣嗎?」我接著問。

「會小很多,基本上應該只會有疲憊感而已。」許醫師回答。

(不過去年全腦放療時,許醫師也是說得很輕鬆,但我卻頭暈了一個多月,這次的可信度???)

「我上次有跟妳說過,如果要做電腦刀的話,除了最大顆那個,我會一起把其他看的見的腫瘤打掉。」許醫師補充道。

留下聯絡電話給護理師後,就回家等候通知了。


看來全腦放療後藥物進入腦部的濃度還是有限......

腦部腫瘤真像打不死的蟑螂,到底怎樣才能根除呢?  

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  • Lo
  • 再加油,任何困難都可以克服的
    第二次頭香
  • 會的,我會努力加油!!

    Cincia 於 2016/04/29 08:51 回覆

  • 三三阿姨
  • 加油~~約會抱抱
  • 先抱一下。。。

    Cincia 於 2016/04/29 08:51 回覆

  • 林宗緯
  • 神一樣的大姐姐
  • XDDD

    Cincia 於 2016/04/29 08:51 回覆

  • 悄悄話
  • 悄悄話
  • ling0037301
  • 加油,加油。記得你是小強(蟑螂)般頑強啊!
  • 哈哈~你還記得我朋友說過的話喔!
    沒錯,我會有小強般堅忍的意志力,絕對會跟癌細胞奮戰到底。

    Cincia 於 2016/04/29 09:36 回覆

  • Hsinfu Huang
  • 您好,日本有做量子軟膏,抹在患部的外面例如頭皮上,軟膏上的太赫茲波會從塗抹處向內照射10公分的範圍(肉眼看不到的光波),癌細胞受到太赫茲波照射就無法增值。癌細胞不會凋亡,但時間一久會被弱化。軟膏完全沒有副作用。我頭痛就抹頭皮,眼花就抹眼皮,效果很快顯現。我女兒內耳前庭發炎昏眩抹在耳朵四周5分鐘就不會昏眩。
  • 這聽起來也是很唬爛,怎麼可能塗個軟膏就可以抑制癌細胞增生,我打了放療都沒有用了。
    你不會真的相信吧!=.=

    Cincia 於 2016/04/29 09:10 回覆

  • Hsinfu Huang
  • 去年8月31日日本和歌山太地町的一家診所的太赫茲量子波莢艙始動,有四名癌友接受治療,在30分鐘內有三名癌細胞當場消失。另外一個比較嚴重的,隔一天再次治療癌細胞也完全消失。
    到今年1月聽說已經有200多位日本癌友體驗奇蹟。
    真想帶人去試試是不是真的。
  • 一聽就覺得是騙人的啊!根本不用花時間去研究吧!
    如果有效的話那個醫師就可以得諾貝爾醫學獎了啦!

    Cincia 於 2016/04/29 09:08 回覆

  • Peter From Toronto Canada
  • I will pray for you,
    hope you are ok with this!
  • 謝謝!我相信我會一切沒事的。
    只是可憐我的小腦袋瓜得忍受放射線一再的摧殘...Q_Q

    Cincia 於 2016/04/29 09:11 回覆

  • 胃出血
  • 心情會陰陰的 , 今晨又放晴了 , 可以去跑步加曬太陽....就是臉跟脖子防曬其他地方不塗....這次感覺是轉機
  • 希望這次是最後一次掃黨行動了。
    今天天氣好好,真不想上班,看著窗外好想去曬太陽啊!

    Cincia 於 2016/04/29 09:12 回覆

  • lin
  • 加油
    兵來將擋,水來土淹
  • 我會加油的。繼續努力!:)

    Cincia 於 2016/04/29 09:12 回覆

  • nini
  • 一定會戰勝的,套一句「太陽的後裔裡劉時鎮的台詞」
    「這麼困難的事,我一向都能做到」
    所以,關關難過,關關過,Cincia 加油~
  • 謝謝nini的鼓勵,沒錯,我都能克服啦!
    只是哀傷我的腦袋一再受到放療的摧殘,嗚嗚~希望這次真的可以一舉殲滅敵軍。

    Cincia 於 2016/04/29 09:19 回覆

  • 新莊小剛
  • 加油,一切順利。我目前也是肺部乾淨,腦袋等待5月MRI檢查在要決定如何處理。
  • 希望你5月腦部MRI順利過關。:)

    Cincia 於 2016/04/29 09:22 回覆

  • Mrs. Rabbit
  • 一定會順利的!!!加油
  • 謝謝鼓勵,Cincia會繼續加油的。

    Cincia 於 2016/04/29 09:35 回覆

  • Ploe
  • 加油 你肯定可以的啦!!你在我心中一直都是創造奇蹟的!
  • 嗯嗯~我也相信我自己,哈哈^^Y

    Cincia 於 2016/04/29 09:35 回覆

  • Hsinfu Huang
  • 我準備在台中榮總附近設一個陶板浴體驗點,以水素水及UP1製家庭用陶板浴完全免費讓化療中的癌友將化療的副作用降到最低。

    抹在我身上的東西效果如何我自知。

    只不過您可以參考這個部落格
    http://16296315.at.webry.info/
    森鈴さん寫的
    我學到很多東西。

    特別是要注意太赫茲光波,1兆赫的頻率會和身體內的水分共振,修復細胞DNA
  • 如果說降低副作用我覺得還有可能,但你說要靠擦藥膏就可以抑制癌症發展,聽起來就很荒謬。
    "抹在我身上的東西效果如何我自知。"-->你應該沒有癌症吧?

    Cincia 於 2016/04/29 09:39 回覆

  • 訪客
  • 要挺住啊!
  • 我沒事的!!^^Y

    Cincia 於 2016/04/29 11:07 回覆

  • David
  • 頑強的敵人那篇 Cincia 把全腦放療形容為地毯式轟炸
    我當時在想 沒有一場戰爭是可以只靠空中轟炸贏的
    一定要地面部隊深入敵軍陣營 進行一對一的巷戰
    這個地面部隊 指的是Cincia 的免疫系統

    電腦刀造成大量癌細胞死亡 會激起妳的抗癌免疫反應
    若造成局部水腫 會吸引免疫細胞進入腦內
    所以吃好睡好 準備戰鬥吧!

    記得如果有水腫 盡量不要用類固醇
    用類固醇 會再次給腫瘤喘息的機會 重新壯大
    在腫瘤微環境 形成抑制免疫的保護傘

    機會只有一次好好把握

    還有建議妳去問問林成龍醫師 看看他有些什麼建議


  • 林醫師我去年有去找過他了。

    Cincia 於 2016/04/29 11:07 回覆

  • Ploe
  • 有回台灣再跟你約出來聚聚囉
  • 好唷!等你!!

    Cincia 於 2016/04/29 11:05 回覆

  • Lin
  • 你好,希望你能繼續加油
    一定可以有好消息的
    腦部真的是最難的挑戰,藥物難以進入放療又擔心後續效果

    另外第三代的ALK臨床的消息是否沒在臨床試驗資訊網張貼呢
    不知道有沒有更詳細的消息能夠分享
    謝謝您!

    祝福 順利
  • 因為才新公佈的,可能還沒有放上去吧!
    我知道的都寫上去了,建議可以詢問主治醫師看看,醫師通常會拿到第一手消息。

    Cincia 於 2016/04/29 11:06 回覆

  • Jhsu
  • 我沒腦轉移的經驗可貢獻。您可以加入 www.smartpatients.com use the tag lung cancer + brain mets.

    國外(大部分美國)病人間的經驗分享。
  • Thanks~有空再來看看。:)

    Cincia 於 2016/04/29 11:08 回覆

  • peichen
  • 加油!戰勝腫瘤!
  • 感謝!!^^

    Cincia 於 2016/04/29 11:11 回覆

  • deepsea926
  • Dear Cincia,

    腦部腫瘤真的非常難纏,雖然我沒有做過全腦放射,但做過2次加馬刀,也許跟電腦刀可能有些不同,但把我的經驗提供給妳參考。

    第一次做加馬刀時效果非常好,2顆全消。但第二次做,3個月後追蹤腫瘤完全沒有反應,還多了很多顆親朋好友,後來追蹤了幾個月,那幾個親朋好友們越來越壯大,神外醫生建議轉放射科全腦放射。

    因為剛好化療無效改吃標靶妥復克,我詢問醫生做全腦後是否會因血腦屏障打開讓藥物更容易進入腦?
    醫生的回覆是,雖然會打開,但只有一小段的時間。後來我決定不做全腦放射把賭注放在妥復克上。3個月後腫瘤縮小,6個月後MRI影像上已縮小到看不見。雖然心理很清楚看不見不代表不存在,但至少能多撐個幾次每3個月一次的MRI檢查穩定沒變化就賺到了。

    希望妳這次電腦刀能將腫瘤全部殺光,戰勝腫瘤,一起努力吧~
  • Dear deepsea,
    妥復克本來就是可以進到腦裡面的,不會被血腦屏障所阻礙,但我的藥進不去阿!
    你根本不需要去管血腦屏障的問題,一定可以進去的啊!你醫師的回覆怪怪的唷!

    Cincia 於 2016/04/29 16:28 回覆

  • ura
  • 希望您手術順利
  • 謝謝鼓勵!

    Cincia 於 2016/04/29 16:28 回覆

  • 路人K
  • 真是令人擔心,電腦刀完成,後續要吃什麼藥控制?希望妳順利度過
  • 繼續吃我原來的標靶藥物啊!因為它對於原位癌還是控制得很好。

    Cincia 於 2016/05/03 10:24 回覆

  • 悄悄話
  • 憂
  • 趕快進行免疫療法吧,再用電腦刀玩打地鼠的遊戲是沒意義的。美國前總統卡特的腦癌先前用電腦刀也是對一直蔓延的腦部癌細胞沒輒,最後只好用免疫療法Keytruda才解決了腦癌,讓腦癌消失。為什麼你要重複他失敗的經驗呢?他採取了有效的方式,而妳卻還在用過時電腦刀傷害生活品質的沒意義老法,實在不解。在水中快淹死時趕緊爬上巨人的肩膀上不是能救命嗎? 所謂忠言逆耳,話說得蠻重的,希望妳聽進去啊!
  • 我用了免疫藥物就要放棄原本的標靶,如果我對免疫藥物沒有反應,我也吃不回原本的標靶(除非自費,一個月20多萬),沒那麼多本錢可以吃很久。

    Cincia 於 2016/05/03 10:27 回覆

  • 光芒萬丈
  • 一般人經常以為只有高血壓、高血脂、高血糖的病患才會腦中風,雙和醫院神經內科主治醫師陳致中表示,放射線治療可能傷及正常血管,導致血管內膜受損,產生斑塊與狹窄的情形,也就是未來血管容易破裂。所以電腦刀並不是妳所以為的只是頭暈撐過就沒事,其實妳的腦血管在經過全腦放療與多次電腦刀後,腦血管內膜已受損,產生斑塊與狹窄即容易破裂,此情形為不可逆。腦血管一旦破裂或阻塞就會被稱為腦中風。
    之前戰友Caspar之所以最後血管破裂而死的遠因正是因為接受了放射線治療所致,他的醫師也告訴過他及他的太太再次接受放射療法就可能血管破裂。我想妳可以問問許醫師就很清楚放射療法的這個不廣為人知的潛在炸彈。
    更不用說放射療法也是很多癌細胞的產生原因,最終妳將無法清楚辨識妳腦中的癌細胞究竟是之後放射療法所致的癌細胞還是原本妳肺腺癌所轉移過來的。
  • Sandy
  • 妳ㄉ廖醫師是不是沒有開放掛號 ??
    因為腫瘤科沒看到他的名字ㄝ。

    這麼多朋友給Cincia 加油,
    大家都想聽到Cincia 的好消息。
    ( 利用些時間,穿短袖短褲去曬曬太陽20~30分鍾
    要曬到皮膚,對癌症絕對有幫助。)


  • 沒錯,廖醫師已經不開放掛號了。
    謝謝你的關心喔!我已有努力在曬太陽,希望讓身體產生更多的維生素D。

    Cincia 於 2016/05/03 10:29 回覆

  • Sandy
  • 我之前癌症持續骨轉移,
    持續吃抗賀爾蒙藥跟打補骨針都沒有效控制住。
    後來實在骨痛的受不了,
    有時痛到沒法睡覺。
    就試試穿短褲短袖去曬太陽(活命為先,放棄美白)。
    冬天也把袖子褲管捲起來曬太陽(30分鐘),
    持續二年下來 骨痛變少 骨頭黑點沒再增加,
    甚至更早之前的黑點竟消失了。

    曬點陽光對癌細胞有些微抑制作用,
    (陽光中的維生素D)
    Cincia 跟大家朋友試試。


  • David
  • Understanding Jimmy Carter’s Surprise Cancer Turnaround: A Conversation with Jedd Wolchok

    https://www.mskcc.org/blog/understanding-jimmy-carter-s-surprise-turnaround-conversation-jedd-wolchok

    Can the combination of radiation and immunotherapy work together in a synergistic way to provide added benefit to patients?

    There is that possibility. The hope is that when you kill a tumor with a tool like radiation therapy, you release cell debris that can trigger an immune response — similar to a kind of vaccination. Then, by blocking an immune checkpoint — in this case PD-1 — you allow that immune response to really take off.

    Are there times when it’s not possible to receive immunotherapy because of brain metastases?

    We have a lot of issues yet to settle here. We know that the same medicines that can have a favorable effect on disease outside of the brain can have a favorable effect in the brain. There was a clinical trial that I participated in and published in Lancet Oncology about two years ago that looked at ipilimumab treatment in melanoma patients with brain metastases.

    The challenge with brain metastases is that sometimes patients require corticosteroid treatments [which can suppress the immune system] to control swelling and symptoms. In the trial I referred to, the benefit of ipilimumab was seen only in the patients who were able to come off corticosteroids. So that’s an important consideration.

    That’s why it’s good to do exactly what Mr. Carter’s physicians did, which was to control the brain metastases to the best of their ability — in this case with stereotactic radiosurgery — get him off the steroids as quickly as possible, and then initiate the immunotherapy.
  • David
  • Dr. Andrew Sloan, director of the Brain Tumor and Neuro-Oncology Center at University Hospitals Case Medical Center in Cleveland, said scientist have only recently understood how “tumors recruit the immune system.”

    “Tumors have figured out how to turn off the immune system,” Sloan said in an interview with ABC News when Carter first announced his diagnosis. “They recruit cells that surround them. ... These are not cells that kill the tumor. They protect cells from part of the immune system.”

    Drugs like pembrolizumab work by keeping the immune system from turning off. Dr. Leonard Lichtenfeld, deputy chief medical officer for the American Cancer Society, said such therapies, first presented in 2010, were the first new drugs for melanoma since the 1970s.

    http://abcnews.go.com/Health/remarkable-cancer-treatment-helped-jimmy-carter-combat-brain/story?id=37467459
  • Hsinfu Huang
  • 我幫您跟UP1石井會長商借一台UP1家用陶板浴,幫您提高體溫1℃,增加血流,自律神經變為副交感神經優位讓您可以很放鬆,改善睡眠。
    不用錢的,您願意試試看嗎?
    據說可以增加治療效果,保護正常細胞。
    您如果願意的話,我跟石井會長談,
    6月份石井先生會來台灣拜訪我。
  • 如果可以免費出借的話,嘗試看看當然好啊!我也不會有損失。

    Cincia 於 2016/05/05 22:44 回覆

  • 胃出血
  • 在我看來..減肥..投資...癌症..這三種資訊最為複雜..前兩項真的不難...但癌症那資訊真的是眼花撩亂...30分鐘內3名癌症患者癌細胞當場消失...應該會上各國新聞頭條吧.....唉...我連估狗都很懶
  • 這我當然也覺得很荒謬,但體溫升高確實對癌友而言是好的沒錯。

    Cincia 於 2016/05/03 10:30 回覆

  • Sandy
  • Cincia 我讚成樓上一些朋友ㄉ看法,
    腦怎能放射再照下去 !!! 又還能再照幾次咧 !!!
    妳目前現在的治療已是瓶頸。

    妳還年輕 經濟金錢也沒顧慮,為什麼不替自己找活路 ?!
    為什麼不到國外 日本或美國,去試最新的治療方式。
    妳真的好好想想。

  • 忍不住的潛水訪客
  • 無良的商人,請你離開這個園地吧!罹患癌症不表示智商會變笨。
  • 悔
  • 用電腦刀等放射療法來消滅癌症,就好比提油滅火一樣,最終終究徒勞無功死路一條。廖醫師嚴肅的一張臉,就已經告訴你最終結果是什麼,只是妳逃避罷了。若電腦刀真能解決妳的腦部腫瘤他大可開心地告訴妳。他也很清楚妳的剩餘時間不多了,只是不忍心對妳明講而已。妳應該趕緊去搜尋全台灣或國外的免疫療法,盡快著手進行療程,因為妳腦部腫瘤的進展速度很快,不容許妳再到處玩浪費僅存不久的生命。甚至我覺得都已經到這地步了,現階段妳應該把工作辭掉,因為汽車廠(保養廠)相較於其他地方,車子進出的頻率及妳會吸到廢氣量會來得多很多,儘管妳只是單純做市場行銷。因為處在房子內一房間告訴別人妳不吸菸,卻看著其中一個房間有人抽菸仍是會免不了吸進二手煙的。對比沒有任何人吸菸的房子,從外界來看妳仍是處於有人抽菸的房子,只是妳沒儀器可偵測心理覺得沒什麼差異罷了。我們行業這種有專業儀器偵測的,很快就測出來差異了。雖然待在其中一間房間沒人抽菸但卻希望沒有吸到任何其他房間有人抽菸所產生的二手煙想法。下這種賭注是毫無勝算的,畢竟空氣無國界。
  • 你講的好像自己是廖醫師肚子裡的蛔蟲一樣,廖醫師嚴肅的臉只是因為有狀況了,並沒有覺得我剩下的日子不多老嗎?目前不選擇免疫療法的原因我已經寫在上面了。
    ps.我在汽車業上班並不是在汽車廠,工作地點是在辦公大樓,沒有你所謂的汽車進進出出。

    Cincia 於 2016/05/03 10:37 回覆

  • Bubu
  • 我的阿姨前陣子在美國被檢查出肺腺癌
    到了最近媽媽才告訴我阿姨的病情
    我總是告訴阿姨跟媽媽要樂觀把心敞開
    既然無法改變那就接受然後作戰跟病毒共處
    在今天看到你的部落格
    希望你的狀況能保持好好的喔!
    加油加油!
  • peter
  • 樓上的不要再澆冷水了,相信星希亞會沒事的,加油,相信自己
  • 悄悄話
  • 放心
  • 你的書才出版,通常作者都要混個9年以上。
    先要慶賀肺部的腫瘤根本就快看不到了,後續無論何種治療,仍然做好該做的飲食及養生,早餐可能多吃固體食物,現階段減少用腦,每天看笑話幽默文章。
  • David
  • 由下面anti PD1治療NSCLC 的各種實驗數據
    你可以發現anti PD1在化療(或放療)後使用
    反應率大增至33%至47%
    這是因為一部份病人(33%)在化療或放療後
    大量死亡的癌細胞 激起對癌症的免疫反應
    化療或放療破壞腫瘤微環境 讓腫瘤抑制免疫反應的能力降到最低
    化療或放療後 緊跟著進行anti PD1 成功率大增
    數字會說話

    http://www.cancernetwork.com/sites/default/files/figures_diagrams/1411kimTable5.gif
  • David
  • Nivolumab

    To assess combination strategies, investigators have launched a large phase Ib multiarm combination study, CheckMate-016. Nivolumab plus ipiliumab was tested in a randomized study with different induction doses (nivolumab 3 mg/kg plus ipilimumab 1 mg/kg [N3+I1] or nivolumab 1 mg/kg plus ipilimumab 3 mg/kg [N1+I3], followed by nivolumab 3 mg/kg every 2 weeks for both arms. N1+I3 had a higher frequency (26%) of treatment-related adverse events leading to discontinuation, including elevations in lipase and alanine transaminase, diarrhea, and pneumonitis. The ORR was 43% (95% CI, 21.8–66.0) in the N3+I1 cohort and 48% (95% CI, 26.8–69.4) in the N1+I3 cohort[29]; these results appear to be more than additive effects. Approximately 80% of these responses were ongoing at the time of data analysis. An additional 24% of patients given N3+I1 and 36% given N1+I3 have achieved stable disease. The 24-week PFS rates were 64% to 65%. In 44 available samples, PD-L1 expression status did not correlate with response. With 1% tumor membrane staining as a cutoff, similar percentages of patients with PD-L1–positive and –negative tumors achieved objective responses (55% and 50%).

    Based on data supporting immune-suppressive effects of vascular endothelial growth factor (VEGF) and FDA-approved antiangiogenic agents for mRCC, nivolumab was tested in combination with either sunitinib (n = 33) or pazopanib (n = 20).[30] Both pretreated and treatment-naive patients responded. Overall confirmed ORRs were 52% (95% CI, 33.5–69.2) in the sunitinib combination arm and 45% (95% CI, 23.1–68.5) in the pazopanib combination arm. As seen with ipilimumab combinations, PD-L1 expression status, regardless of the staining cutoff, did not predict response to combination therapy with either sunitinib or pazopanib. The most common side effects were consistent with known toxicity profiles of these tyrosine kinase inhibitors and included diarrhea, fatigue, and hypertension. Two grade 3 pneumonitis events (3%) were observed.

    http://www.cancernetwork.com/supplements/prospects-targeting-pd-1-and-pd-l1-various-tumor-types/page/0/2#sthash.Giv8A4rZ.dpuf
  • Buenos Dias
  • 我媽也是四期,最近也是要開始放射,相信菩薩會保佑大家一切平安順利的。
  • David
  • 抱歉 #45 資料是Renal Cell Carcinoma 請略過
    NSCLC資料如下:

    兩種免疫治療 anti CTLA4 + anti PD1: 反應率 = 14% to 19%
    化療+ anti PD1: 反應率 = 33% to 47%

    免疫治療在化放療之後進行可以收到最大效益

    Combination studies in NSCLC

    Several combination strategies are being tested in large, multicohort phase I trials. Nivolumab, pembrolizumab, MEDI-4736, and MPDL3280A are being evaluated in combination with chemotherapies, oral epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors, anti–CTLA-4 antibodies, or other targeted therapies.

    Nivolumab and ipilimumab in combination were tested in chemotherapy-naive advanced NSCLC in the ongoing CA209-012 study.[37] At the time of data analysis, 8 of 29 patients (16%) had objective responses. Six of these patients (75%) had ongoing responses at the time of analysis. Most of the responses were seen by the time of the first tumor assessment (10 weeks). In an exploratory analysis based on PD-L1 status, responses were seen in both PD-L1–positive and PD-L1–negative patients, with ORRs of 19% (3/16) and 14% (3/22), respectively.

    The CA209-012 study also tested nivolumab in combination with various platinum-doublet chemotherapy regimens, including gemcitabine/cisplatin, pemetrexed/cisplatin, and paclitaxel/carboplatin. The safety data showed an adverse event profile reflecting the additive toxicities of nivolumab and chemotherapy. No dose-limiting toxicities were seen during the first 6 weeks of treatment.[38] ORRs were 33% (95% CI, 10–65) to 47% (95% CI, 21–73) across all arms. One-year OS rates were 50% (95% CI, 21–74) to 87% (95% CI, 56–96).

    Nivolumab plus erlotinib was tested in 21 patients with chemotherapy-naive, EGFR-mutant, advanced NSCLC.[39] All except one patient had acquired resistance to the EGFR tyrosine kinase inhibitor. The overall ORR was 19% (95% CI, 5.4–41.9). Of 20 patients who had erlotinib resistance, 3 (15%) achieved a partial response. One erlotinib-naive patient achieved a near CR, and all responses were durable beyond 78+ weeks. Nine patients (45%) had stable disease. The most common treatment-related adverse events were rash, fatigue, paronychia, diarrhea, and skin fissures. No pneumonitis of any grade was observed.

    - See more at: http://www.cancernetwork.com/supplements/prospects-targeting-pd-1-and-pd-l1-various-tumor-types/page/0/2#sthash.Giv8A4rZ.uItpb3aH.dpuf
  • Qing Jonse
  • 这次你一定会成功的!我想请教:我现住美国,去年查出肺腺癌四,口服Tarceva。当时脑部转移,我读了你的放疗是全脑,我也选择了全脑15次去年12月31结束。以后医生会诊我要做MRI医生一直说半年才做。我现在也不知道放疗以后脑部的肿瘤怎样?请问你有无症状与你的脑瘤长大?另外查血CEA近一月来逐渐升高,这个是不是药物失效的症状?我现在生活和治疗在美国,因为语言障碍和医生沟通不是很好,他叫怎样做我就做。谢谢你的精神鼓舞了我们!
  • David
  • Combining Radiation and Immunotherapy: A New Systemic Therapy for Solid Tumors?

    anti CTLA4 + anti PD1 併用或是 anti PD1 + chemo 併用都有毒性的問題
    (會讓病人吃不消)
    然而放療(特別是電腦刀)除了局部控制外 能讓腫瘤釋放抗原 激起免疫反應
    增進免疫系統辨識腫瘤的能力

    Cancer immunotherapy has come of age and is becoming one of the pillars, along with surgery, chemotherapy, and radiotherapy, for the treatment of patients with cancer. Combination therapies are also being investigated, including inhibition of both CTLA-4 and PD-1, or use of one immunotherapy agent with chemotherapy or with other molecular-targeted agents. Although such combinations may improve antitumor efficacy, their toxicity may prove to be a major obstacle.

    In contrast, combinations of radiation (preferably stereotactic ablative radiotherapy) with immune checkpoint inhibitors have the advantage that radiation can provide local control and may also prompt the release of tumor antigens that activate immune response and enhance immune recognition on a systemic level.

    http://cancerimmunolres.aacrjournals.org/content/2/9/831.full
  • 翠芳
  • 何不試試浩鼎obi-822 obi-833免疫疫苗,聽說適用於16種癌症,但目前只有乳癌末期進入臨床3期,最近鬧得沸沸揚揚的,徹底去了解一下,搞不好對你有幫助,就在南港.
    www.facebook.com/serenitysjourney 參加臨床者可參考.
  • 抗癌有悔
  • 「我上次有跟妳說過,如果要做電腦刀的話,除了最大顆那個,我會一起把其他看的見的腫瘤打掉。」許醫師補充道。

    許醫師不是說得很清楚了嗎?就像冰山一樣,許醫師只會打"看得見"的腫瘤,冰山海面下的無數癌細胞根本無法打到,也就是說你每隔幾個月就必須做電腦刀來打掉又長出來的腫瘤。問題是只要電腦刀未來再多打個幾次妳就會腦血管爆裂,更糟的是還沒有再多打幾次之前妳大腦的認知能力早因電腦刀無法避免打到正常的腦細胞因而無法避免智力嚴重退化。電腦刀並沒有橫跨空間的能力,也就是放射線束射進妳腦部所有經過沿途路線細胞DNA都會受損破壞(甚至這些被破壞DNA的正常腦細胞再接下來也會演變成癌細胞)。如此重複不斷施作電腦刀終會邁向死亡的結局。大學學理工的妳,難道還看不出現在還不趕快做免疫療法,真的只有等待死亡這種不可避免的結果嗎?。這是任何智商沒問題的戰友都可以預見結局的~ 也不需要醫師或其他人直接告訴妳~苦口婆心無非是希望妳能活下去,但現在再不做免疫療法,等妳之後智力退化就再也來不急了,因為那時也沒人可以有智慧地替妳做決定了~當然妳也可以選擇這樣的過程來度過接下來的剩餘生命,沒有人能強迫妳做什麼選擇,畢竟人生不就是一連串自我選擇的結果嗎?
  • Joy
  • 樓上翠芳,obi-822實驗適應症是乳癌,obi-833一期臨床也未以肺腺癌為適應症~
  • 翠芳
  • 不好意思我因家母2年半前音肺腺癌兒潛水於此,對興西亞的勇氣及樂觀感到敬佩,也給癌友莫大的鼓勵,見今日星西亞面對此狀況而想提一下建議沒別的意思,並希望星西亞能平安. obi-833不是以乳癌臨床實驗就只能治乳癌而以,他適用16種癌症,肺癌好像也是一種,GH癌抗原譜遍於各種癌細胞中,打去公司問看看,搞不好有機會,也可以聯合用藥爭取時間.
  • 看不下去了
  • 樓上的某人,你該不會想借cincia版面打廣告吧~她會思考會判斷,但不會每個患者或家屬都這樣...好心點,癌症患者已經得花很多錢了,請讓他們都能花在刀口上好嗎??
  • 薄曦
  • 面對生死日久,真的不再視之為天大地大!
    但是對有所為有所不為,卻變成更加堅持的底線。
    網路可以輕易隱藏,卻逃脫不出自我,
    發言前,還是多想想吧!
    不然,很快便會開始厭惡自己,
    不值得的。
  • 可可
  • 領頭雁加油! 星西亞永遠都可以克服難關的!加油!加油!
  • 薄曦
  • Cincia加油,
    廖醫生會做正確的治療,我和你一樣,信任他。
    別把網路上的半桶水,甚至比病人還盲的無聊漢當回事。
    祝福你。
  • 謝謝薄曦大哥,我做了全腦放療只是記憶力減退,智力沒有下降啦!
    我當然是非常信任廖醫師,也相信他會為我做最佳的安排。

    Cincia 於 2016/05/03 09:59 回覆

  • 冷眼
  • 廖醫師神不神我不知道,但我知道抗癌戰友會社團的目前管理員之一:大姊:Joyce Hsu 的母親肺腺癌主治醫師也是廖醫師,但廖醫師也是救不回來因而過世了。先前社團癌症成員前仆後進相繼過世了,比較知道的有之前的小炎的肺腺癌老公過逝於台大,以及大家很懷念的已過世的肺腺癌年輕美女:Pauline Wu她的醫師是榮總肺腺癌權威主治醫師:蔡主任。接下來有Kate與Caspar,其他已經過世的成員族繁不及記載,在社團中每天都可以看到。別當鴕鳥視而不見,那些過世的人帶給我們的有價值訊息就是:那些過時的主流療法已經行不通了,趕緊進行最新的免疫療法吧。妳去找手中握有鐵鎚的人幫妳把釘子打進去,他當然只會用鐵鎚,難道他會用釘槍幫妳打進去嗎? 我是個直腸子的人,有話直說且喜歡切中問題核心的人。我說的都是事實,若有感覺不爽,請見諒。
  • 為什麼要去消費已經去世的人呢?而且這些都是我的朋友,你應該一個都不認識吧!
    你知道肺腺癌對免疫療法的反應率多少嗎?20%而已。怎麼可能放棄現在還可以控制好好的標靶去做免疫,到時候若免疫沒效,也吃不回來原本的標靶藥物(除非自費,每月20多萬)。
    如果我有很多錢,沒問題,我會去嘗試,但是我沒有,只能在有限的經濟條件下做最好的安排。

    Cincia 於 2016/05/03 10:07 回覆

  • Andrew Chen
  • 回冷眼,其實有些人已做過免疫療法。
  • 丹鳳MRT-Wimax Wang
  • To cincia:分享給妳,抗癌成功的2個案例,祝福妳,加油!

    案例1:
    長庚醫院已退休的皮膚科主任:官裕宗
    1994年50歲時,莫名其妙得到胃腺癌第三期,開刀後堅持不做放、化療,
    只施打以「日本蓮見疫苗 Hasumi Vaccine」治愈好他的胃腺癌,二十多年從未復發。書中第157 -201頁,說明抗癌成功的經歷,去書店可以看看,抗癌經驗(蓮見疫苗)詳情可以去問作者。

    書籍:【官裕宗醫師真心話:治癌心得與5W1H醫療藝術】
    http://www.books.com.tw/products/0010681753
  • 感謝分享,我之前就有找過關於"蓮見疫苗"的資訊了,但覺得有效案例好像都屬於前期的癌症,我在想說不定那些人本來不治療也都沒事?

    Cincia 於 2016/05/03 10:13 回覆

  • David
  • 1. 免疫細胞療法若是有效 效果也是短暫的
    癌症能利用免疫系統抑制打入體內的免疫細胞

    2. 免疫疫苗和樹突細胞 比較適合於初期癌症 在經過傳統治療後
    預防復發 對於4期病人不適用
    乳癌疫苗NeuVax目前進行第3期 臨床實驗

    3. Anti CTLA4, Anti PD1 和Anti PDL1是目前少數通過3期臨床實驗
    證實有效的免疫療法 作用機制是阻斷免疫系統抑制免疫反應的機制
    讓癌症無法利用免疫系統來抑制免疫反應

    4. Anti PD1真正與癌症作戰的是T細胞 而不是Anti PD1藥品
    過度看重反應率讓人(包括部份台灣醫師)見樹不見林
    而乎略了”癌症之所以會發生就是因為癌症有能力抑制免疫反應”
    真正的重點是”癌症抑制免疫反應”(tumor burden) 與”抗癌症免疫反應” (anti-tumor response)
    誰比較強? Anti PD1 讓這橇橇板 不再向腫瘤一面倒
    未來癌症治療應該包括設法讓病人的免疫系統重新控制癌症

    5. 癌細胞是不穩定的生命體 生命會找到自己的出路
    許多標靶治療最後失效 就是因為癌細胞不斷突變
    然而免疫系統可以偵測到新的突變 產生新的免疫反應
    這是Anti PD1治療俱有長效性的原因
  • 悄悄話
  • 逆轉勝
  • 樓上冷眼說得確實沒錯 電腦刀打地鼠只能治標用來爭取一段時間
    電腦刀不能當作主要治療手段

    找一下林口長庚神經外科系主任魏國珍看看吧

    長庚醫療團隊領先國際,開發出「高效能腦瘤聲熱治療法」,利用近年熱門的「奈米石墨烯」作為載體,搭配聚焦超音波技術,兼具化療與熱治療效果,能把藥物帶到深部腫瘤,研究顯示,比起傳統技術深達十倍以上,動物實驗發現,能抑制腫瘤細胞生長,未來可望不只讓腦瘤、甚至是其他癌症患者,有新的治療選擇

    https://www1.cgmh.org.tw/intr/intr2/c3s000/document/research_plugger/20130828.htm
  • "動物實驗"發現,能抑制腫瘤細胞生長....
    這離人體試驗還很遠耶!

    Cincia 於 2016/05/03 10:18 回覆

  • WINNER
  • 心情常常時高時低 一定不好受呢 我們都會在遠方默默的給大家支持 證明大家都不是自己1個人 我們都同時在努力著 陪伴著大家 每一天的醒來都代表新的希望 謝謝你一路的分享 給了好多人從絕望中看到希望 謝謝你
  • 三連休去台中走走後,心情好的不得了呢!繼續加油~
    希望可以再繼續寫10年、20年的Blog。

    Cincia 於 2016/05/03 10:24 回覆

  • 悄悄話
  • 悄悄話
  • kelly
  • 電腦刀沒有那麼恐怖啦~~治標不治本沒錯,但遠水救不了近火,近火要趕快撲滅是優先,爭取時間該打就是要打~
  • peichen
  • 我看過李鳳山先生的這本書
    http://www.books.com.tw/products/0010591296

    裡面有許多練平甩功的案例,
    但是他們每天都練好幾次,練的時間也很長,
    或許你可以研究一下,
    看看是否增加練功的時間。
    祝擊退腫瘤!
  • 我也在想應該要增加運動時間,調整一下現在的做法,可能還什麼地方可以改善。

    Cincia 於 2016/05/05 22:42 回覆

  • Sandy
  • Cincia,
    妳必須要相信 來到這個平台網業的朋友們,
    都是關心妳的。(打商業廣告的除外)。
    大家有大家的看法,每個癌友也有自身的治療經驗,
    都不會是惡意 是關心。
    樓上很多朋友打了那麼多字(一百以上) ,
    她們就是擔心跟關心 給自己的建議沒惡意。
    (要不她們很閒ㄛ!),
    Cincia,妳能感受的到ㄇ。

  • 天平之女
  • 其實妳不用管大家的想法,就按自己所做的選擇進行吧。無怨無悔,畢竟生死交關,最終抉擇的結果也只能自己承擔了,旁人毋需再置喙。祝福妳能成功~
  • David
  • Crizotinib Tops Chemo for ALK-Positive NSCLC With Brain Metastases

    April 04, 2016

    First-line crizotinib therapy offered better intracranial disease control rate (IC-DCR) than chemotherapy in patients with ALK-positive non–small-cell lung cancer (NSCLC) and stable treated brain metastases, according to results of a phase III study.

    Earlier results from the ongoing PROFILE 1014 trial showed that crizotinib offers better progression-free survival (PFS) and response rates compared with pemetrexed-platinum chemotherapy. “Although the development of targeted therapies has improved outcomes for selected patient populations with oncogenic driver mutations, brain metastases are frequent and result in significant morbidity and mortality in patients with lung cancer,” wrote study authors led by Benjamin J. Solomon, MBBS, PhD, of the Peter MacCallum Cancer Centre in East Melbourne, Australia.

    The new analysis included 343 PROFILE 1014 patients in an intent-to-treat population, 79 of whom (23%) had stable treated brain metastases at baseline; 39 of those patients were treated with crizotinib, and 40 were treated with chemotherapy. The results of the study were published online ahead of print in the Journal of Clinical Oncology.

    Among those with brain metastases at baseline, 27% had intracranial progressive disease (IC-PD); the median intracranial time to tumor progression (IC-TTP) was 15.7 months for crizotinib-treated patients and 12.5 months for chemotherapy-treated patients.

    Crizotinib was associated with non-significant improvements in IC-TTP in the intent-to-treat population, with a hazard ratio (HR) of 0.60 (95% CI, 0.34–1.05; P = .069); in the brain metastases present group, with an HR of 0.45 (95% CI, 0.19–1.07; P = .063); and in the group without brain metastases, with an HR of 0.69 (95% CI, 0.33–1.45; P = .323).

    Crizotinib was significantly associated with better disease control (complete or partial response, or stable disease) than chemotherapy in patients with brain metastases at baseline. The intracranial disease control rate at 12 weeks was 85% with crizotinib and 45% with chemotherapy (P < .001); at 24 weeks, the rates were 56% and 25%, respectively (P = .006). There were four intracranial complete responses with crizotinib, and two with chemotherapy.

    In those with brain metastases at baseline, the median PFS with crizotinib was 9 months vs 4 months with chemotherapy, for an HR of 0.40 (95% CI, 0.23–0.69; P < .001). Crizotinib also yielded better PFS in those without brain metastases, with a PFS of 11.1 months vs 7.2 months with chemotherapy, for an HR of 0.51 (95% CI, 0.38–0.69; P < .001). This was also the case in the intent-to-treat population. The median OS had not yet been reached in the intent-to-treat or in the with/without brain metastases groups.

    “Prospective assessment of [central nervous system] activity in the PROFILE 1014 study demonstrated superior intracranial disease control by crizotinib over chemotherapy and indicated that crizotinib should be the standard first-line therapy for patients with ALK-positive NSCLC, including those with [brain metastases],” the authors concluded.

    - See more at: http://www.cancernetwork.com/lung-cancer/crizotinib-tops-chemo-alk-positive-nsclc-brain-metastases#sthash.33hA4Ls7.dpuf
  • David
  • Alectinib in Crizotinib-Refractory ALK-Rearranged Non–Small-Cell Lung Cancer: A Phase II Global Study

    Purpose Crizotinib confers improved progression-free survival compared with chemotherapy in anaplastic lymphoma kinase (ALK)-rearranged non–small-cell lung cancer (NSCLC), but progression invariably occurs. We investigated the efficacy and safety of alectinib, a potent and selective ALK inhibitor with excellent CNS penetration, in patients with crizotinib-refractory ALK-positive NSCLC.

    Patients and Methods Alectinib 600 mg was administered orally twice daily. The primary end point was objective response rate (ORR) by central independent review committee (IRC).

    Results Of the 138 patients treated, 84 patients (61%) had CNS metastases at baseline, and 122 were response evaluable (RE) by IRC. ORR by IRC was 50% (95% CI, 41% to 59%), and the median duration of response (DOR) was 11.2 months (95% CI, 9.6 months to not reached). In 96 patients (79%) previously treated with chemotherapy, the ORR was 45% (95% CI, 35% to 55%). Median IRC-assessed progression-free survival for all 138 patients was 8.9 months (95% CI, 5.6 to 11.3 months). CNS disease control rate was 83% (95% CI, 74% to 91%), and the median CNS DOR was 10.3 months (95% CI, 7.6 to 11.2 months). CNS ORR in 35 patients with baseline measurable CNS lesions was 57% (95% CI, 39% to 74%). Of the 23 patients with baseline CNS metastases (measurable or nonmeasurable) and no prior radiation, 10 (43%) had a complete CNS response. At 12 months, the cumulative CNS progression rate (24.8%) was lower than the cumulative non-CNS progression rate (33.2%) for all patients. Common adverse events were constipation (33%), fatigue (26%), and peripheral edema (25%); most were grade 1 to 2.

    Conclusion Alectinib is highly active and well tolerated in patients with advanced, crizotinib-refractory ALK-positive NSCLC, including those with CNS metastases.
  • David
  • Posted by Dr. Guneet Walia on September 18th, 2015

    Approximately 3-5 % patients with non-small cell lung cancer patients (NSCLC) harbor abnormal rearrangements of the ALK (Anaplastic Lymphoma Kinase) gene, whereby the ALK gene abnormally fuses with another gene, EML4, resulting in a fusion oncogene, EML4-ALK. This gene rearrangement causes aberrant downstream signaling leading to the development of cancer.

    Though these percentages of ALK-driven lung cancer patients seem small, given the total number of patients diagnosed with lung cancer each year, these percentages actually translate into a sizable number of NSCLC patients.

    Testing for the ALK rearrangement is critical because highly active, targeted therapies exist for this subset of patients. One of the most common ALK rearrangement-targeted inhibitors is crizotinib (Xalkori), which was approved by the FDA on November 20, 2013 for the treatment of patients with locally advanced or metastatic ALK+ NSCLC. Crizotinib is a highly effective, orally active, ALK inhibitor demonstrating response rates in the 60-70% range and median progression-free survival of ~8-11 months.

    Unfortunately, despite initial responses most patients on crizotinib invariably develop resistance during the first year on treatment with this therapy and their disease relapses. This acquired resistance is one of the major challenges in treating ALK+ lung cancer patients. Most often in these crizotinib-resistant NSCLC patients, new tumors emerge in the central nervous system (CNS), typically the brain, which is a difficult area to reach with current medications. Multiple mechanisms have been identified for crizotinib resistance, several of which involve the development of unique new mutations in the ALK gene.

    Till very recently, treatment options for patients who failed crizotinib were limited to toxic chemotherapy, palliative radiotherapy or supportive care. However, things are rapidly changing in this space and there are currently over 10 new next-generation inhibitors under preclinical and clinical development for ALK+ NSCLC patients that have developed resistance to crizotinib. Since the CNS (brain) is a frequent site of progression in ALK+ NSCLC treated with crizotinib, CNS efficacy is a critical point to look for in the new ALK inhibitors.

    Ceritinib (Zykadia, LDK378) is one of the first next generation ALK- targeted inhibitors that has been granted an accelerated approval by the FDA for the treatment of ALK+ metastatic NSCLC patients who experienced disease progression on, or who are intolerant to crizotinib.

    Data on 3 promising ALK inhibitors was presented at the recently concluded 16th World Conference on Lung Cancer (WCLC) in Denver, CO in which the Addario Lung Cancer Foundation participated- Alectinib, Brigatinib and Loralitinib.

    Alectinib
    Alectinib is a highly-selective, orally available, ALK inhibitor with 10-fold greater potency than crizotinib, and has shown activity in both crizotinib-naïve and crizotinib-resistant patients. Alectinib has been shown to cross the blood-brain barrier and is very effective against central nervous system (brain) metastases that are commonly seen in patients that progress on crizotinib.

    This CNS penetrable ALK inhibitor has been approved in Japan and has received breakthrough therapy designation in United States for patients who have failed crizotinib.

    Pooled efficacy data from two phase 2 studies evaluating alectinib in ALK+ NSCLC patients previously treated with crizotinib was presented at the WCLC meeting. These findings showed that alectinib has promising efficacy against CNS metastases in ALK+ NSCLC patients previously treated with crizotinib, irrespective of whether these patients received any prior radiotherapy. Interestingly, this CNS activity was sustained for an equivalent duration of time as that seen for systemic response. Therefore, this inhibitor is capable of inducing very durable response rates in this subset of patients. Alectinib was also well tolerated overall, with mild side effects such as constipation, fatigue, myalgia, edema, etc.

    Ongoing, randomized phase 3 clinical studies, such as ALEX, will assess the systemic and CNS efficacy of alectinib versus crizotinib as front-line therapy for ALK+ NSCLC patients.

    Brigatinib (AP61223)
    Brigatinib is an investigational, oral, ALK-targeted inhibitor that has demonstrated promising antitumor activity in ALK+ NSCLC patients with or without prior treatment with crizotinib, including patients with brain metastases.

    Brigatinib has received a Breakthrough Therapy designation by the U.S. FDA for the treatment of patients with ALK+ metastatic NSCLC whose tumors are resistant to crizotinib. This designation is based on results from the ongoing Phase 1/2 trial that show anti-tumor activity of brigatinib in patients with ALK+ NSCLC, including patients with active brain metastases.

    Updated analyses of data from this ongoing trial were presented at the WCLC meeting in Denver, demonstrating a median progression-free survival (PFS) of 13.4 months in patients with prior crizotinib therapy, and a median PFS not reached so far for crizotinib-naïve patients. Brigatinib demonstrated excellent intracranial activity with a median intracranial PFS of 15.6 months and a median duration of intracranial response of 18.9 months.

    In summary, based on data presented on brigatinib so far, this experimental agent has a high activity against brain metastases typically seen in ALK+ NSCLC patients, and durable intracranial responses.

    A global, phase 2 trial (ALTA) of brigatinib in crizotinib-resistant ALK+ NSCLC patients is ongoing and results from this trial are eagerly awaited to get a complete picture of brigatinib’s CNS activity as well as systemic efficacy.

    Lorlatinib (PF-06463922)
    Lorlatinib, which mostly goes as ‘3922’, is a highly potent, selective, brain-penetrant ALK inhibitor that is active against not just ALK rearrangements but also the resistance mutations that arise in the ALK gene driving resistance to current clinical ALK inhibitors such as crizotinib. One of these mutations is G1202R and Lorlatinib is currently the only ALK-targeted inhibitor that is active against this resistance mutation in the ALK gene. Based on preclinical studies, Lorlatinib is believed to be the one ALK inhibitor that covers the broadest spectrum of ALK resistance mutations.

    Early data from the ongoing phase 1 study evaluating Lorlatinib in NSCLC patients shows that this experimental agent is active against both crizotinib-naïve as well as crizotinib-resistant non-small cell lung cancers.

    In this Ph 1 study, Lorlatinib has demonstrated robust clinical activity in ALK+ NSCLC patients who have been previously treated with other ALK-directed inhibitors. In this heavily pretreated population of ALK+ NSCLC patients, Lorlatinib demonstrated high activity against brain metastases.

    Other agents under development: There are several other ALK-targeted inhibitors currently in early stages of development, such as X-396, TSR-011, CEP-37440 and RXDX-101 (entrectinib).

    In summary, there’s a currently a lot of activity in the drug development arena for ALK targeted agents. For ALK+ NSCLC patients that relapse on crizotinib, there are several CNS- and extra-CNS active next-generation ALK inhibitors currently under development. Each of these agents have variable side effect profiles, and may have varying levels of activity against brain metastases in ALK+ patients. There is currently no data available on a head-to-head comparison of these agents to identify which ones patients must go on after they stop responding to crizotinib. It will also be very interesting to see how these agents perform in the front-line setting; studies to this effect are currently underway for ceritinib and alectinib, while those for brigatinib are planned.

    https://www.lungcancerfoundation.org/patients/news/whats-new-for-alk-rearrangement-positive-lung-cancer-patients/?loggedin
  • David
  • Brigatinib (AP61223) has good CNS penetration according to #74.
    Here is the clinical trial info (not yet open)

    Trial of Brigatinib After Treatment With Second-Generation ALK Inhibitors

    https://clinicaltrials.gov/ct2/show/NCT02706626

  • David
  • #77 requires subscription, so I post the article here.

    Alectinib Shrinks Brain Metastases in Advanced ALK-positive NSCLC

    Becky McCall
    October 07, 2013

    AMSTERDAM — A new ALK inhibitor, alectinib (under development by Roche/Chugai), for patients with non-small cell lung cancer (NSCLC) positive for anaplastic lymphoma kinase (ALK) rearrangement has shown activity in patients resistant to crizotinib (Xalkori, Pfizer). It also markedly reduces brain metastasis, a finding unseen with other agents in this patient population.

    The new data on alectinib were presented here at the European Cancer Congress 2013 (ECCO-ESMO-ESTRO) by Sai-Hong Ignatius Ou, MD, PhD,health science associate clinical professor at the University of California, Irvine School of Medicine.


    He emphasized that the findings related to brain metastasis are a first for patients whose lesions are progressing. "These patients normally require radiotherapy or surgery, and such metastases will usually be fatal. Previously we had nothing to offer them, but now these results show that potentially they'll have a pill."

    Matthias Preusser, MD, from the Medical University of Vienna, Austria, and cochair of the European Organization for Research and Treatment of Cancer (EORTC) Brain Tumor Group, welcomed the findings. He explained that brain metastases are found in around half of all NSCLC patients, and that local treatments such as radiotherapy, stereotactic radiosurgery, and neurosurgical resection are typically used to treat such advanced cases. "Limited data are available on systemic therapies, but many drugs do not achieve adequate concentrations in brain metastases due to the blood-brain barrier," he said.

    Crizotinib-naïve and Crizotinib-resistant Populations

    Crizotinib is so far the only ALK inhibitor available globally for the treatment of ALK-positive advanced NSCLC. It is approved for use as any-line treatment in the United States and as second-line therapy in Europe. In a phase 3 trial, crizotinib was found to be superior to standard chemotherapy in advanced NSCLC with ALK gene rearrangement (N Engl J Med. 2013;368:2385-2394).

    However, the majority of patients treated with crizotinib usually progress after an average of 8 months, so a more potent ALK inhibitor is needed to overcome resistance, Dr. Ou noted.


    He explained that the phase 1 alectinib results he presented are the beginning of a therapy that could move the treatment of advanced and resistant NSCLC forward.

    In their study, Dr. Ou's team enrolled 47 crizotinib-resistant patients from 6 sites in the United States.

    All study participants had an ALK rearrangement and had failed crizotinib treatment but had not been exposed to any other ALK inhibitors. All had asymptomatic brain metastases, including leptomeningeal carcinomatosis, but were clinically stable for at least 2 weeks without steroid treatment.

    In this dose-escalation study, patients were treated with twice-daily alectinib of 300 mg, 460 mg, 600 mg, 760 mg, or 900 mg until progression or lack of clinical benefit.

    The primary objective was to establish a dose for the phase 2 study. It was determined that the dose would be 600 mg twice a day.

    So far, the overall response rate (ORR), measured by tumor shrinkage and lack of new lesions or growth of existing tumors, has been relatively good — at 54.5% for all cohorts, Dr. Ou said. At the twice-daily dose of 600 mg or above, the ORR was 59.5%.

    The median duration has not yet been reached in the ongoing study, "but currently it is longer than 4 months," Dr. Ou reported.

    Before enrollment in the phase 2 trial of alectinib in ALK-positive NSCLC that has failed crizotinib, which has started in the United States, patients must undergo a mandatory biopsy after crizotinib failure; they must also undergo a mandatory biopsy after progression on alectinib.

    The global phase 2 (Accalia G2L) trial is actively enrolling patients.

    Dr. Ou noted that Roche is planning a global phase 3 head-to-head comparison of alectinib and crizotinib with a secondary end point of time to brain relapse. It should start in early 2014.

    Reduction in Brain Metastasis

    The considerable reduction in brain metastasis with alectinib was the other significant finding in the study, Dr. Ou pointed out. "Control of brain metastasis is a real unmet need in NSCLC. People do progress in the brain as a late 'tumor escape' phenomenon. This occurs at the 7- or 8-month stage, and is due to selection pressure of the crizotinib in this molecular subset of patients where systemic control is excellent."

    At baseline, 21 of the 47 patients had central nervous system metastases, which is unusually high for a trial of this size, he noted. "We started out with a high number of patients with brain metastases, but only 4 patients went off study because of progression; all others are active on study," Dr. Ou reported.

    He used MRI scans from before and after treatment with alectinib in a patient with brain metastases. The lesions, which were 2.5 cm at the start of treatment, shrank by 47% in 3 weeks.

    Two patients with leptomeningeal carcinomatosis, a carcinoma that infiltrates the lining of the meninges, also responded well. One was treated under single-patient compassionate use and achieved a complete response, demonstrated by spinal fluid clear of metastases. This 29-year-old patient was a nonsmoker and had been battling her disease for 7 years, Dr. Ou noted. "With the development of leptomeningeal carcinomatosis, she suffered facial numbness and stroke-like effects, but within 6 weeks she was clear and better."

    According to Dr. Ou, alectinib is distinct from other agents used to treat NSCLC because it has very good brain penetration, crossing the blood-brain barrier and reaching higher levels within the brain. '"Unfortunately, with crizotinib, there is a strong selection pressure on the tumor. While it provides excellent control in most of the body, such control elsewhere can actually precipitate relapse in the brain," he told Medscape Medical News.

    The clinical activity of alectinib in brain metastasis from ALK-positive NSCLC patients will be presented in more detail at the World Conference in Lung Cancer, being held in Sydney, Australia, later this month.

    Although the patient numbers were small in this phase 1 study, the results with this novel ALK inhibitor are of great interest, said Alba A. Brandes, MD, from the Medical Oncology Department at the Azienda USL Bellaria-Maggiore in Bologna, Italy.

    "The role of targeted agents in the treatment of brain metastases remains a challenge," she told Medscape Medical News in an interview. "However, many signals from other agents and in other cancer types seem to point in the same direction, suggesting that the biological sensitivity of specific tumor types — such as ALK-mutant or EGFR-mutant NSCLC, HER2-positive breast cancer, and BRAF-mutant melanoma — is much more important than the site of metastases."

    "Moreover, because of the specific activity of this potent anti-ALK agent, even after crizotinib failure, brain metastases should not be considered exclusion criteria for further clinical trials," she said.

    "The authors must be congratulated for opening their early clinical trial to patients with brain metastases, a population that has unfortunately been excluded from most clinical studies in the past," Dr. Preusser added.

    This study was funded by Roche/Chugai, the manufacturer of alectinib. Dr. Ou reports consulting for Pfizer, Chugai, and Genentech, and serving on the speaker's bureau for Pfizer, Genentech, and Boehringer Ingelheim. Dr. Preusser reports receiving research funding and travel grants for scientific meetings from Roche, Novocure, Boehringer Ingelheim, and GlaxoSmithKline. Dr. Brandes has disclosed no relevant financial relationships.

    European Cancer Congress 2013 (ECCO-ESMO-ESTRO): Abstract 44. Presented October 1, 2013.

    http://www.medscape.com/viewarticle/812159
  • David
  • ARIAD Presents Updated Phase 1/2 Clinical Data on Brigatinib in Patients with ALK+ Non-Small Cell Lung Cancer

    April 15, 2016 07:35 AM

    GENEVA & CAMBRIDGE, Mass.--(BUSINESS WIRE)--ARIAD Pharmaceuticals, Inc. (NASDAQ: ARIA) today announced updated clinical data on its investigational tyrosine kinase inhibitor, brigatinib, in patients with advanced malignancies, including anaplastic lymphoma kinase positive (ALK+) non-small cell lung cancer (NSCLC), from an ongoing Phase 1/2 trial. This report includes updated data on the brigatinib safety profile and pharmacokinetics (PK) from all patients treated in the trial, with a focus on brigatinib clinical activity in patients with ALK+ NSCLC, including those with intracranial CNS metastases at study entry. The report also details overall survival outcomes of patients in the study.

    The updated results were presented at the 6th European Lung Cancer Conference (ELCC) being held in Geneva, Switzerland.

    Phase 1/2 Study

    The data presented at ELCC include pharmacokinetics and safety analyses on all patients in the trial (n=137) and efficacy analyses on patients with ALK+ NSCLC (n=79). The presentation is based on patient data as of February 2015 with a median time on treatment for ALK+ NSCLC patients of 12.6 months (range, 0.03 – 35.5+ months). Patient enrollment in the trial is complete, with the last patient enrolled in July 2014. The primary endpoint in the Phase 2 portion of the trial is overall response rate. Secondary endpoints include safety and tolerability, pharmacokinetic parameters, progression free survival, and overall survival.

    “The updated data from the Phase 1/2 trial of brigatinib show a one year overall survival rate of 100 percent in crizotinib-naive patients, and 81 percent in patients with prior crizotinib treatment,” stated Rafael Rosell, M.D., Director, Cancer Biology & Precision Medicine Program Catalan Institute of Oncology, Germans Trias i Pujol Health Sciences Institute and Hospital in Barcelona, Spain. “In addition, the new data show predictable pharmacokinetics, with drug exposure increasing proportionally with dose. The Phase 1/2 trial has provided important long-term follow-up data on the safety and efficacy of this promising drug candidate.”

    Key Data Update from Study

    Anti-tumor Activity – ALK+ NSCLC Patients:

    Of the 70 evaluable ALK+ NSCLC patients with prior crizotinib therapy treated with brigatinib, median progression-free survival (PFS) was 13.4 months. Median PFS was not yet reached in ALK+ NSCLC patients who were crizotinib-naive (n=8).
    The “waterfall plot” analysis demonstrated tumor shrinkage in nearly all evaluable ALK+ NSCLC patients, with 25 patients experiencing 100% shrinkage of the target lesion.
    Of the eight evaluable TKI-naive ALK+ NSCLC patients treated with brigatinib, all demonstrated an objective response (100%), including three complete responses. Seven responses were confirmed.
    Of the 70 evaluable ALK+ NSCLC patients with prior crizotinib therapy treated with brigatinib, 50 (71%) demonstrated an objective response, including four complete responses. Forty-three responses were confirmed.
    The one-year overall survival (OS) rate in ALK+ NSCLC crizotinib-naive patients (n=8) was 100 percent and the projected two-year OS is also estimated to be 100 percent. Of the 71 ALK+ NSCLC patients who received prior treatment with crizotinib, the one-year OS was estimated to be 81 percent with projected two-year OS estimated to be 71 percent.
    An evaluation of the efficacy of brigatinib in ALK+ NSCLC patients with intracranial CNS metastases at baseline was also included in the ELCC presentation. In an independent central review of brain magnetic resonance imaging (MRI) scans, 50 of 79 ALK+ NSCLC patients were identified to have intracranial CNS metastases at baseline.
    Of these 50 patients, 17 had measurable intracranial CNS metastases (15 evaluable), and 33 patients had only non-measurable intracranial CNS metastases (31 evaluable).
    8 of 15 (53%) patients with measurable intracranial CNS metastases had at least 30% reduction in intracranial target lesion diameter, and 11 of 33 (33%) with only non-measurable intracranial CNS metastases had complete disappearance of intracranial lesions.
    Median intracranial PFS for evaluable ALK+ NSCLC patients with intracranial CNS metastases at baseline was 15.6 months.
    Pharmacokinetics:

    The brigatinib plasma steady-state parameters increased proportionally with dose over the dose range of 60 to 240 mg once daily.
    The geometric mean average plasma concentrations of brigatinib at steady state at 90 mg once daily and 180 mg once daily exceed the IC50 values for native ALK and all clinically relevant ALK resistance mutants tested.
    Safety and Tolerability – All Patients Enrolled:

    The most common treatment-emergent adverse events (TEAEs; ≥ 30%), regardless of treatment relationship, were nausea (52%), fatigue (42%), diarrhea (40%), headache (33%), and cough (32%).
    TEAEs, grade 3 or higher, occurring in three or more patients were increased lipase (9%), dyspnea (7%), hypertension (5%), hypoxia (5%), neoplasm progression (5%), pneumonia (5%), increased amylase (4%), fatigue (4%), and pulmonary embolism (≥3%).
    Serious AEs, all causality, occurring in three or more patients were dyspnea (7%), pneumonia (6%), hypoxia (5%), neoplasm progression (5%), pulmonary embolism (3%), malignant pericardial effusion (2%), and pyrexia (2%).
    A subset of pulmonary events, including dyspnea, hypoxia, pneumonia and/or pneumonitis, often with radiographic findings of linear or ground-glass pulmonary opacities, were observed in 8% (11/137) of patients within 7 days of dosing. The incidence of these early-onset pulmonary events was lower with a starting dose of 90 mg (1/50 patients, 2%) vs. 180 mg (6/44 patients, 14%). In addition, no early-onset pulmonary events were observed after dose escalation in the 32 patients started at 90 mg and escalated to 180 mg after seven days.
    “As we continue to study brigatinib in the ongoing Phase 1/2 trial, the pivotal Phase 2 ALTA trial and the new Phase 3 ALTA 1L trial in the front-line setting, we are encouraged by the potential of this targeted drug candidate for patients with ALK positive NSCLC and are looking forward to an NDA submission later this year,” stated Timothy P. Clackson, Ph.D., president of research and development and chief scientific officer at ARIAD. “The safety, PK and efficacy results reported with this update provide the potential for differentiation of brigatinib in the crizotinib-resistant patient population.”

    http://www.businesswire.com/news/home/20160415005047/en/ARIAD-Presents-Updated-Phase-12-Clinical-Data
  • 胃出血
  • 對於放療之後,我能力可給的建議是..寬心飲....優點....1.平價..打開就喝...2..很有名數據多...我也沒完全查完啦..只是作為輔助..你可以參考一下..這是我剛看到的一部分......中醫癌症關懷病友會12月6日寬心飲,癌症與中醫(youtube)..我不會貼影片
  • MINA
  • 姐姐加油~我們一起加油~
    我因為乳癌所以正在治療當中...

  • Zozo
  • 雖然不認識你 不過我好佩服妳 加油喔
  • su3741
  • 最近常聽佛樂,心靈獲得很大撫慰,

    "諸苦猶如夢子死,妄執實有起憂惱,故於違緣會遇時,觀為虛妄佛子行。"

    這一句話感觸很深,所有的苦難都是虛妄,都會過去,

    加油! 願佛菩薩保佑妳!
  • 悄悄話
  • ezioshen1203
  • Dear Cincia

    加油,希望妳後續的治療可以很順利!!!

  • 感謝你。Cincia會加油的。

    Cincia 於 2016/05/05 22:40 回覆

  • 顏榮郎
  • (看你的部落格討論串是個蠻奇妙的經驗。)
  • Q_Q

    Cincia 於 2016/05/05 22:41 回覆

  • 癌友
  • #51 "抗癌有悔" 說的是真話. 我親戚一發現是肺腺癌四期, 在榮總治療一年多, 最後醫生給他用電腦刀打腦腫瘤, 連續幾次, 打到醫生說不能再打了, 一個月後就往生.
    抗肺腺癌六年的單國璽樞機主教2012年五月連續兩次電腦刀打腦腫瘤, 八月就蒙主寵召. 用電腦刀殺腦腫瘤是傷敵一百, 自損三千, 絕對是不划算的"治療". Your life, your call. God bless you.

  • 薄曦
  • Cincia的好戰友,經常在網路發文的Kim,
    2014年9月25日,採伽瑪刀,第一次治療肺腺癌腦轉移;
    2015年4月9日,採全腦放療,第二次治療肺腺癌腦轉移;
    全程都做過忠實的記錄和檢討,
    目前持續在網路發文,思路清晰,走筆流暢。
    請問諸位僅得一知半解的網友,是否仍思提供走馬看花、甚至理解錯誤的信息,
    繼續干擾Cincia專心接受治療嗎?
    光陰寶貴,請好好用心照顧自己的生活吧。
  • Kim姐的智力應該是完全沒有影響的,損人的功力仍然不減XDDDD
    不過她加馬刀後有出現半邊身體麻的後遺症,任何腦部的治療真的風險都不小;我也覺得我記憶力有變差,不知道是全腦放療的影響還是初老現象?^^"

    Cincia 於 2016/05/22 17:30 回覆

  • 悄悄話
  • 悄悄話
  • ann88097
  • 看了這篇讓我好擔心.................希望醫師為Cincia各種檢查治療做正確的判斷
  • 我當然相信廖醫師會為我做最好的處理,謝謝Ann的關心。

    Cincia 於 2016/05/09 10:31 回覆

  • 薄曦
  • 美國執業醫生,平均的誤診率是30%,台灣也不會低於這個數字。
    所以不必把醫生當神,要求他們做到100%完美。
    不過也不必因為徬徨不安,而流於意、必、固、我,最後把自己當成了神!
    請問生病了,不問醫生,問誰?不信醫生,信誰?
    徵詢第二意見時,是聽專業看法是否一致?還是堅持我執,挽甲攻乙,聯乙擊丙?
    徵詢的對象,是合格的執業醫生?還是連背景都不明不白的「神網友」?
    真的不必擔心,現實環境中,多數人都擁有足夠,而不真實的世界,也原非所有。
    你僅需勇敢的飛,更擺脫諸多漫無目標、漂蕩攀纏的閒人便好。
  • 悄悄話
  • hank
  • 雖然是在我太太過世後才看到妳的部落格,但斷斷續續都會上來看看,也推薦給有需要的人.我太太發現時也是肺腺4期, 經過1循環化療, 後續標靶從愛瑞沙,得舒緩, 到最後的妥復克 她是歷經5年. 以妳的樂觀積極, 超過5年絕對沒問題, 好好加油!

    以我陪伴5年的經驗, 癌症治療不管是手術,藥物對晚期病患, 都在於控制延緩時間,但這也是機會, 醫學的進步,或許很快會有突破的療法. 要治本,一定要從強化自我免疫系統,以自我免疫力消滅癌細胞, 才是根本.但這真的不容易, 因為化療,標靶期間還是對身體有不同程度的傷害,所以必需付出更大的決心,意志力與樂觀的心(這是最困難, 因為那麼的努力配合治療, 定期檢驗報告不如預期時,心情真的不會好, 而且又會胡思亂想).

    要增強免疫力, 我的經驗是:
    1. 要有足夠的營養, 可諮詢營養師,營養夠才有體力治療,才能培養免疫軍隊打仗
    每天喝蔬果汁, 前1,2 年我每天都打蔬果汁(約1200 cc)給我太太喝(甜菜根,紅蘿
    蔔,蘋果,葡萄, 蕃茄), 為確保安全, 除洗淨外, 會用熱水燙一下
    2. 規律持續運動, 前1-2年, 每天做甩手功 1500下 及 每天早上上班前健走約40分鐘

    3. 親人的陪伴鼓勵,

    在前2年雖然腫瘤還在, 但癌指數都在 5上下. 後來因為有看中醫, 要喝中藥有要喝果汁,沒辦法就把果汁停了,因為家住基隆, 有段期間連下2個月的陰雨又冷, 走路也沒持續了.後來每種標靶服用約半年,就多出現抗藥性,我太太不想化療,隨後 指數也慢慢升高,體力也慢慢弱下來,最後還是不敵戰敗.



  • 感謝Hank的經驗分享,尊夫人和你五年來也做了不少努力,真的很棒。
    你要好好照顧自己喔!感謝鼓勵,Cincia也會繼續加油的。
    我也覺得心情好和規律運動真的很重要。:)

    Cincia 於 2016/05/22 17:23 回覆

  • 悄悄話
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