破癌解謎－組織嚴密的疾病 Breaking cancer puzzle - organized disease
突 變 │ Ras 基因 │ DNA │ 癌 細胞的染色體 │ 色 素體 │ 愛 滋病毒 Mutation │ Ras gene │ DNA │ cancer chromosome │ chloroplasts │ HIV │ 癌 細胞 │ DNA 晶片 │ cancer │ DNA chip

琳朵兒邵德恩住在美國奧克拉荷馬州，她今年41歲，一輩子跟 癌一起生活，曾經四度長癌，她18個月大時鼻子上第一次長骨肉瘤，也就是惡性骨瘤；14歲時下顎骨再長骨肉瘤，她動過無數次外科手術、接受放射治療、整形 手術，後來她結婚生下三個女兒，現在她離婚獨力扶養三名女兒。 Lin Shao Deen Dor live in the United States, Oklahoma, her 41-year-old, living with life with cancer, had cancer four times longer, when she was 18 months the first time in a long nose, osteosarcoma, malignant bone tumor that is; 14 years of age and then a long mandible osteosarcoma, she moves, numerous surgeries, radiotherapy, plastic surgery, and later she gave birth to three daughters married, and now she divorced, raising three daughters alone. 她32歲時生第三個孩子，癌又在她的右乳房肆瘧，她動了乳房 切除術，35歲時又失掉左乳房，她想不通為什麼自己一連四次長癌。 Her third child, 32 years old students, cancer again in her right breast is rampant, and she moved mastectomy, 35 years old has lost the left breast, she can not imagine why his fourth consecutive long cancer.

以46個譜代表46個染色體，A、T、G、C等4個字母，分成60億對寫在譜上，這些字母代表化學名稱，分別是 Adenine腺嘌呤、Thymine胸腺嘧啶、Guanine鳥嘌呤、Cytosine胞嘧啶。 With 46 chromosomes representing 46 spectra, A, T, G, C and so on 4 letters, divided into six billion pairs of written spectrum, these letters stand for chemical name, namely Adenine Adenine, Thymine Thymine, Guanine Guanine, Cytosine Cytosine. 這四個字母的順序改變，或是部份遺失就會突變。 Change the order of the four letters, or some mutations will be lost.

大約有十萬個地方，排列這四個字母成基因，目前發現200種 基因，跟癌有關連，其中一些基因顯示在此，每一種都能在適當時候，令細胞分裂或是停止分裂。 About 100 000 places, arrange the four letters into the gene, now found 200 genes with cancer-related, some of which appear in this gene, each of which can in due course, so that cells divide or stop dividing.

在細胞核內藍色蛋白質是防止細胞分裂的蛋白質，這種蛋白質是 要限制ras蛋白質的同工，不它們自由活動，藍紅兩種蛋白質交戰，讓細胞分裂不超過所需，紅色蛋白質連接壓制分裂的蛋白質，然後受限制的蛋白質得到釋放， 連接DNA複製基因之後，細胞開始分裂。 Blue protein in the nucleus is to prevent cell division protein, this protein is to limit the ras protein with the workers, not their freedom of movement, blue and red two proteins at war, so that no more than the required cell division, red to connect to suppress separation of protein protein, and then restricted the release of proteins by linking DNA replication genes, the cells began to divide.

假如ras蛋白質有失誤，就持續地發分裂信號。 If ras proteins errors made on a continuing split signal. 目前發現大約有兩百種癌，與基因有關，Ras基因首先被發 現，會讓細胞增殖。 Now found that about 200 kinds of cancer, and genes, Ras gene was first found, allow cell proliferation. 為什麼正常的細胞，會變成癌細胞？ Why do normal cells become cancer cells? 起初以為謎底是基因突變，使細胞倍增，另一種功能迥異的基因，是致癌的要角。 At first thought the answer is gene mutation, the cell multiplication, another function of different genes, is a cancer of the key players. 在日本，東京醫學院領導基因研究，從幾千名癌病患採下細胞， 發現基因怎麼突變，什麼時候跟癌有關連。 In Japan, the Tokyo School of Medicine leadership genes, collected from thousands of cancer patients under the cells and found how gene mutations, when associated with cancer. 中村有助教授經常為癌病患動手術，他想到不可能以傳統療法征 服癌，於是研究基因，他們現在鑽研p53基因，基本上這個癌的基因不正常的頻率很高，不正常的p53基因存在於大半數的癌內，研究發現p53防止細胞癌 化，因此不論作為診斷或治療的法寶，東京醫學院都把這種基因，視為最大的目標。 Professor Nakamura will help cancer patients often undergo an operation, he thought not possible with traditional therapies to conquer cancer, so of genes, they are now studying p53 gene, basically this cancer is high frequency of abnormal gene, abnormal p53 genes in a majority of cancer, the study found that p53 prevent cell carcinoma, thus, regardless of diagnosis or treatment as a magic weapon, Tokyo Medical regarded this gene, as the biggest target.

p53蛋白質，從p53基因生出，連接DNA，p53蛋白質總是四個一組，與DNA連接，為了防止細胞失控倍增，p53蛋白 質和同工把關，Ras基因內發生突變時，激發細胞分裂，不停地發出細胞分裂的指令，P53蛋白質察覺有突變，就會有行動。 p53 protein, p53 gene from birth, to connect DNA, p53 protein is always a group of four, and the DNA connection, in order to prevent the cells multiply out of control, p53 protein, and check with the workers, Ras gene mutation occurred, stimulate cell division, non-stop to the instructions issued by cell division, P53 protein detected a mutation, there will be action. 細胞受ras基因影響，不停地分裂，是正常的細胞，癌化的初期階段紅蛋白質激發細胞分裂之後，如果還連接DNA，細胞分裂就 不會停止，壓制分裂的藍蛋白質，要拉紅蛋白質離開基因，ras蛋白質的信號一個接一個地發出，P53的支援者招架不住，這時候就要看p53，鎮壓細胞分裂 的本領了。 Cells affected by the ras gene, constantly splitting, is the normal cells, cancer of the early stages of red proteins stimulate cell division, if it is connected DNA, cell division will not stop, suppress separatist blue protein, protein to pull red leave the gene, ras protein signal sent one by one, P53 supporters Zhaojiabuzhu, this time depends on p53, the ability to suppress cell division.

P53不單是連著紅蛋白質壓制細胞增殖，P53蛋白質是四員一組，連接DNA的特定部位，然後釋出強大無匹的蛋白質援 軍，P53釋出的蛋白質援軍，急行軍去支援藍蛋白質，於是把ras的指令消滅，以生出援軍的方式，防止正常細胞變化成癌細胞。 P53 suppression is not simply a row of red cell protein, P53 protein is a group of four to connect the specific parts of DNA, and then release powerful reinforcements matchless protein, P53 protein released reinforcements, forced march to support the blue protein, so the ras of the command elimination to give birth to reinforcements and the prevention of changes in normal cells into cancer cells. 大約半數的癌病患有突變的p53基因，琳朵兒四度長癌，就因 為p53基因突變。 About half of the cancer with mutant p53 gene, Lin bud long cancer four times, because of p53 gene mutation.

MD安德生癌症中心的露易絲史壯教授發現，琳朵兒的一組p53基因有突變，突變複製遺傳的機率有15%，所以她全身都容易長 癌。 MD Anderson Cancer Center found that Louise Professor Shi Zhuang, Lin bud of a p53 gene mutation, mutation probability of genetic replication, 15%, so long her body is easy to cancer. 琳朵兒的p53基因，這部位應該有一對T和一個A，她卻失掉 這一對T，因此以後的一對就失序了，這些突變基因很少產蛋白質，若遍及其他p53基因，就只會生出變形蛋白質，不正常的p53蛋白質不能連接DNA，生出 蛋白質幫手。 Lin bud of the p53 gene, this site should have a pair of T and an A, she has lost the right T, so after a pair of the disorder, and the mutant gene produced very little protein, if over other p53 gene, the only give birth to a deformed protein, abnormal p53 protein can not connect to DNA, proteins birth helper. 細胞有不正常的p53基因，才會失調而無節制地增殖。 Cells have abnormal p53 gene, will offset the uncontrolled proliferation.

琳朵兒在保險公司當秘書，扶養三個女兒。 Lin bud in the insurance company as a secretary, raising three daughters. 大女兒今年16歲，從14歲長顎骨癌開始，琳朵兒一心就想生孩子，她認為兒女是她活著的證明，目前她無意追究她孩子們，是否 承襲了突變基因，她認為要等她們成人後，自己決定要不要檢查。 16-year-old daughter, 14-year-old long jaw bone from the beginning, Lin bud as one wanted to have children, she thinks her children are living proof, she had no intention at present pursue her children, whether inherited the mutant gene, she finds it necessary so they are adult, to decide or not to check. 基因突變不僅得自遺傳，化學品和紫外線也是導因，癌症的遺傳 機率為5%或10%，所以90%以上的癌症，非先天遺傳而是後天罹患。 Not only derived from genetic mutations, chemical and UV is also the reason leading to the genetic risk of cancer is 5% or 10%, so 90% of the cancer, risk of non-congenital genetic but acquired.

癌細胞的染色體 Chromosomes of cancer cells

突變不是先天遺傳，而是後天罹患。 Genetic mutation is not innate, but acquired suffering. 地球乃是生命的搖籃，有害的紫外線恆常地照射著地表，有少量的紫外線從臭氧層洩出籠罩地球，會傷害我們的基因導致突變。 Earth but the cradle of life that regular exposure to harmful ultraviolet radiation with the surface, a small amount of UV escape from the ozone layer enveloped the earth, will hurt our genes cause mutations. 紫外線射到身體時，驅動皮膚的色素體或色素細胞，紫外線射到 皮膚時，色素體生出黑色素。 UV rays reach all parts of the body, the driven body or skin pigment pigment cells, when UV rays reach all parts of the skin pigment melanin physical birth.

有些人容易長癌是因為基因突變，患乾皮症的兒童又稱為XP， 他們臉上有許多色斑，都是細胞被日晒的疤痕，這情形惡化下去就是皮膚癌。 Some people tend to cancer because of gene mutation long, children suffering from dry skin disorder, also known as XP, they face many spots, all cells are the sun and the scar, this situation is getting worse skin cancer. 患XP的兒童受紫外線傷害，無法完全修復，不過p53基因有 最後一招防止細胞癌化，p53蛋白質用不同的助力，讓無法修復的細胞死亡，DNA碎片到處散落，這是細胞自殺。 Children suffering from XP by UV damage, can not be completely repaired, but the p53 gene are a last resort to prevent the cell cancerous, p53 protein with different help, so can not repair cell death, DNA fragments strewn everywhere, which is cell suicide.

人類的皮膚細胞，在紫外線下進行自殺，細胞以自殺來阻擋不正 常的基因，避免波及周圍的細胞，患XP的兒童無法修復損壞的p53基因，所以很容易罹患皮膚癌。 Human skin cells commit suicide under ultraviolet light, cells commit suicide to stop the abnormal gene, to avoid spread to surrounding cells, for children suffering from XP can not repair a damaged p53 gene, so it is easy to skin cancers.

XP的兒童住在一個營地中，對於患XP不能在白天到戶外玩耍的兒童，這個營地為他們提供了少許交友的機會，義工在這個營地 舉辦各種活動，晚上九點有輛冰淇淋車來這裏販賣，病童可跟動物玩。 XP's children live in a camp for people with XP can not be children playing outdoors during the day, the camp provided them with some friends the opportunity to volunteer in various activities organized by the camp nine at night with vehicles selling ice cream truck to come here , children can play with the animals. XP兒童的家長擔心，神經併發症導致癱瘓，要看突變的部位而定，有些兒童從五歲起，喪失聽覺、行動失控。 XP parents worried about children, neurological complications may result in paralysis, depending on the site of mutation may be, some children from the age of five, loss of hearing, action out of control.

基因密碼破解之後，各種致病的基因包括致癌的基因都被發現了，這些基因在細胞正常時，扮演重要的角色，但這些基因發生突變 時，疾病也就發作。 After cracking the genetic code, a variety of disease-causing genes, including cancer-causing genes have been identified, these genes in normal cells, play an important role, but mutations in these genes, the disease also attacks. 例如有一種與特應性皮炎有關的基因是在11號染色體上，與阿茲海默症有關的基是在14號染色體上。 One example of atopic dermatitis and related genes in chromosome 11, with Alzheimer's disease is related to the base chromosome 14. 不過基因突變並非通通不利，美澳兩洲有許多原住民，體內有8 號染色體突變基因，每三個日本人就有一個有這種突變基因，目前由於吃得太好，這種突變很有可能引發糖尿病，不過人類歷史上還是挨餓的時候多，這種突變使人 類挨過食物不足的世代，如此一來熬過困境的記憶，都記錄在基因裏。 But mutation is not detrimental to them altogether, United States and Australia and Asia, many indigenous people, in vivo gene mutation on chromosome 8, one of every three Japanese have such a mutation, present, because eating too well, this mutation is very may lead to diabetes, but still hungry human history when more of this mutation to the generation of human to survive the food shortage, this way survive the difficulties of memory, are recorded in the genes.

愛滋病毒溜進免疫細胞，一個接一個地破壞，最後侵占了整個身體。 HIV slipped into the immune cells, one by one, destroy, and finally occupied the entire body. 紫色病毒先附著免疫細胞的巨噬細胞，愛滋病毒黏著巨噬細胞表面的化學受體，然後溜進去，愛滋病毒的巨噬細胞，因為基因的協助 暴增而溢出，終於破壞了全身的免疫細胞。 Purple virus before attachment of immune cells macrophages, HIV-macrophage cell surface adhesion of chemical receptors, and then slipped to the AIDS virus in macrophages, because the genes to help explosion and spill, and finally destroy the body's immune cells . 由於基因突變，然後使得像史蒂芬這樣的人，有了形狀不同的化學受體，防止愛滋病毒溜進去。 As the gene mutation, and then makes such people as Stephen, with the shape of different chemical receptors to prevent HIV Mitnick.

研究人員從基因散佈的頻率，發現這種突變可能是最近發生的，在這群白種族裔的祖先，大約是在過去的十萬年中，因為某種原因， 在那群人裏產生基因突變。 Researchers from the gene frequency distribution and found that this mutation may be recent, in the group of white ethnic ancestors, about the past million years, for some reason, the crowd in produce gene mutation. 歐布萊教授鑑於這種突變，大部份發生於歐美白人，因此假設這種突變曾經對這些人有利。 O'Brien Professor of view of this mutation, the majority occurred in Europe and the United States whites, so assume that this mutation has been beneficial to these people.

根據歐布萊教授的人口統計，大約是七百年前歐洲的確有病變，發生過鼠疫，這場鼠疫在短短的六年內，把歐洲的人口消滅 30%，不過還是有人撐過，歐布萊教授相信在這場大瘟疫中，有人帶著這種突變活下來，所以有同樣受體的相同細胞，成了HIV的目標，引發了愛滋病，就像耶 爾森氏鼠疫桿菌引發黑死病，這是發生高頻率的潛在原因。 According to O'Brien, Professor of Population, about 700 years ago in Europe there is indeed a disease, the occurrence of plague, this plague in just six years to eliminate 30% of the population of Europe, but people still make it through, O'Brien Professor Lai believes in this big plague, some people survive with this mutation, so the same receptors in the same cell, HIV has become the goal, causing AIDS, like Yersinia pestis, the plague caused This is the high frequency of occurrence of potential causes. 歐布萊教授假設這基因突變，在七百年前救了許多人，如今再出 現可能成為壓制愛滋病毒的基因。 Professor O'Brien assumed that mutations in the 700 years ago to save a lot of people, now and then there may be suppression of HIV genes.

隨著基因研究的進展，新的療法一個接一個，目前研究員正努力，把p53基因殖入癌細胞，這種腺病毒，引發傷風遺傳工程，帶 p53基因人的腦瘤是受這種病毒感染，這種腺病毒能在細胞裏，產生p53蛋白質，一天之後這細胞，快速地萎縮。 With the progress of genetic research, new treatments one by one, now researchers are trying to p53 gene was cloned into the cancer cells, this adenovirus, cause colds genetic engineering, human brain tumors with p53 gene is infected by this virus This adenovirus in cells, the p53 protein production, one day after the cells rapidly shrinking. 腺病毒大量地送進癌細胞內產生p53蛋白質，激發細胞自殺， 三天之後癌細胞死亡，裏面有突變基因。 Adenovirus sent large numbers of cancer cells to generate p53 protein to stimulate cell suicide, three days after the death of cancer cells, which have mutations.

目前基因治療法正在臨床試用p53基因，德州休斯頓一家生化科技公司，研究注入p53基因的腺病毒，已經用於治療，由於基因 治療需要高品質的特級細胞，生產過程幾乎是密而不宣。 Recently, the gene therapy clinical trial is p53, a biotechnology company in Houston, Texas, to study the injection of adenovirus p53 gene has been used to treat, because gene therapy requires high-quality super cell, the production process is almost Silent .

高德開業行醫已有四十多年，兩年前十二月，診斷出他患早期肺癌，診斷結果目前無法可治，他正好符合條件，於是立刻接受 p53基因治療。 De-opening practice has 40 years, two years ago in December, he was diagnosed with early lung cancer diagnosis is not possible to rule, he happened to meet the conditions, p53 gene therapy was immediately accepted. 帶p53基因的腺病毒，由長針頭注入肺部癌細胞，高德在兩個月內，接三次這樣的治療，治療前高德的癌直徑有八公分，三個月以 後癌的直徑縮到三公分，而且肺壞掉的部位，又恢復正常，p53基因使癌細胞自殺。 P53 gene with adenovirus, the long needle into the lung cancer cells, high German in two months, then three such treatments, the cancer treatment with high moral and eight centimeters in diameter, three months after the cancer to shrink in diameter three centimeters, and the broken parts of the lung, but also to restore normal, p53 gene to cancer cells commit suicide. 基因治療的好處是中毒率低，而且可以跟記波治療，放射治療配 合進行，而毒性並沒有增加，所以基因治療的好處是可以用於大量的病人，配合其他療法。 The benefits of gene therapy is low toxic and can be credited with the wave treatment, with radiotherapy, whereas no increase in toxicity, so the benefits of gene therapy can be used for a large number of patients with other therapies.

不過到現在只有初期癌病患，接受這種療法，所以很少有高德這樣的結果，因為癌症初期，不僅p53基因，還有許多其他的基因 突變。 However, there are only the initial cancer patients receiving this therapy, so very few results of such high moral, because the early cancers, not only the p53 gene, there are many other mutations. 癌細胞的產生是因為正常細胞的基因突變，如果基因突變限制分裂，當正常細胞分裂增殖時，細胞分裂會失控，這是正常細胞癌化的 開始。 Cancer arise because of mutations in normal cells, if the gene mutation restricted to split, when normal cell division and proliferation, the cells divide out of control, this is the beginning of the normal cell cancerous. 如果其中的細胞裏又發生突變，這細胞的形狀功能會改變，如果有若干基因突變，細胞會現出前所未有的特性，這個細胞脫離四周的 細胞，到處遊走，不久它就會溜到正常細胞中間，進入血管淋巴管，流到另一個地點，然後溜進另一部位長新的瘤。 If one cell in another mutation, this cell will change the shape of the function, if the number of gene mutations, cells features than ever, the cell from surrounding cells, roam, and soon it will slip off to the middle of normal cells into the lymphatic vessels, to flow to another location, and then slipped into the other parts of the tumor grows new.

癌細胞裏的基因突變累積的方式很複雜，有各樣的力量發動毫無節制，要戰勝癌症的關鍵在於，更精確迅速地判定癌細胞內的基因突 變。 Cancer gene mutations accumulated in a complex manner, with all sorts of unbridled power to launch, is the key to overcoming cancer, more precise cancer cells quickly determine the gene mutation.

由於科技革新，諸如DNA晶片顯微排列，可以同時分析成千上萬的基因，用這個方法可以掌握廣大的情報，與現在情報侷限的光 景，不可同日而語。 As the new technology, such as DNA micro array chip that can analyze thousands of genes simultaneously, using this method can grasp the general intelligence, and intelligence is now limited circumstances, can not compare.

基因情報愈來愈明朗，突變的意義也會劇變，包括癌症的許多疾 病的治療，因基因研究而有進展，基因好像主宰了命運，但是當我們解開，基因內的疾病之謎時，我們治病的方法，可能會大大地改觀，而這一天也不會太久了。 Genetic information more and more clear, the significance of mutations will be drastic changes in the many diseases including cancer treatment, because of genetic research progresses, seems to dominate the fate of the gene, but when we unlock the genetic mystery of the disease, we method of treatment may be greatly changed, and this day will not be too long.

（原翻者：姜金龍；公視研發部整理） (Original translation by: Jiang Jinlong; public order, as the R & D)