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【資源】Cell-of-Origin for Human Prostate Cancer Identified for First Time 已有1人參與
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ScienceDaily (July 29, 2010) — UCLA scientists have identified for the first time a cell-of-origin for human prostate cancer, a discovery that could result in better predictive and diagnostics tools and the development of new and more effective targeted treatments for the disease. The researchers, from UCLA's Jonsson Comprehensive Cancer Center, proved that basal cells found in benign prostate tissue could become human prostate cancer in mice with suppressed immune systems, a finding that bucks conventional wisdom. It had been widely believed that luminal cells found in the prostate were the culprits behind prostate cancer because the resulting malignancies closely resembled luminal cells, said Dr. Owen Witte, a Jonsson Cancer Center member and director of the UCLA Broad Stem Cell Research Center. "Certainly the dominant thought is that human prostate cancer arose from the luminal cells because the cancers had more features resembling luminal cells," said Witte, senior author of the study and a Howard Hughes Medical Institute Investigator. "But we were able to start with a basal cell and induce human prostate cancer and now, as we go forward, this gives us a place to look in understanding the sequence of genetic events that initiates prostate cancer and defining the cell signaling pathways that may be at work fueling the malignancy, helping us to potentially uncover new targets for therapy." The study appears July 30, 2010 in the peer-reviewed journal Science. The researchers took healthy tissue from prostate biopsies and separated the cells based on their surface marker expression into groups of luminal cells and groups of basal cells. Using viral vectors as vehicles, they then expressed altered genes known to cause cancer into both cell populations and placed the cells in mice to see which developed cancer, said Andrew Goldstein, a UCLA graduate student and first author of the study. "Because of the widespread belief that luminal cells were the root of human prostate cancer, it would have been those cells examined and targeted to treat the disease," said Goldstein. "This study tells us that basal cells play an important role in the prostate cancer development process and should be an additional focus of targeted therapies." In normal prostate tissue, basal cells have a more stem cell-like function, Goldstein said, meaning they proliferate more to re-grow human prostate tissue. Luminal cells don't proliferate as much, but rather produce major proteins that are important for reproduction. Something is going awry in the basal cells that results in cancer and Witte and Goldstein plan to study those cells to uncover the mechanisms that result in malignancy. Currently, there is a dearth of knowledge about how prostate cancer develops to treat it effectively in a targeted way, as Herceptin targets an out-of-control production of growth factor receptors in breast cancer cells. The major targeted therapy used for prostate cancer is directed at the androgen receptor and it is not always effective, Witte said. The new human-in-mouse model system developed in the study -- created by taking healthy human prostate tissue that will induce cancer once it is placed in mice instead of taking malignant tissue that is already cancerous and implanting it -- can now be used to evaluate the effectiveness of new types of therapeutics. By using defined genetic events to activate specific signaling pathways, researchers can more easily compare therapeutic efficacy. The new model, by deconstructing tissue and then reconstructing it, also will aid in analyzing how the cells change during cancer progression. "There are very few examples of taking benign cells and turning them into cancer experimentally," Goldstein said. "We usually study cancer cell lines created from malignant tumors. This study resulted in the creation of a novel model system that is highly adaptable, such that we can test any cellular pathway and its interactions with other genes known to induce cancer, and we can start with any type of cell as long as it can be reproducibly purified." In this system, Witte and Goldstein know the "history" of the cells that became cancer, unlike the cancer cells lines used in other work. "We know those cells are malignant, but we don't know how they got there," Goldstein said. "By starting with healthy cells and turning them into cancer, we can study the cancer development process. If we understand where the cancer comes from, we may be able to develop better predictive and diagnostic tools. If we had better predictive tools, we could look earlier in the process of cancer development and find markers that are better than the current PSA test at catching disease early, when it is more treatable." Rising PSA levels can indicate the presence of cancer that is already developing in the prostate. However, now that it is known that basal cells are one root of human prostate cancers, scientists can study pre-malignant basal cells and uncover what they express that the healthy ones don't, perhaps revealing a new marker for early detection, Goldstein said. Also, a therapy directed at the pre-malignant basal cells about to become malignant could provide a way to prevent the cancer before it becomes dangerous. This year alone, more than 217,000 men will be diagnosed with prostate cancer. Of those, more than 32,000 will die from their disease. The study was funded by a Prostate Cancer Foundation Challenge Award, the Howard Hughes Medical Institute and the Department of Defense. |
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首次發(fā)現(xiàn)前列腺癌細(xì)胞來源 今日科學(xué)2010年7月29日報(bào)道，UCLA科學(xué)家們首次發(fā)現(xiàn)了人前列腺癌的細(xì)胞來源，該發(fā)現(xiàn)可能更好地成為前列腺癌預(yù)測和診斷工具，并可開發(fā)新的和更加有效的靶向治療方法。 來自于UCLA's Jonsson 綜合癌癥中心的研究人員采用免疫系統(tǒng)抑制的小鼠，證明了良性前列腺組織中的基底細(xì)胞可能變成前列腺癌，該研究發(fā)現(xiàn)顛覆了傳統(tǒng)觀點(diǎn)。Jonsson癌癥中心成員，也是UCLA組干細(xì)胞研究中心主任Owen Witte博士說現(xiàn)在人們廣泛認(rèn)為前列腺腔上皮細(xì)胞是前列腺癌細(xì)胞來源，因?yàn)閻盒陨掀し浅ｎ愃朴谇簧掀ぜ?xì)胞。 “人前列腺癌起源于腔上皮細(xì)胞的觀點(diǎn)為主是因?yàn)榍傲邢侔┘?xì)胞特征更加類似于腔上皮細(xì)胞，”該項(xiàng)研究的高級作者，Howard Hughes醫(yī)學(xué)研究所調(diào)查人員Witte說。“但是我們能從一個(gè)基底細(xì)胞開始并誘導(dǎo)出人前列腺癌，現(xiàn)在，隨著我們繼續(xù)努力，必將給我們提供了一個(gè)理解誘發(fā)前列腺癌發(fā)生的遺傳學(xué)時(shí)間的順序和定義可促使惡性轉(zhuǎn)化的細(xì)胞信號途徑的機(jī)會，有助于我們可能揭示新的治療靶點(diǎn)�！� 該項(xiàng)研究以同行評論的方式發(fā)表在2010年7月30日的《科學(xué)》雜志上。 研究人員采用前列腺活檢的健康組織，根據(jù)它們的表面標(biāo)記物表達(dá)將這些細(xì)胞分為腔細(xì)胞和基底細(xì)胞組。使用病毒載體作為賦形劑，然后他們將已知的能致癌的基因?qū)脒@2組細(xì)胞中，并將這些細(xì)胞注入小鼠細(xì)胞中觀察哪個(gè)發(fā)展為癌。UCLA研究生和本研究的第一作者Andrew Goldstein說。 “由于人們普遍認(rèn)為腔細(xì)胞是前列腺癌的細(xì)胞來源，所以這些細(xì)胞被檢查和靶向治療這種疾病，”Goldstein說：“這項(xiàng)研究告訴我們基底細(xì)胞在前列腺癌發(fā)展進(jìn)程中發(fā)揮重要作用，應(yīng)該成為靶向治療的另一個(gè)焦點(diǎn)�！� 在正常前列腺組織中，基底細(xì)胞具有更多的干細(xì)胞樣功能，Goldstein說，意味著這些細(xì)胞可以增生并重新生長為前列腺組織。腔細(xì)胞雖然不增生，但可產(chǎn)生主要蛋白對再生具有重要作用。有時(shí)候基底細(xì)胞發(fā)生差錯(cuò)可導(dǎo)致癌，Witte和Goldstein計(jì)劃研究這些細(xì)胞并揭示其發(fā)展為癌的機(jī)制。 Witte said.Witte說，目前還缺乏前列腺癌應(yīng)如何更有效的靶向治療，雖然赫賽汀可靶向乳腺癌細(xì)胞中生長因子受體的失控性產(chǎn)生。前列腺癌的主要靶向治療是直接針對雄激素受體，而且它不是總是有效的。 本研究中發(fā)展了一種新的人鼠模型，該模型是采用可誘發(fā)癌的健康人前列腺組織，將其注入小鼠中，而不是采用已經(jīng)成為癌的惡性前列腺癌組織種植到小鼠中�，F(xiàn)在使用該模型能評估新的治療方法的有效性。能夠使用明確的遺傳學(xué)事件活化特異性信號途徑，研究人員較能容易比較不同治療方法的有效性。這種新的模型通過破壞組織和重構(gòu)組織，也將有助于分析在癌癥進(jìn)展過程中這些細(xì)胞是如何變化的。 “有一些較少的例子是采用良性細(xì)胞，采用實(shí)驗(yàn)方法將這些細(xì)胞變?yōu)榘┘?xì)胞，”Goldstein說：“我們通常研究惡性腫瘤的癌細(xì)胞系，而本研究可導(dǎo)致一種高度可適應(yīng)性的新的動(dòng)物模型系統(tǒng)，采用這種系統(tǒng)我們能檢測任何細(xì)胞途徑和與其他已知的能誘導(dǎo)癌癥的其他基因的相互作用。只要能夠可重復(fù)性純化，我們能從任何一種類型細(xì)胞開始�！� 在這個(gè)系統(tǒng)中，Witte和Goldstein知道變成癌的細(xì)胞的歷史，不想過去在其他工作中使用的癌細(xì)胞系。 “我們知道這些細(xì)胞是惡性的，但我們不知道他們?nèi)绾蔚竭_(dá)那里的，”Goldstein說�！巴ㄟ^從健康細(xì)胞開始，將它們變?yōu)榘┘?xì)胞，我們能研究癌癥發(fā)展過程。如果我們理解了癌癥起源于哪里，我們可以能夠開發(fā)出更好的預(yù)測和診斷工具。如果我們有較好的預(yù)測工具，我們能在癌癥發(fā)展過程中較早看到，發(fā)現(xiàn)比目前PSA檢測更好的標(biāo)記物早期診斷，從而達(dá)到更好的治療�！� PSA增高能預(yù)測前列腺癌的存在，然后，現(xiàn)在知道基底細(xì)胞是前列腺癌的來源，科學(xué)家們能研究癌前基底細(xì)胞，揭示它們在正常健康人不表達(dá)的東西，或許能發(fā)現(xiàn)早期檢測的新的標(biāo)記物，Goldstein說。而且，針對將變?yōu)閻盒缘陌┣盎准?xì)胞的治療能提供一種預(yù)防癌癥的方法。 每年大約有217,000名男性被診斷為前列腺癌，其中有32,000人死于該病。 這項(xiàng)研究由前列腺癌基金會挑戰(zhàn)資金、霍華德休斯醫(yī)學(xué)研究所和國防部資金資助。 |
2樓2010-08-07 23:41:40
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