結腸癌和直腸癌實際上是相同的


  【24drs.com】根據腫瘤基因圖譜(TCGA)網絡進行的癌症綜合分子特徵分析,在多種基因圖譜分析中,結腸和直腸癌結果幾乎沒有區別;這項針對224種腫瘤進行的分析,線上登載於7月18日自然期刊。
  
  根據國家癌症研究中心(NCI)提供的資料,腫瘤基因圖譜獲得的癌症基因組資料有助於治療的特定標靶。
  
  哈佛醫學院醫學教授暨基因學名譽教授Raju Kucherlapati博士等研究者結論表示,不論在結腸內或直腸內的解剖位置或來源,結腸和直腸組織的基因組變化類型幾乎相同,因此,這兩種癌症類型可分為同組。最初,TCGA研究網絡探討結腸腫瘤時認為它們和直腸腫瘤不同。
  
  腫瘤基因圖譜計畫是獲NCI和國家人類基因組研究中心資助,每年100億美元左右。
  
  國家健康研究中心的Francis S. Collins博士在新聞稿中表示,發現結腸癌和直腸癌的真正基因特質,對於我們了解此病之基礎而言,是一項卓越成就,獲得的這些資料和知識將有助於改變某些癌症的診斷及治療。
  
  Kucherlapati博士表示,對於結腸癌和直腸癌發展之所有類型變化的關鍵,我們確實有了更好且更全面的觀點,這次或許是這類癌症最大型且最綜合的研究,以前沒有人同時分析過這麼多不同類型的癌症樣本。
  
  這篇研究也發現造成結腸直腸癌復發的多項基因狀況,例如,已知大腸腫瘤的侵略性和突變之間有負向關連,基因突變比率異常地高,因為正常的DNA修補機制被損害。
  
  目前的研究中,16%的樣本被發現是過度突變,其中,四分之三表現出微隨體(基因組中、DNA的重複片段)不穩定,有時候這是預後更佳的徵兆。
  
  根據NCI指出,如果突變發生在維持基因組的這些區域的基因,微隨體可能會變得更長或更短。
  
  該研究顯示,多數案例有24種基因發生突變,除了之前研究提及的基因(如 APC、ARIDIA、FAM123B/WTX、TP53、SMAD4、PIK3CA和KRAS),研究者發現了其他基因(ARIDIA、SOX9和FAM123B/WTX)是突變發生時的可能致癌因子。
  
  NCI主任Harold E. Varmus醫師在發表時表示,雖然還要許多年才可以將這些有關結腸直腸癌的基因資料發展為新的治療策略和監測方法,這些基因資料無疑地將是有助於臨床決定何者有益於結腸直腸癌的重要跳板。
  
  研究者也確認了ERBB2和IGF2在結腸直腸癌中為突變或過度表現,因此,有可能作為藥物標靶;這些基因和調節細胞增生有關,在結腸直腸腫瘤中經常被發現過度表現。
  
  NCI聲明指出,這項結果提出了可能的藥物治療策略,抑制這些基因的產物將可延緩癌症病程。
  
  Kucherlapati博士認為,這篇研究將會催生藥物檢測的新世代。
  
  他表示,突然之間,對於治療方式有限的某種腫瘤,現在這些研究開啟了可以檢查的新方式。有相當好的機會對這些新策略進行臨床檢測,為每個病患檢測腫瘤,釐清他們有哪些變化,嘗試將他們引領到適當的臨床試驗,如果成功治療,那麼,它們在未來將可能變成標準療法。
  
  資料來源:http://www.24drs.com/professional/list/content.asp?x_idno=6888&x_classno=0&x_chkdelpoint=Y

Colon and Rectal Cancers Are Truly the Same

By Fran Lowry
Medscape Medical News

July 20, 2012 — In multiple types of genomic analyses, colon and rectal cancer results were nearly indistinguishable, according to a comprehensive molecular characterization of these cancers by the Cancer Genome Atlas (TCGA) Network.

Their work, which is based on a study of 224 tumors, was published online July 18 in Nature.

The Cancer Genome Atlas generates genomic data for cancers that point to potential targets for treatment, according to information provided by the National Cancer Institute (NCI).

The pattern of genomic alterations in colon and rectal tissues was the same, regardless of anatomic location or origin within the colon or the rectum. Because of this, the 2 cancer types can be grouped as 1, conclude the researchers, led by Raju Kucherlapati, MD, PhD, who is the Paul C. Cabot Professor of Genetics and Professor of Medicine at Harvard Medical School, Boston, Massachusetts, Initially, the TCGA Research Network studied colon tumors as though they were distinct from rectal tumors.

The Cancer Genome Atlas project is funded by the NCI and the National Human Genome Research Institute to the tune of $100 million a year.

"This finding of the true genetic nature of colon and rectal cancers is an important achievement in our quest to understand the foundations of this disease," Francis S. Collins, MD, PhD, director of the National Institutes of Health, said in a news release. "The data and knowledge gained here have the potential to change the way we diagnose and treat certain cancers."

"We really have a much better and more comprehensive view of all the types of changes that are critical for colon cancer and rectal cancer to develop," Dr. Kucherlapati told Medscape Medical News. "This is probably the largest and most comprehensive study of its nature in this cancer. Nobody in the past has analyzed this many tumor samples with all of these different applied forms at the same time."

The study also found several recurrent genetic errors that contribute to colorectal cancer. For example, there is known to be a negative link between the aggressiveness of colorectal tumors and hypermutation, a phenomenon in which the rate of genetic mutation is abnormally high because the normal DNA repair mechanisms are disrupted.

In the current study, 16% of the samples were found to be hypermutated. Of these, three quarters exhibited microsatellite (a repetitive section of DNA in the genome) instability, which can sometimes be a sign of a better prognosis.

If mutations occur in the genes responsible for maintain those regions of the genome, the microsatellites may become longer or shorter, according to the NCI.

The study showed that 24 genes were mutated in a significant number of cases. In addition to genes found through prior research (eg, APC, ARIDIA, FAM123B/WTX, TP53, SMAD4, PIK3CA, and KRAS), the researchers identified other genes (ARIDIA, SOX9, and FAM123B/WTX) as potential drivers of this cancer when mutated.

In the release, Harold E. Varmus, MD, director of the NCI, said: "While it may take years to translate this foundational genetic data on colorectal cancers into new therapeutic strategies and surveillance methods, this genetic information unquestionably will be the springboard for determining what will be useful clinically against colorectal cancers."

The researchers also identified the ERBB2 and IGF2 as being mutated or overexpressed in colorectal cancer, and therefore, as potential drug targets. These genes are involved in regulating cell proliferation and were seen to be frequently overexpressed in colorectal tumors.

This finding "points to a potential drug therapy strategy in which inhibition of the products of these genes would slow progression of the cancer," the NCI stated.

A new era of drug testing may be spawned by the research, suggested Dr. Kucherlapati.

"Suddenly, for a tumor type for which there was a limited therapeutic approach, these studies now open up a whole spectrum of approaches that can be tested," he said. "There is a great opportunity to clinically test all of these new targets by testing the tumors from each patient, finding out what kinds of changes they have, and trying to direct them into an appropriate clinical trial. And if the therapies are successful, then of course they will become the standard therapy in the future."

Dr. Kucherlapati has disclosed no relevant financial relationships.

Nature. 2012;487:330-337.

    
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