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　　12月17日于舊金山召開(kāi)的美國細胞生物學(xué)協(xié)會(huì )年會(huì )上，美國威斯康辛大學(xué)卡邦癌癥中心發(fā)現了一種人類(lèi)細胞分裂的新形式，并稱(chēng)之為“核分裂”（klerokinesis）。這種新分裂形式是一種對錯誤細胞分裂的天然補救機制，能預防某些細胞步入“癌”途。

　　正常細胞分裂每次都是一個(gè)母細胞變成兩個(gè)子細胞。細胞先按照原有成分復制出一套完全一樣的副本，包括細胞核中的DNA染色體；然后進(jìn)入有絲分裂階段，將這兩套完全一樣的成分朝相反方向分開(kāi)，此時(shí)它們還在同一個(gè)細胞內；最后是胞質(zhì)分裂，一個(gè)細胞分成兩個(gè)子細胞，時(shí)間恰好在有絲分裂結束時(shí)。

　　一個(gè)世紀前，德國生物學(xué)家西奧多·博韋里通過(guò)海膽卵實(shí)驗提出假說(shuō)，錯誤分裂會(huì )導致細胞染色體倍數異常和細胞不受遏制地生長(cháng)，這就是癌癥。在癌細胞的細胞核中，染色體常常會(huì )在分裂過(guò)程中形成不止兩套而是多套，約14%的乳腺癌和35%的胰腺癌細胞會(huì )有3套或更多染色體，沒(méi)有多余染色體的癌細胞則含有錯誤染色體。

　　研究小組給人類(lèi)細胞復制出了多倍染色體，以模擬癌癥。他們用一種常規化學(xué)物質(zhì)阻止了胞質(zhì)分裂，結果發(fā)現分裂并未顯出異常，子細胞在大部分情況下看起來(lái)都很正常，這和博韋里假設相悖。

　　他們進(jìn)一步觀(guān)察了人類(lèi)細胞是怎樣恢復正常染色體倍數的。該校醫學(xué)與公共衛生學(xué)院醫學(xué)部血液—腫瘤學(xué)副教授、主管研究員馬克·博卡德說(shuō)：“我們從一個(gè)細胞變成兩個(gè)核開(kāi)始觀(guān)察，吃驚地發(fā)現細胞沒(méi)經(jīng)過(guò)有絲分裂，而是直接由一個(gè)細胞變成了兩個(gè)細胞。”每個(gè)新細胞都遺傳了一個(gè)完整無(wú)缺的細胞核，包含一套完整染色體。分裂發(fā)生的時(shí)間出乎預料，是在延遲生長(cháng)階段，而不是在有絲分裂結束時(shí)。他們還做了大量額外實(shí)驗，以確定這種分裂和正常的細胞分裂形式“胞質(zhì)分裂”不同。

　　他們還發(fā)現，有90%的子細胞恢復為正常的配對染色體。博卡德認為，在一個(gè)生物經(jīng)過(guò)的所有細胞分裂周期中，每次的胞質(zhì)分裂偶爾也會(huì )失敗。這種新分裂是一種補救機制，讓細胞能從故障中恢復正常。

　　“如果我們能促進(jìn)這種新形式的細胞分裂，就可能預防某些癌癥的發(fā)展。”博卡德說(shuō)，他希望能把這一數字提高到99%。現在他們的目標是為有多倍染色體的乳腺癌患者開(kāi)發(fā)出新的治療方案。

　　Researchers at the University of Wisconsin Carbone Cancer Center have discovered a new form of cell division in human cells.

　　They believe it serves as a natural back-up mechanism during faulty cell division, preventing some cells from going down a path that can lead to cancer.

　　"If we could promote this new form of cell division, which we call klerokinesis, we may be able to prevent some cancers from developing," says lead researcher Dr. Mark Burkard, an assistant professor of hematology-oncology in the department of medicine at the UW School of Medicine and Public Health.

　　Burkard presented the finding on Monday, Dec. 17 at the annual meeting of the American Society for Cell Biology in San Francisco.

　　A physician-investigator who sees breast cancer patients, Burkard studies cancers in which cells contain too many chromosomes, a condition called polyploidy.

　　About 14 percent of breast cancers and 35 percent of pancreatic cancers have three or more sets of chromosomes, instead of the usual two sets. Many other cancers have cells containing defective chromosomes rather than too many or too few.

Burkard

　　"Our goal in the laboratory has been to find ways to develop new treatment strategies for breast cancers with too many chromosome sets," he says.

　　The original goal of the current study was to make human cells that have extra chromosomes sets. But after following the accepted recipe, the researchers unexpectedly observed the new form of cell division.

　　Until now, Burkard and most cell biologists today accepted a century-old hypothesis developed by German biologist Theodor Boveri, who studied sea urchin eggs. Boveri surmised that faulty cell division led to cells with abnormal chromosome sets, and then to the unchecked cell growth that defines cancer. With accumulated evidence over the years, most scientists have come to accept the hypothesis.

　　Normal cell division is at the heart of an organism's ability to grow from a single fertilized egg into a fully developed individual. More than a million-million rounds of division must take place for this to occur. In each division, one mother cell becomes two daughter cells. Even in a fully grown adult, many kinds of cells are routinely remade through cell division.

　　The fundamental process of cells copying themselves begins with a synthesis phase, when a duplicate copy is made of cell components, including the DNA-containing chromosomes in the nucleus. Then during mitosis, the two sets are physically separated in opposite directions, while still being contained in one cell. Finally, during cytokinesis, the one cell is cut into two daughter cells, right at the end of mitosis.

　　Burkard and his team were making cells with too many chromosomes-to mimic cancer. The scientists blocked cytokinesis with a chemical and waited to see what happened.

　　"We expected to recover a number of cells with abnormal sets of chromosomes," Burkard explains.

　　The researchers found that, rather than appearing abnormal, daughter cells ended up looking normal most of the time. Contrary to Boveri's hypothesis, abnormal cell division rarely had long-term negative effects in human cells.

　　So the group decided to see how the human cells recovered normal sets of chromosomes by watching with a microscope that had the ability to take video images.

　　"We started with two nuclei in one cell," Burkard says. "To our great surprise, we saw the cell pop apart into two cells without going through mitosis."

　　Each of the two new cells inherited an intact nucleus enveloping a complete set of chromosomes. The splitting occurred, unpredictably, during a delayed growth phase rather than at the end of mitosis.

　　The scientists did a number of additional experiments to carefully make sure that the division they observed was different than cytokinesis.

　　"We had a hard time convincing ourselves because this type of division does not appear in any textbook," Burkard says.

　　Over time, they found that only 90 percent of daughter cells had recovered a normal complement of chromosomes. Burkard would like to leverage that statistic up to 99 percent.

　　"If we could push the cell toward this new type of division, we might be able to keep cells normal and lower the incidence of cancer," he says.

　　Burkard now thinks that among all those rounds of cell division an organism goes through, every once in a while cytokinesis can fail. And that this new division is a back-up mechanism that allows cells to recover from the breakdown and grow normally.

　　The group has dubbed the new type of division klerokinesis to distinguish it from cytokinesis. Burkard enlisted the help of William Brockliss, UW assistant professor of classics, to come up with the name; klero is a Greek prefix meaning "allotted inheritance."

　　Collaborators on the project include Beth Weaver, UW assistant professor of cell and regenerative biology; Dr. Alka Choudhary; Robert Lera;  Melissa Martowicz and Jennifer Laffin.