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

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

　　一個世紀(jì)前，德國生物學(xué)家西奧多·博韋里通過海膽卵實驗提出假說，錯誤分裂會導(dǎo)致細(xì)胞染色體倍數(shù)異常和細(xì)胞不受遏制地生長，這就是癌癥。在癌細(xì)胞的細(xì)胞核中，染色體常常會在分裂過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(xì)胞會有3套或更多染色體，沒有多余染色體的癌細(xì)胞則含有錯誤染色體。

　　研究小組給人類細(xì)胞復(fù)制出了多倍染色體，以模擬癌癥。他們用一種常規(guī)化學(xué)物質(zhì)阻止了胞質(zhì)分裂，結(jié)果發(fā)現(xiàn)分裂并未顯出異常，子細(xì)胞在大部分情況下看起來都很正常，這和博韋里假設(shè)相悖。

　　他們進一步觀察了人類細(xì)胞是怎樣恢復(fù)正常染色體倍數(shù)的。該校醫(yī)學(xué)與公共衛(wèi)生學(xué)院醫(yī)學(xué)部血液—腫瘤學(xué)副教授、主管研究員馬克·博卡德說：“我們從一個細(xì)胞變成兩個核開始觀察，吃驚地發(fā)現(xiàn)細(xì)胞沒經(jīng)過有絲分裂，而是直接由一個細(xì)胞變成了兩個細(xì)胞。”每個新細(xì)胞都遺傳了一個完整無缺的細(xì)胞核，包含一套完整染色體。分裂發(fā)生的時間出乎預(yù)料，是在延遲生長階段，而不是在有絲分裂結(jié)束時。他們還做了大量額外實驗，以確定這種分裂和正常的細(xì)胞分裂形式“胞質(zhì)分裂”不同。

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

　　“如果我們能促進這種新形式的細(xì)胞分裂，就可能預(yù)防某些癌癥的發(fā)展。”博卡德說，他希望能把這一數(shù)字提高到99%?，F(xiàn)在他們的目標(biāo)是為有多倍染色體的乳腺癌患者開發(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.