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  Haomin Huang


My current focus is to address how cells detect and fix the problems that potentially threat to their genetic stability, in particular, the mitotic checkpoint system and kinetochore proteins, that form a core scaffold to facilitate cell division in human cells.
Genetic instability was one of the first characteristics to be postulated to underlie cancer development. In recent years scientists began to realize that an abnormal chromosome number (aneuploidy) may be the more common reason for genetic instability. The physiological and molecular basis of this pervasive abnormality are still not very clear, but to a large extent are ascribed to the defects in cell division. In fact, all cancers involve the malfunction of genes that control cell growth and division. 

When cell divides, the genetic materials (DNA or chromosomes) are faithfully copied and equally segregated into two daughter cells. In addition to cancer, defects in cell division are also believed to be major causes of birth defects such as Down’s Syndrome. The most important question we are addressing is how the accuracy of cell division is achieved in normal cells and why aneuploidy happens in cancer cells. Together with other scientists, we have uncovered a monitoring system during cell division called mitotic checkpoint. Mitotic checkpoint detects the connection of the separating machinery (microtubules) to unique points (centromeres) on chromosomes. In normal cell division all centromeres have to be connected by microtubules before the chromosomes are equally distributed into two daughter cells. If the mitotic checkpoint is defective, cells will divide before all the chromosomes are properly attached by microtubules, and thus produce daughter cells with unequal numbers of chromosomes (aneuploidy), that can cause cancer. Indeed, defects in mitotic checkpoint genes have been observed in colorectal cancer, hepatocellular carcinoma, lung cancer, leukemia among others.










Postdoctoral fellow


Fox Chase Cancer Center
7701 Burholme Ave
Philadelphia, PA 19111

Lab tel.: 215 728-2472; 215 728-4311
Fax: 215 728-2412


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Huang H, Hittle J, Zappacosta F, Annan R, Hershko A, Yen TJ 
Phosphorylation sites in BubR1 that regulate kinetochore attachment, tension and mitotic exit
J Cell Biol. 2008 (in press)
Huang H, Fletcher L, Beeharry N, Daniel R, Kao G, Yen TJ, Muschel RJ.
Abnormal cytokinesis after X-irradiation in tumor cells that override the G2 DNA damage checkpoint
Cancer Res. 2008 May 15;68(10):3724-32
Huang H, Feng J, Famulski J, Rattner JB, Liu ST, Kao GD, Muschel R, Chan GK, Yen TJ
Tripin/hSgo2 recruits MCAK to the inner centromere to correct defective kinetochore attachments.
J Cell Biol. 2007 May 7;177(3):413-24
Feng J, Huang H, Yen TJ. 
CENP-F is a novel microtubule-binding protein that is essential for kinetochore attachments and affects the duration of the mitotic checkpoint delay.
Chromosoma. 2006 Aug;115(4):320-9.