What Is the Cancer Research of Henry Heng at Wayne State University?

Question by Kevin7: What is the cancer research of Henry Heng at Wayne State University?

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Answer by Ted H
DETROIT, June 8, 2010 – For decades, cancer has been believed to be caused by a sequential accumulation of common gene mutations, with the identification, characterization and targeting of common genetic alterations and their defined pathways dominating the field. A Wayne State University researcher is challenging this notion, however, with evidence that the general mechanism of cancer occurs at the level of the genome, not the gene. Henry Heng, Ph.D., associate professor in WSU’s Center for Molecular Medicine and Genetics and resident of Detroit, published a study in a recent edition of the Journal of Cellular Biochemistry in which he says, “Considering cancer as an evolutionary process is vital to both basic research and clinical applications. Unfortunately, most previous efforts have focused on individual cancer genes, which represent only a small part of the evolutionary story of cancer. A growing body of evidence suggests that no distinguishable pattern can be discerned from single gene studies. Instead, it appears that finding a general mechanism will require us looking to the system as a whole – the genome.” According to the theory, most genetic information cannot be defined at the gene level because the function of an individual gene is dependent on the genome context – its position relative to other genes and environmental factors. The theory is supported by previous discoveries that cancer progression requires evolution of the genome as a whole, or macroevolution.

Despite the impressive amount of data accumulated from studies of gene mutations, epigenetic dysregulation and pathway alterations, an overwhelming amount of diverse molecular information has offered only a limited understanding of the general mechanism. To solve this paradox, Heng’s group applied the newly established genome theory to describe how somatic cells evolve within individual patients. Using cell culture and animal models, they identified three key components of somatic cell evolution that are responsible for cancer formation: increased dynamics induced by stress, elevated genetic and epigenetic heterogeneity, and natural selection mediated by genome alteration. Results of the study showed a correlation between cancer progression events – immortalization, transformation, metastasis and drug resistance – and changes at the genome level. No common pattern of gene mutations was discovered. In fact, cancer risk was found to be associated with higher levels of genetic diversity.

As a result of this and previous findings, Heng said, the field of cancer research should begin to shift its search for evolutionary mechanisms to the genome level.

Cancer is commonly viewed as a disease of the stepwise accumulation of gene mutations. However, genetic and epigenetic heterogeneity (GEH) is pervasive in cancer, playing a key role in promoting cancer progression. GEH occurs at three primary levels, the genome, gene and epigenetic levels and increases during the aging process and during stress. GEH at the genome level plays the largest role of the three in cancer evolution, as genome level change creates new cellular systems whereas genetic and epigenetic level change mainly modify the existing system. This system replacement achieved by genome level change is essential for cancer evolution. GEH challenges traditional molecular-based cancer research that focuses on common gene mutations in linear models of progression. Clinically, GEH must be monitored in order to determine the evolutionary potential of a tumour. Increased knowledge about GEH will benefit basic research and cancer treatment.

Key Concepts:
**** Cancer progression is a typical process of somatic evolution of which system heterogeneity is a key component.
**** Genetic and epigenetic heterogeneity occurs at three levels: the genome level, the gene level and the epigenetic level. The three levels of genetic and epigenetic heterogeneity are highly interactive. Genome level heterogeneity can influence gene and epigenetic level heterogeneity and vice versa.

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