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J Med Oncl Ther 2017 Volume 2 | Issue 3

International Conference on

Oncology and Cancer Therapeutics

October 30- November 01, 2017 | Chicago, USA

Onco-histone H3.3K36M reprograms the epigenome of chondroblastomas

Fang Dong

Columbia University, USA

ith the expansion of cancer genome sequencing,

many chromatin-regulating genes are found mutated.

The surprising finding is that of histone proteins, the basic

structural components of the human chromatin and is

mutated in a variety of cancers. Specifically, a somatic histone

H3.3 lysine 36 to methionine (K36M) mutation is identified in

over 90% of chondroblastomas. In human genome, there are

13 genes encoding canonical histone H3 proteins that differ

from two H3.3 genes by four or five amino acids. H3K36 is

conserved among all these histone proteins. Therefore, it

is unknown how mutations at one allele of 15 histone H3

genes are linked to Tumorigenesis. We have shown that

the levels of H3K36 di- and tri-methylation (H3K36me2/

me3) are reduced dramatically in chondroblastomas and

chondrocytes bearing the same the genetic mutation as

chondroblastomas. Mechanistically, we show that H3.3K36M

mutant proteins inhibit enzymatic activity of some, but all

H3K36 methyltransferases. In addition, chondrocyte cells

with H3.3K36M mutant proteins exhibit several hallmarks

of cancer cells. Based on these studies, we propose that

H3.3K36M mutant proteins alter epigenomes of specific

progenitor cells, which in turn lead to cellular transformation

and tumorigenesis.

Speaker Biography

Fang Dong is an Associate Research Scientist in Institute of Cancer Genetics of

Columbia University. He has expertise in evaluation and passion in improving the

health and wellbeing. His open and contextual evaluation model based on responsive

constructivists creates new pathways for improving healthcare. He works under the

Leadership of Dr. Zhiguo Zhang.