Unlocking Cancer’s Molecular Processes

New research, led by a medical student and a cancer biologist at the College of Osteopathic Medicine (NYITCOM), aims to continue the historic work of a world-renowned Nobel laureate and explain why some human cells become cancerous, spread, and resist treatment.

Our bodies depend on a tightly controlled and well-executed process of cellular reproduction to create and maintain healthy tissues and organs. When cells reproduce, the genetic materials (DNA) inside them are duplicated and passed on to new cells. However, for duplication to occur precisely and correctly, the cell’s “replication machinery” must overcome structural or molecular roadblocks in the process. The ends of chromosomes are genomic regions full of roadblocks, and failure to overcome these blocks can lead to damage, preventing proper duplication.

When damaged chromosome ends fuse with other broken chromosome ends, this initiates a cycle in which chromosomes break, fuse, form a bridge, and break again. Known as the “breakage-fusion-bridge (BFB) cycle,” this series of events causes a cascade of DNA mutations that eventually leads to tumor formation, metastasis (spreading), and drug resistance.

The BFB cycle was first discovered in the late 1930s by the world-renowned geneticist and Nobel laureate Barbara McClintock, Ph.D. While McClintock’s hypothesis of the BFB cycle was groundbreaking, the technology did not yet exist to pin down the molecular cause that triggers the cycle.

Now, as seen in the journal Nucleic Acids Research, an innovative study led by Manrose “Manny” Singh, a fifth-year student in the Osteopathic Medicine, D.O./Medical and Biological Sciences, Ph.D. (D.O./Ph.D.) program, builds upon McClintock’s work to provide a possible answer. The research was primarily conducted in the laboratory of Professor and Director of the Center for Cancer Research Dong Zhang, Ph.D., located on New York Tech’s Long Island campus.