Confronting Tumor Cells Head On
Cells within tumors are as individual and unpredictable as the people they attack – and the tumor is as complex as the body it is assaulting. Diverse in character and content, the cells constantly change as they multiply. “Our goal is to understand how this happens, which pathways can influence the identity they will acquire and how to use this knowledge as a potential means of effective therapy, ” says Dr. Ittai Ben-Porath, PhD, who heads a research team in the Faculty of Medicine’s Department of Developmental Biology and Cancer.
Dr. Ben-Porath and his team are studying the molecular mechanisms that determine tumor growth and metastasis – the functions cancer cells acquire – and the genes controlling them. “Our work is aimed at uncovering the genetic regulators whose activity dictates poor differentiation of breast cancers, focusing on regulatory genes known to play a role in controlling normal stem cell function.” Analysis of the gene expression data they derived led them to identify previously unknown functions of several stem cell-associated regulatory genes.
Cellular senescence – a program of cellular aging – is another central mechanism controlling cancer growth. Senescence represents an important “brake” on cancer development.
When the tumor cells start to multiply, this program leaps into action and prevents them from further dividing. Tumors must therefore get rid of this brake in order to develop. Since this is one of the most universal features of tumors, understanding how senescence works is very important. “The flip side of blocking tumors is aging. As we age, senescent cells accumulate in our body, contribute to disease – and in fact, shorten our life span.”
The aim of both research avenues is to turn the tables on the tumors using their unique characteristics to develop a treatment as individual as the person they are trying to destroy.
“When we know as much as we can, molecularly, about the tumor,” Dr. Ben-Porath says, “we can then determine which drugs apply to which tumor.”
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