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Original research carried out on the Rambam campus holds promise for developing new methods for controlling cancer’s growth, and new therapies that may transform cancer from a rapidly lethal disease to a chronic manageable disorder.
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The study was conducted jointly by Rambam Medical Center and the Technion’s Rappaport Faculty of Medicine and Research Institute. The investigation was led by Prof. Karl Skorecki, Director of Medical and Research Development at Rambam and Director of the Rappaport Research Institute, and Dr. Maty Tzukerman, Senior Scientist and Project Director at Rambam’s Molecular Medicine Laboratory. The findings were first published online on February 14, 2012 in the journal STEM CELLS (30:415-424).
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Professor Karl Skorecki giving a lecture on "the power of DNA," during the 2010 Rambam Summit
Koko-RHCC |
The team built on previous studies in which they had determined that some tumor cells appear to differentiate (mature and specialize) while others retain the property of self-renewal that makes cancer so deadly. The new research attempts to understand how cancer grows, and to find ways to halt cancer cells’ runaway replication.
The researchers used a carrier mouse as a platform for artificially growing a variety of human stem cell lines. From these cell lines, they created a benign teratoma (a tumor comprised of a heterogeneous mix of cells and tissues). They then took cells from one woman’s ovarian clear cell carcinoma for their source of human cancer cells. They injected the malignant cells either into or alongside the benign teratoma, rendering it cancerous. Their aim was to mimic the human cancer environment as closely as possible, and then to monitor the behavior and proliferation of human cancer cells. Using this human stem cell derived platform, the scientists were able to tease out a remarkable six different kinds of self-renewing cancer cell subpopulations based on their molecular profiles and behavior — how quickly they grew, how aggressive they were, and how they differentiated.
Until now, it had not been known that one cancerous tumor might have such a diversity of cells with fundamental growth properties. When the researchers cloned and expanded the six distinct cell subpopulations, this led them to another key observation: some cancer cells, which had not self-replicated in any other environment, became self-replicating when exposed to non-cancerous human stem cells.
“We noticed, rather strikingly, that human cancer cells grow and proliferate more robustly when exposed to a population of human cells compared to any other environment in which we grew them, such as in a mouse muscle or under the skin of a mouse,” says Prof. Skorecki. He adds that while he wasn’t surprised that the human environment affected the growth, he was in fact surprised by the magnitude of influence.
The researchers concede that they do not yet know the cues that enhance cancer’s proliferation. The team is now working on isolating the factors in human cells that promote cancerous plasticity and self-renewal. An important next step will be to pursue targeted drug discovery aimed at blocking cancer cell lines’ self-renewal mechanisms. This hoped-for discovery may eventually allow physicians to manage cancer as a chronic disease.
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