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The molecular basis of cancer metastasis: multi-step metastasis process and anti-metastasis therapeutic development

Part 2 of 2
Published on April 30, 2023   26 min

Other Talks in the Series: The Molecular Basis of Cancer

Other Talks in the Series: Periodic Reports: Advances in Clinical Interventions and Research Platforms

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0:05
One major concept I would like to discuss is this multi-step metastasis model. In there the EMT program is actually not a one-way street. The reason I say that is because we all know that when the patient developed distant metastasis, the distant metastasis actually present many of the same features of the primary tumor. What I mean is, if you have a breast cancer, the distant metastasis also is a breast tumor and may still express ER, or still express HER2 and still maintain a relative epithilioid morphology. There are a lot of debate in the field. If the distant metastasis do not look like a sarcoma does not look like a mesenchymal tumor, how can EMT program play a role? I think that brought up to this very important concept that EMT is not a one-way street. Tumor cells actually appear on this program to allow the invasion and intravasation, the extravasation. By that distant site, we think this program probably needs to be turned off to allow this migrated cell to actually now stay in a distant site to start to regrow and colonize the distance site. In the next few slides, I would like to show you some of the evidence from animal models to show the importance of this plasticity.
1:30
But before I go on, I want to show you the evidence why we think EMT plasticity exists in human cancer. I think the best place to look at this plasticity in human patient is in circulating tumor cells. This is the early study from Ming Hu, the isolated circulating tumor cells from breast cancer patients. You can see there's 17 patients than they stained for either epithelial or mesenchymal markers defined the circulating cell either they're E or EM or M. As you can see here in the majority of the patient, there are highly enriched sub population of the cell that present a mesenchymal signature. And this has been reported not only in breast cancer, but also in many type of human eye carcinomas. So what this suggests is that the enrichment of this more mesenchymal phenotype, this is a much higher than present in a primary tumor. Usually the more mesenchymal cell cannot be, go over 10 percent. Is that turning on this program probably gave this tumor cell the advantage to be able to enter the circulation to become CTC.

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