Slashdot Mirror
Method For Fooling Cancer Cells Into Fat Cells Can Stop Cancer's Spread (technologynetworks.com)
Researchers from the University of Basel in Switzerland have discovered that they can prevent the formation of metastases by fooling breast cancer cells into fat cells. The proof-of-concept study was published in the journal Cancer Cell. Technology Networks reports: Malignant cells can rapidly respond and adapt to changing microenvironmental conditions, by reactivating a cellular process called epithelial-mesenchymal transition (EMT), enabling them to alter their molecular properties and transdifferentiate into a different type of cell (cellular plasticity). Cancer cells can exploit EMT -- a process that is usually associated with the development of organs during embryogenesis -- in order to migrate away from the primary tumor and form secondary metastases. Cellular plasticity is linked to cancer survival, invasion, tumor heterogeneity and resistance to both chemo and targeted therapies. In addition, EMT and the inverse process termed mesenchymal-epithelial transition (MET) both play a role in a cancer cell's ability to metastasize.
Using mouse models of both murine and human breast cancer the team investigated whether they could therapeutically target cancer cells during the process of EMT -- whilst the cells are in a highly plastic state. When the mice were administered Rosiglitazone in combination with MEK inhibitors it provoked the transformation of the cancer cells into post-mitotic and functional adipocytes (fat cells). In addition, primary tumor growth was suppressed and metastasis was prevented. Since both drugs used in the preclinical study were FDA-approved the team are hopeful that it may be possible to translate this therapeutic approach to the clinic.
Using mouse models of both murine and human breast cancer the team investigated whether they could therapeutically target cancer cells during the process of EMT -- whilst the cells are in a highly plastic state. When the mice were administered Rosiglitazone in combination with MEK inhibitors it provoked the transformation of the cancer cells into post-mitotic and functional adipocytes (fat cells). In addition, primary tumor growth was suppressed and metastasis was prevented. Since both drugs used in the preclinical study were FDA-approved the team are hopeful that it may be possible to translate this therapeutic approach to the clinic.
The idea is to make the cancer behave like a fat cell, so it'll not metastasize or grow uncontrollably. It'll still be well-behaved cancer so depending on where it is, age and so on you still may want to have further treatment but it is much easier to treat cancer if it isn't metastatic. Even if this was a light sci-fi comedy, it'd be better to get fat than to have metastatic cancer.
The "fit and fat" hypothesis has been disproved.
Fat is not healthy (BMI should be 25)
Heart disease, stroke, diabetes, cancer rates all higher in fat people.
I don't read your sig. Why are you reading mine?
I am a bit suspicious of the value of studies that have not been replicated for more than one case. This is one of those. It is very clever work but I don't think the chances that it will lead to a cancer therapy are particularly high. The idea behind the work is that cells from breast cancer are one type (epithelial), but they need to convert into another type (mesenchymal) so they can leave the tumor and form metastasis. The clever part is that they nudge the mesenchymal cells to convert to fat cells and stop dividing. The problem is that the occurrence of the epithelial to mesenchymal transition in tumors is a bit of a controversial topic. The idea has a devoted cult following, but it has not been convincingly shown to be true. We know that the breast cancer tumors are epithelial and we know that their metastasis are epithelial. Genetic tagging to detect the transition in actual tumors so far have failed to do so and have shown that you don't need this transition to form metastasis. We also can see epithelial cells leaving the tumor without the need to convert to a different cell type. In the work, they use cell lines (cell cultured in a dish) that either readily undergo the epithelial to mesenchymal transition when exposed to a hormone that is abundant in the tissue and the blood (TGF-Beta), or a cell line that is mesenchymal (MDA-MB-231). These experiments show that when you inject these cell lines in a mouse you can reprogram them into fat cells. To make sure the reprogramming also works on tumors they use a human patient derived tumor that is grown in mice. Here is where my major problem with the work is. There are hundreds of these patient derived tumors that are available but they do the experiments on just one. Why just one? Why this particular one? If you are developing a cancer therapy one of the major questions is what are the chances that it will work. You answer that question by testing as many tumors as you can.