In the meantime, Pawelek’s work has inspired other labs—75 scientists attended the first meeting on cell fusion and cancer in Sweden in October 2007, where Pawelek was a featured speaker. The hybrid theory, it seems, is spreading once more.
Note: This article was originally printed with the title, "A Theory of a Deadly Fusion".
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3 Comments
Add CommentPawelek's hypothesis is very interesting and seems plausible, but unfortunately, the evidence in support of his hypothesis is not strong.
Reply | Report Abuse | Link to thisThe forensic DNA analysis approach seems to be the obvious way to go to provide stronger support for this hypothesis. An experiment could be conducted to determine whether macrophage DNA is present or comingled with tumor cell DNA. A fairly simple experiment would be to take bone marrow cells from a donor, label the DNA in the donor cells, then take some tumor cells from the host and label the DNA with another chemical marker. Then put both donor and host cells back into the host and when the cancer spreads to a new area, remove tumor cells from the new area and look for donor DNA mixed with the host's DNA in the tumor cells.
I would guess that this type of experiment has already been done...maybe no one has come up with results that would back up Pawalek's hypothesis?
Actually it may be worth taking the cell fusion theory one step further beyond metastasis, in an attempt to justify oncogenesis itself based on the following assumptions.
Reply | Report Abuse | Link to thisGenomic fusion between cells generates diversity. This diversity can be selected upon by its environment. In the case of cancer the selection is for uncontrolled cell growth. In theory if one shuffles the genome of a cell most of the cell progeny will be not be viable however the possibility exist that the shuffling event will generate the genetic fusions that we often see in tumor cells.
Whether or not a macrophage are involved is not the soul issue, indeed a prearranged epigenome of a macrophage should give an advantage for metastasis as compared to other cells when fused to a non metastatic tumor. However the role of cell fusion may not limited to metastasis alone, but rather contribute to the genomic instability that is often seen in cancer.
Which raises the question, is genomic fusion the driving force in oncogenesis that leads to oncogenes? Maybe the experiment to do would be to take cells that are amendable to fusion such as stem cells, and fuse them together then select for uncontrolled growth as compared to non-fused cells. The hypothesis would be that the diversity generated by the fusion would introduce the necessary mutations to initiate oncogenesis. The counter would be that reverse fusion (mitosis) directs the rearrangement. In any event pursuing the cause of metastasis/oncogenesis whether it is fusion or reverse fusion contributes to our knowledge regardless of the outcome.
One aspect that should be incorporated into any experiments with cell fusion is using a fusible cell lines such as stem cells.
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