It’s clear why melanoma cells are so dangerous when you watch them in action.
Researchers recently did just that, documenting in real time (and in 3D) how melanoma cells form tumors. The cells waste no time finding their cancerous cousins, slashing their way through a lab-prepared gel to quickly join other melanoma cells and form tumors.
For a new study, published in PLOS ONE, the scientists used unique computer-assisted 3D reconstruction software to chronicle how both breast tissue cancer cells and melanoma cells form tumors.
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The video above shows healthy skin cells in action. The video below shows how melanoma cells aggressively move and join with other melanoma cells to mostly form one large tumor. It’s believed to be the first time that melanoma tumor creation has been shown in continuous, real time. (Credit: Soll Laboratory)
The two cancers act similarly in the joining stages of tumor formation. With that knowledge, they screened more than four dozen monoclonal antibodies—unique agents that can stop cells from growing or forming tumors and can be mass produced—before finding two that block tumor creation in both types of cancer.
“It upholds our hypothesis that coalescence is so similar that there’s got to be the same molecules and mechanisms that do it, and we may be able to find a drug that shuts tumor formation down without being toxic to healthy cells in the body,” says David Soll, professor of biology at the University of Iowa and the paper’s corresponding author.
In earlier work, Soll’s team showed that human breast cancer cells form tumors by extending cables—bridges of sorts—between small aggregates of cancer cells. In the current study, the group reports that melanoma cells behave in a similar way, but with variations in timing and speed.
For one, melanoma cells are on the go immediately and at all times; they appear to both divide into more cells and rush to join clusters simultaneously.
“…there might be a magic bullet (to stop tumor formation) for all cancers.”
One lab test showed a single cell moving a distance three times its diameter and joining with a small cancerous cluster in just four hours. In another instance, within 72 hours, 24 individual melanoma cells or small clusters of cells had mostly repositioned themselves into one large cancerous clot—an 80 percent accretion rate. Melanoma cells are “fast as lightning,” Soll says. “They don’t sit still. They’ve got ants in their pants.”
Breast cancer cells, in contrast, are more ponderous and lumbering in both their movements and in forming tumors, waiting on average 100 hours—dividing into more cells during much of that interval—before forming “clonal islands,” or small clusters that then gradually join to form large tumors.
The reason why melanoma cells seem to always be on the move could lie in their evolutionary origin, Soll says. Melanocytes, healthy skin cells that form the pigment melanin, come from neural crest cells, which are created in the spinal column. Once programmed, melanocytes migrate through the tissue to take their place in the upper layer of the skin. “They’re professional crawlers,” Soll says. “They were born to move.”
Because melanoma cells are derived from melanocytes, it stands to reason that melanoma cells would retain the same mobile profile. Study tests appear to show that is the case.
Still, how melanoma cells join into tumors—whether by individual cells coming together or small or large clusters of cells doing so—follows the same pattern as breast tissue cancer cells: Cables are extended to reel in other cells or clusters.
That was an interesting revelation to Soll, who then screened 51 monoclonal antibodies before finding two, anti-beta 1 integrin/(CD29) and anti-CD44, that blocked tumor creation in both cancers.
“What’s so cool is the same drug that stops breast cancer cells from undergoing coalescence also stops melanoma cells from undergoing coalescence, despite these cancers’ whole history being different,” Soll says. “That means there’s a commonality despite the different origins. And that also means there might be a magic bullet (to stop tumor formation) for all cancers.”
The Monoclonal Antibody Research Institute and the Developmental Studies Hybridoma Bank, the latter a national resource created by the National Institutes of Health housed at the University of Iowa, funded the work.
Source: University of Iowa
Original Study DOI: 10.1371/journal.pone.0173400
Article by Richard Lewis-Iowa