October 6, 2015

Artificial Intelligence Uncovers Clues to Why Embryos Develop Abnormally

Left: A normal tadpole. Right: A tadpole in which the pigment cells’ normal bioelectrical
signaling was interrupted, inducing the cells to develop melanoma-like characteristics.
Photo: Courtesy of the Levin Lab/Tufts University

(October 6, 2015)  Melanoma-like cells in tadpoles may mimic variability in human responses to cancer stimuli

Uncle Joe smokes a pack a day, drinks like a fish and lives to a ripe old age. His brother, leading a similar lifestyle, succumbs to cancer at age 55. Why do some individuals develop certain diseases or disorders while others do not? In newly reported research that could help provide answers, scientists at Tufts University, in collaboration with the University of Florida, have developed a novel approach that uses artificial intelligence to illuminate cellular processes and suggest possible targets to correct aberrations. 

The findings, published Oct. 6 in Science Signaling online in advance of print, are believed to mark the first time artificial intelligence has been used to discover a molecular model that explains why some groups of cells deviate from normal development during embryogenesis, said senior author Michael Levin, Ph.D., the Vannevar Bush Professor of Biology at Tufts and director of the Tufts Center for Regenerative and Developmental Biology.

The paper builds on the center's earlier studies to understand development and metastasis of melanoma-like cells in tadpoles as well as work applying artificial intelligence to help explain planarian regeneration. The new findings, Levin said, indicate that "our methodology can be taken well beyond simple organisms and applied to the physiology of cell behavior in vertebrates."

For the Science Signaling work, the researchers applied a type of artificial intelligence called evolutionary computation to pinpoint the molecular mechanisms underlying earlier research in which they induced normal pigment cells in embryonic Xenopus laevis frogs to metastasize. Researchers used a series of drugs to disrupt the cells' normal bioelectrical and serotonergic signaling at a crucial stage of development. Even in the absence of DNA damage or exposure to carcinogens, the pigment cells of the affected embryos acquired bizarre, branch-like shapes and developed other melanoma-like characteristics, proliferating uncontrollably and invading the frogs’ internal organs.

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