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Genes encode proteins, and proteins often work like minuscule molecular switches, activating yet other proteins and inactivating others, turning molecular switches \u201con\u201d and \u201coff\u201d inside a cell. Thus, a conceptual diagram can be drawn for any such protein: protein A turns B on, which turns C on and D off, which turns E on, and so forth. This molecular cascade is termed the signaling pathway for a protein. Such pathways are constantly active in cells, bringing signals in and signals out, thereby allowing a cell to function in its environment.<\/p>\n\n\n\n
Proto-oncogenes and tumor suppressor genes, cancer biologists discovered, sit at the hubs of such signaling pathways. Ras, for instance, activates a protein called Mek. Mek in turn activates Erk, which, through several intermediary steps, ultimately accelerates cell division. This cascade of steps, called the Ras-Mek-Erk pathway\u2014is tightly regulated in normal cells, thereby ensuring tightly regulated cell division. In cancer cells, activated \u201cRas\u201d chronically and permanently activates Mek, which permanently activates Erk, resulting in uncontrolled cell division\u2014pathological mitosis.<\/p>\n\n\n\n
But the activated ras pathway (Ras? Mek ? Erk) does not merely cause accelerated cell division; the pathway also intersects with other pathways to enable several other \u201cbehaviors\u201d of cancer cells. At Children\u2019s Hospital in Boston in the 1990s, the surgeon-scientist Judah Folkman demonstrated that certain activated signaling pathways within cancer cells, ras among them, could also induce neighboring blood vessels to grow. A tumor could thus \u201cacquire\u201d its own blood supply by insidiously inciting a network of blood vessels around itself and then growing, in grapelike clusters, around those vessels, a phenomenon that Folkman called tumor angiogenesis.<\/p>\n\n\n\n
Folkman\u2019s Harvard colleague Stan Korsmeyer found other activated pathways in cancer cells, originating in mutated genes, that also blocked cell death, thus imbuing cancer cells with the capacity to resist death signals. Other pathways allowed cancer cells to acquire motility, the capacity to move from one tissue to another\u2014initiating metastasis. Yet other gene cascades increased cell survival in hostile environments, such that cancer cells traveling through the bloodstream could invade other organs and not be rejected or destroyed in environments not designed for their survival.<\/p>\n\n\n\n
Cancer, in short, was not merely genetic in its origin; it was genetic in its entirety. Abnormal genes governed all aspects of cancer\u2019s behavior. Cascades of aberrant signals, originating in mutant genes, fanned out within the cancer cell, promoting survival, accelerating growth, enabling mobility, recruiting blood vessels, enhancing nourishment, drawing oxygen\u2014sustaining cancer\u2019s life.<\/p>\n\n\n\n
These gene cascades, notably, were perversions of signaling pathways used by the body under normal circumstances. The \u201cmotility genes\u201d activated by cancer cells, for instance, are the very genes that normal cells use when they require movement through the body, such as when immunological cells need to move toward sites of infection. Tumor angiogenesis exploits the same pathways that are used when blood vessels are created to heal wounds. Nothing is invented; nothing is extraneous. Cancer\u2019s life is a recapitulation of the body\u2019s life, its existence a pathological mirror of our own. Susan Sontag warned against overburdening an illness with metaphors. But this is not a metaphor. Down to their innate molecular core, cancer cells are hyperactive, survival-endowed, scrappy, fecund, inventive copies of ourselves.<\/p>\n\n\n\n