How cancer begins
Cells become cancerous after acquiring a series of mutations in their DNA, which occur as a result of exposure to radiation, cigarette smoke, dietary components or a genetic predisposition.
Mutations may intensify or eliminate the messages cells use to grow, stop growing or die. Cells then begin to divide too often and are unable to die, forming tumors. Identifying the mutations, signals and mechanisms that promote and sustain tumors creates new opportunities to target human cancer.
We’ve brought together scientists with expertise in developmental and stem cell biology with investigators who focus on RNA biology and the signaling pathways that regulate cell growth and cell fate. The diversity of our faculty members, along with our shared interests in what drives cancer cell growth, is fostering strong interactions that will lead to breakthrough treatments for brain, breast and prostate cancers, as well as melanoma and leukemia.
– Robert Wechsler-Reya, Ph.D., Program Director
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PTEN and DNA-PK determine sensitivity and recovery in response to WEE1 inhibition in human breast cancer.
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Zika Virus Targets Glioblastoma Stem Cells through a SOX2-Integrin α<sub>v</sub>β<sub>5</sub> Axis.
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