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Cancer biologist Piyush Gupta joins the Whitehead Institute faculty in September on a mission to shed new light on the mechanisms that determine why some cells in our bodies behave appropriately while others venture down destructive, malignant paths.

Human embryonic stem (ES) cells and adult cells reprogrammed to an embryonic stem cell-like state—so-called induced pluripotent stem or iPS cells—exhibit very few differences in their gene expression signatures and are nearly indistinguishable in their chromatin state, according to Whitehead Institute researchers.

Researchers at Whitehead Institute and Children’s Hospital Boston have identified a protein, called Musashi 2, that is predictive of prognosis in acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) patients. High levels of Musashi 2 protein is associated with increased cell proliferation, decreased cell maturation, and multiple cancer-related cellular pathways in human leukemias.

Cells from frozen human blood samples can be reprogrammed to an embryonic stem-cell-like state, according to Whitehead Institute researchers. These cells can be multiplied and used to study the genetic and molecular mechanisms of blood disorders and other diseases.

Whitehead Institute Founding Member Gerald Fink has been awarded the 2010 Genetics Prize of The Peter and Patricia Gruber Foundation for his groundbreaking research in yeast genetics.

Oxygen levels in the lab can permanently alter human embryonic stem (ES) cells, specifically inducing X chromosome inactivation in female cells, according to Whitehead Institute researchers.

Whitehead Institute researchers have determined a key part of how cells regulate the chromosome/microtubule interface, which is central to proper chromosomal distribution during cell division.

Whitehead Institute researchers have converted established human induced pluripotent stem (iPS) cells and human embryonic stem (ES) cells to a base state of greater pluripotency. 

Whitehead Institute researchers have identified the mechanism that the protein c-Myc uses to regulate gene transcription, which affects one-third of the expressed genes in the genome. The work also reveals a general role for this mechanism in gene control, which is called transcriptional pause release.

According to Whitehead Institute researchers, cells take advantage of a biologically ancient compartment to sequester prions, an action that can initially prevent the prions’ phenotypic expression. While in this compartment, less stably heritable prion plaques also mature to a more transmissible state.