A new study from Cold Spring Harbor Laboratory suggests the tumors might not be as invincible as previously thought.
More than half of all human cancers have mutations that disable a protein called p53. When cells lose p53, tumors grow aggressively and often cannot be treated.
Researchers report that another protein called TAp63, an older sibling of p53 that's usually intact and not mutated in most cancers may be the answer.
Using chromosome engineering researchers noted that they have succeeded in shutting off the growth of tumors in which p53 is missing by turning up the production of TAp63 proteins, which make up one class of proteins produced by the p63 gene.
They completely blocked tumor initiation by inducing a state of growth arrest in which tumor cells are still metabolically alive but fail to divide.
The study, funded by a Research Scholar Award from the American Cancer Society, appears online ahead of print on November 8th in Nature Cell Biology. Some 1.4 women were diagnosed with cancer over the past 12 months according to the American Association for Critical Illness Insurance and over 565,000 Americans die each year from cancer.
Researchers reported that of the six different proteins that are produced from the p63 gene, three promote activities that could lead to cancer. The remaining three, which are TAp63 versions, do the opposite: prevent cancer by triggering senescence -- a process that shuts down the tumor.
The medical scientists found that TAp63 could also substitute for p53 in its ability to halt tumor growth. When TAp63 was turned on in Ras-producing cells that were missing p53, tumors never started. The team went a step further and showed that in addition to blocking the initiation of tumors, TAp63 could also shut down tumors that were already established.
Written by Mindy Hartman
Los Angeles, CA
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