Good news! Cancer is history! Perhaps new forms of treatments are on the horizon!
"Researchers at the Weizmann Institute of Science, in collaboration with the National Cancer Institute, USA, and other institutions, have now revealed a mechanism that accounts for the spread of a particularly aggressive type of breast cancer.
The study began with a large-scale computational analysis of data from several databases, including information on patient survival and the genes that are overly active in fast-spreading cancers. The scientists came up with a list of some 20 genes, out of about 25,000, that the most aggressive breast cancers appeared to need in order to spread. The top two are genes that play a role in cell division, and they already serve as targets for anticancer drugs. But the third puzzled researchers: It encoded a protein called NUP93, one of the numerous components of the pores, or tunnels of sorts, in the envelope enclosing a cell’s nucleus. ...
The researchers found that NUP93 was present in abnormally large amounts in breast cancer patients with the poorest survival records. As the disease progressed, the genomes of some of these patients came to contain two or three copies of the gene for NUP93 instead of the usual one. Strikingly, many of these patients had tumors that were not sensitive to estrogen. Such tumors, which make up about a third of all breast cancers, are particularly difficult to treat because they lack the estrogen receptors that are targeted by hormonal anticancer drugs. ...
Next, the scientists unraveled the mechanism by which NUP93 plays its grim role in cancer. Because this protein forms a tunnel in the nuclear membrane, it can allow the passage of shuttle proteins called importins, which, among their cargo loads, deliver growth and migration commands from the cytoplasm into the nucleus and thus to the DNA. In this manner, cancer gets access to the cell’s genome, harnessing it for its own needs, namely, increasing the cell’s ability to migrate and revving it up so as to spread the disease. ..."
The researchers found that NUP93 was present in abnormally large amounts in breast cancer patients with the poorest survival records. As the disease progressed, the genomes of some of these patients came to contain two or three copies of the gene for NUP93 instead of the usual one. Strikingly, many of these patients had tumors that were not sensitive to estrogen. Such tumors, which make up about a third of all breast cancers, are particularly difficult to treat because they lack the estrogen receptors that are targeted by hormonal anticancer drugs. ...
Next, the scientists unraveled the mechanism by which NUP93 plays its grim role in cancer. Because this protein forms a tunnel in the nuclear membrane, it can allow the passage of shuttle proteins called importins, which, among their cargo loads, deliver growth and migration commands from the cytoplasm into the nucleus and thus to the DNA. In this manner, cancer gets access to the cell’s genome, harnessing it for its own needs, namely, increasing the cell’s ability to migrate and revving it up so as to spread the disease. ..."
From the abstract:
"By establishing multi-omics pipelines, we uncover overexpression and gene copy-number alterations of nucleoporin-93 (NUP93), a nuclear pore component, in aggressive human mammary tumors. NUP93 overexpression enhances transendothelial migration and matrix invasion in vitro, along with tumor growth and metastasis in animal models. ..."
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