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Researchers in Hong Kong and the United States have announced discovery of a protein that blocks the effects of insulin and other hormones on cancerous tumors, causing them to spread.

Blocking Production of a Production May Keep Keep Tumors from Becoming Deadly

The hormone, called CPE-delta N, is present in large amounts when a primary tumor has spread. Individual cancer cells or tiny clusters of cancer cells break off from primary tumors and get into the bloodstream and lymph canals. The interior plumbing of the human body carries them to other parts of the body where they are trapped and multiply.
The secondary tumor is the same kind of cancer as the primary tumor. Breast cancer, for example, can form tumors in the lungs, but these tumors continue to respond to the same treatments as breast cancers, not lung cancers.

Cancers that spread to other parts of the body usually result in death. Cancers that can be treated before they spread usually do not result in death. Stopping the spread of cancer gives doctors, and the immune system, a chance to kill the cancer where it begins.

The researchers tested patients who had stage 2 liver cancer, which has spread, but only within the liver, colon cancer, and a rare form of adrenal cancer. The presence of absence of the protein was invaluable in choosing the right follow-up treatment.

What Doctors Do When They Know Cancer Will (or Won't) Spread

When patients are treated for stage 2 liver cancer, or primary colon cancer, or certain kinds of cancerous tumors of the adrenal glands, they are usually told that the cancer will not spread and that there is no need for follow-up chemotherapy or other treatment. In a small number of cases, however, this prediction proves wrong with deadly consequences.

In the 18 patients in the study who had stage 2 liver cancer, 13 had low levels of CPE-delta N, and 5 had high levels of CPE-delta N. Of the 13 who had low levels of the protein, 10 were cancer-free three years after treatment. Of the 5 who had high-levels of the protein, 4 suffered recurrence of the cancer.

These results suggest that testing for CPE-delta N is helpful, but not perfect. But that is true of all treatments for cancer. Simply identifying cancer patients whose tumors are producing large amounts of the protein that makes tumors turn on to insulin and other hormones tells doctors which are most likely to benefit from chemotherapy and which are likely to be OK without it.

The hope of this research is that eventually doctors will be able to turn off the gene that codes the protein and stop these tumors from ever spreading at all. This has already been accomplished in tests involving mice in the laboratory. When researchers used a technique called antisense to deactivate the CPE-delta N gene, transplanting tumors into the mice did not result in their spread throughout the body.
Mouse and human genes are thought to be similar, but this technique is at least a few years away for humans. It is more likely that researchers will develop a pill to block the protein than antisense techniques to switch off the gene.

In the meantime, oncologists have a new tool for identifying who needs chemo and who may not. Eventually there may be a pill to prevent the spread of cancer, but for now, doctors at least know who is more likely to need treatment.

  • Lee TK, Murthy SR, Cawley NX, Dhanvantari S, Hewitt SM, Lou H, Lau T, Ma S, Huynh T, Wesley RA, Ng IO, Pacak K, Poon RT, Loh YP. An N-terminal truncated carboxypeptidase E splice isoform induces tumor growth and is a biomarker for predicting future metastasis in human cancers. J Clin Invest. 2011 Feb 1. pii: 40433. doi: 10.1172/JCI40433. [Epub ahead of print]
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