Designing DNA

The future of pancreatic cancer

Pancreatic cancer is one of the deadliest diseases. It is difficult to diagnose, so it is usually found in advanced stages. It also spreads rapidly and is notoriously resistant to many chemotherapy and radiation treatments that are usually used. Only about 3% of people with pancreatic cancer live more than five years after diagnosis. Despite the small number of diagnostic, is the fourth most common fatal cancer.

Do not know or fully understand the molecular basis of pancreatic cancer, making it very difficult to treat, but there are several being brought to market research to try to understand this terrible disease.

In 2007 we identified a small group of cells, called cancer stem cells in tumors of patients with pancreatic cancer. It is estimated that these stem cells are the key to finding effective treatment and possibly cure the disease someday.

These cells are a small number of cancer cells that replicate to allow tumor growth. Researchers believe current cancer treatments sometimes fail because they are attacking these cells. Laboratory studies have shown that pancreatic cancer stem cells are particularly resistant to chemotherapy, but identifying these cells can develop drugs that identify and kill.

This is particularly crucial for pancreatic cancer, where no significant improvements have been achieved long-term survival in recent decades.

Cellular origin of cancer

The cancer is in all or almost all cases the mutation or some other abnormal activation of cellular genes that control cell growth and mitosis. The abnormal genes are called oncogenes and have discovered 100 different types.

In all cells there are also anti-oncogenes, which suppress the activation of specific oncogenes, ie, the loss or inactivation of anti-oncogenes allows the activation of oncogenes that lead to cancer.
Only a tiny fraction of mutated cells in the body once produced a cancer, which has several explanations. First, most of the mutated cells have a lower survival capacity and normal cells simply die.

Secondly, only some of the mutated cells are cancer survivors, because even most mutated cells have normal feedback controls that prevent excessive growth.

Third, the potentially cancerous cells are destroyed, if not always, almost always, in the body’s immune system before they grow and develop cancer, what happens because they form abnormal proteins within the cell that activate mutant the immune system to destroy them.

Fourth, we need simultaneous presence of several activated oncogenes to cause cancer. For example, one of these genes could promote rapid reproduction of a cell line, but cancer does not occur because there is no simultaneous mutant gene to form blood vessels necessary.

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