Cutting off the fuel supply: A new approach to the treatment of pancreatic cancer
By Dorothy L. Tengler

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Do you think this new understanding of pancreatic cancer cells could lead to future drug targets?
  • 1. Yes
  • 2. No

Pancreatic cancer kills about 38,000 Americans each year and has the highest mortality rate of all major cancers. We know pancreatic cancer is a disease caused by damage to the DNA, and these mutations can be inherited from our parents or acquired as we age. After diagnosis with metastatic disease, patients have a life expectancy of three to six months. It is no wonder that researchers are hard at work searching for new treatment possibilities for such a lethal disease.

It has been well established that a mutant form of the protein K-Ras plays a pivotal role in the initiation and progression of pancreatic cancer by stimulating the growth and survival of the cells, generating a strong signal to constantly grow and ignore environmental cues to stop growing. While these cells are known to have specific nutrient requirements, the way in which they obtain these nutrients has been poorly understood.
Fast Facts

  • Tobacco use is the most important important avoidable risk factor for pancreatic cancer, accounting for up to 30 percent of the cases.

  • Exercise lowers the risk of this cancer. Obese people and those who have limited physical activity are more likely to develop exocrine pancreatic cancer.

  • Individuals who consume three or more drinks of hard liquor a day are more likely to die of pancreatic cancer.

  • However, in a recent landmark study, researchers at NYU School of Medicine have begun to understand the mystery about how pancreatic tumor cells feed themselves. The findings of this study, led by Cosimo Commisso, a postdoctoral fellow in the Department of Biochemistry and Molecular Pharmacology at NYU School of Medicine, suggest Ras cancer cells are dependent on a process called macropinocytosis. In this process, the vesicles transport nutrients deep into a cell, to swallow up the protein albumin, thereby allowing the cancer cells to meet their excessive nutrient demands.

    The researchers used a chemical to block the uptake of albumin via macropinocytosis in mice with pancreatic tumors. What happened next was crucial to cancer research: the tumors stopped growing and in some cases even shrank considerably. It is important to note that pancreatic cells in mice featured more macropinosomes than normal mouse cells.

    This breakthrough in the understanding of how pancreatic cancer cells ingest nutrients suggests that the prevention of macropinocytosis in Ras cells could stop the spread of cancerous cells without causing damage to healthy cells.

    Dorothy L. Tengler, MA, is a freelance medical writer/communication specialist with nearly 20 years of experience in the pharmaceutical and medical communication industries. She has developed educational and medical marketing materials, including monographs, slide kits, health articles, primary and review manuscripts, and pharmaceutical sales training materials.