A journal on of mice and

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A journal on of mice and

November 21,University of Tokyo Researchers at the University of Tokyo studied a cell membrane receptor, LRP1, and an enzyme, tPA, for their roles in metastasis of melanoma in mice. CC-BY-NC Melanoma skin cancer tumors grow larger and are more likely to metastasize due to interactions between a pair of molecules, according to experiments in mice and human cells.

The results may restore the potential for a type of cancer therapy previously abandoned in clinical trials.

A journal on of mice and

The results also implicate one molecule already connected to obesity and dementia as a potential cause of metastasis, or spread of cancer cells to other areas of the body. Melanoma accounts for about 1 percent of skin cancers, but causes a large majority of skin cancer deaths, according to the American Cancer Society.

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Few treatments exist to prevent melanoma from metastasizing. Heissig's research team proposes blocking the metastasis-promoting action of tPA by preventing it from connecting to LRP1.

Other studies have linked LRP1 to chronic diseases including diabetes, obesity, and Alzheimer's disease. It's normally a receptor for fat molecules," said Heissig. Controlling cancer's spread InHeissig's research group discovered that mice given extra tPA had greater numbers of a specific type of cell.

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This same cell type usually increases within the melanoma tumors and can enhance tumor growth. Based on that potential connection, the current project was designed to investigate what role tPA might play in skin cancer.

When cancer cells metastasize, they use proteases to cut through the matrix of protein chains that holds healthy cells in place. When cancer cells arrive in a new part of the body and begin to form new tumors, they corrupt nearby cells to build a niche, or supportive home for themselves.

Clinical researchers have attempted to prevent metastasis by stopping proteases. However, completely blocking all proteases causes unintended side effects. No protease-based cancer therapy has succeeded in clinical trials.


Better understanding of the specific interactions of LRP1 and tPA will hopefully lead to protease cancer treatments that maintain the normal, healthy protease actions of tPA," said Yousef Salama, first author of the research paper and postdoctoral researcher in Heissig's lab.

Salama also suggests that tPA may be linked to cancer immunotherapy, the life-saving treatment awarded the Nobel Prize in Physiology or Medicine. Blocking tPA could enhance the immune system's action and potentially boost the effectiveness of cancer immunotherapy treatments," said Salama.

Suppression of DKK3 protein thwarts pancreatic tumor progression and prolongs survival More information: Fibrinolytic crosstalk with endothelial cells expands murine mesenchymal stromal cells, Blood View Notes - Dialectical Journals; Of Mice and Men from APLC at Basic High School.

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The software mice appeared in the year as an S-PLUS library, and in as an R package.

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