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UV light accelerates cancer cells that creep along outside of blood vessels

Date:
March 7, 2014
Source:
University of California, Los Angeles (UCLA), Health Sciences
Summary:
Deadly skin cancer (melanoma) cells spread by creeping along the outside of blood vessels: extravascular metastatic migration (EVMM). Ultraviolet light exposure accelerates EVMM in a mouse model, new research has found. Now researchers are targeting new drugs that slow or stop EVMM, potentially reducing the death rate from melanoma.

Based on the pioneering work of Dr. Claire Lugassy and Dr. Raymond Barnhill at UCLA's Jonsson Comprehensive Cancer Center, a new study provides additional support for a process by which melanoma cells, a deadly form of skin cancer, can spread throughout the body by creeping like tiny spiders along the outside of blood vessels without ever entering the blood stream, and that this process is exacerbated by exposure to ultraviolet (UV) light.

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In collaboration with the husband and wife team of Dr. Barnhill, professor of pathology and Dr. Lugassy, associate professor of pathology, the study was published March 6, 2014 in the journal Nature. Lugassy and Barnhill's team at UCLA collaborated with a team from the University of Bonn, Germany, led by Dr. Thomas Tuting.

It is well established that melanoma cells can spread through the blood to accumulate and form new tumors (metastases) in other parts of the body away from the original tumor. Thus, a small skin cancer becomes life-threatening by spreading to the brain, lungs, liver, or other organs.

Lugassy and Barnhill began studying the way cancer, especially melanoma, spreads (metastasizes) more than fifteen years ago, when they conceived and developed a process that they termed extravascular migratory metastasis (EVMM). They found that besides traveling in the bloodstream, melanoma cells could also move along the abluminal, or outside, surface of blood vessels by way of angiotropism, a biological interaction between the cancer cells and the blood vessel cells. Lugassy and Barnhill continue to assemble a body of scientific studies confirming the reality of this metastatic pathway of cancer cells.

With angiotropism and EVMM, the cancer cells may replace a type of cell called a pericyte, which normally resides on the outsides of blood vessels. While imitating the tendril-like pericytes, which Lugassy and Barnhill called pericytic mimicry, the melanoma cells creep along the length of blood vessels like spiders until they reach an organ or other point where they accumulate to form new tumors, "potentially explaining the delay between the detection of the primary cancer and the appearance of distant metastasis," Barnhill said.

"At first our idea was controversial," Lugassy said. "But mounting evidence confirming angiotropism and EVMM has revolutionized the knowledge of how cancer spreads through the body to the point that other scientists have confirmed the process in other solid tumor cell types such as pancreatic cancer."

In this new Nature study, EVMM was observed again by Tuting, Lugassy, Barnhill, and colleagues in a genetically engineered mouse model. The researchers also found that when the mice with melanoma were exposed to ultraviolet radiation (UV light) their immune systems responded with inflammation that accelerated the angiotropism, increasing the amount of EVMM, and leading to more lung metastases in the mice than those not exposed to UV light. This very exciting new study has been performed in the Laboratory for Experimental Dermatology in Bonn, Germany, under the direction of Dr. Tuting. "We have known for a long time that UV radiation is a factor in the development of melanoma," Barnhill said, "but in this study the melanoma was already present in the mice." Tuting observed that UV light provoked inflammation at the site of the tumor, which caused the mouse immune system to attract neutrophils, a type of white blood cell, and the neutrophils promoted angiotropism.

With this knowledge and the confirmation of the works of Lugassy and Barnhill on angiotropism and EVMM, the researchers in the scientific community can now begin looking for a drug target that will interfere with this EVMM process, with the hope of creating a treatment that would stop EVMM. Because the danger of melanoma comes from its metastasis from the skin to the vital organs, being able to slow down or stop metastasis could turn a disease that was often a death sentence into a manageable chronic illness with relatively little risk of death.


Story Source:

The above story is based on materials provided by University of California, Los Angeles (UCLA), Health Sciences. Note: Materials may be edited for content and length.


Journal Reference:

  1. Tobias Bald, Thomas Quast, Jennifer Landsberg, Meri Rogava, Nicole Glodde, Dorys Lopez-Ramos, Judith Kohlmeyer, Stefanie Riesenberg, Debby van den Boorn-Konijnenberg, Cornelia Hömig-Hölzel, Raphael Reuten, Benjamin Schadow, Heike Weighardt, Daniela Wenzel, Iris Helfrich, Dirk Schadendorf, Wilhelm Bloch, Marco E. Bianchi, Claire Lugassy, Raymond L. Barnhill, Manuel Koch, Bernd K. Fleischmann, Irmgard Förster, Wolfgang Kastenmüller, Waldemar Kolanus, Michael Hölzel, Evelyn Gaffal, Thomas Tüting. Ultraviolet-radiation-induced inflammation promotes angiotropism and metastasis in melanoma. Nature, 2014; 507 (7490): 109 DOI: 10.1038/nature13111

Cite This Page:

University of California, Los Angeles (UCLA), Health Sciences. "UV light accelerates cancer cells that creep along outside of blood vessels." ScienceDaily. ScienceDaily, 7 March 2014. <www.sciencedaily.com/releases/2014/03/140307100050.htm>.
University of California, Los Angeles (UCLA), Health Sciences. (2014, March 7). UV light accelerates cancer cells that creep along outside of blood vessels. ScienceDaily. Retrieved October 31, 2014 from www.sciencedaily.com/releases/2014/03/140307100050.htm
University of California, Los Angeles (UCLA), Health Sciences. "UV light accelerates cancer cells that creep along outside of blood vessels." ScienceDaily. www.sciencedaily.com/releases/2014/03/140307100050.htm (accessed October 31, 2014).

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