Following a path to a possible treatment for NF2, a disease Tumor

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The proteins, the cells with a sense of personal space offer could cause type 2 (NF2), an inherited cancer disease, researchers at the Wistar a therapeutic target for neurofibromatosis Institute according to. Their results, which appear in the 12 April issue of the journal cancer cell, would have profound implications for nf2 and related cancers, such as such as mesothelioma.

The researchers describe, interact for the first time that Merlin, which encoded within the NF2 gene protein with a protein called Angiomotin. This link between Merlin and Angiomotin combines two important information networks in cells that have brought numerous forms of cancer in context. There is a link, say the researchers between the sensor, the interactions between cells and the signalling see networks, that drive cell division.

"Angiomotin for the movement of the cells is required, the form of new blood vessels, so is fascinating, it see as closely with Merlin, the product of the NF2 gene loss of which to the tumor formation is linked," said Joseph Kissil, PhD., senior author of the study and associate professor in the molecular and cellular oncogenesis program of the Wistar Institute Cancer Center. "The discovery opened a potential new method for the treatment of NF2 by attacking the tumor cells directly and through hunger, a strategy already in certain cancer treatments."

"Drugs like AVASTIN, for example." "The aim of growing blood vessels," said Kissil, "but what makes Angiomotin a tempting target is that it offer these blood vessels of blood vessels and the growing tumor cells need nutrients used."

NF2 is caused mutations in both copies of a person of NF2 gene a genetic disorder. It occurs in about one of 30,000 people, and it is usually hereditary. NF2 is generally a benign tumors of the nervous system of young adults, often deafness caused tumors of the auditory nerve nerves affect. While the tumors are usually benign, finally more malignant tumors can arise. Moreover, even the benign tumors cause often debilitating pain how to spread to the nervous system. There is currently no treatment for NF2 except remove tumors surgery, as they appear.

Mutations in the gene NF2 interfere with the function of the gene protein product, Merlin, who is in a complex molecular pathway that regulates how cells grow and divide. These paths are similar to information channels and disrupt a protein the function of other proteins upstream and downstream along the channel may change. Merlin is especially interesting for cancer biologists as the mutations in about half of all cases have been found from the deadly lung cancer mesothelioma, and in some cases of the thyroid, bladder and other types of cancer.

According to Kissil stops Merlin usually cells grow, as soon as they come with adjacent cells into contact. In other words, Merlin at the Angiomotin at "Crossings," binds where cells with each other coming into contact areas. Together bound the interacting proteins include the arrangement a signal of the cell to further set you, growth and movement primarily. It is a way for cells to coordinate their growth within a tissue. For example, often the feel of the inhibition is missing cancer cells, and they will continue to grow unchecked.

The Kissil lab plans, their exploration of the Angiomotin as a potential therapeutic target for the treatment of NF2, as well as look into the role of Angiomotin in other cancers known NF2 mutation will be affected.

Notes:

Funding for this study was provided by a grant of Kissil of the National Cancer Institute part of the national institutes of health. The study was also by a Young Investigator Award from the tumor foundation to Chunling Yi, PhD, a postdoctoral supports children in the laboratory Kissil.

Wistar collaborators include research assistant Scott Troutman and Neepa Christian; Student Jacqueline L. Avila and Daniela fera; and Wistar professors David W. memory, PhD. and Ronen Marmorstein, PhD. co-authors are also Akihiko Shimono, PhD., the cancer Science Institute of Singapore at the National University of Singapore; Lars Holmgren, PhD., and Nathalie L. Persson of the Karolinska Institute in Stockholm, Sweden; and Anat stemmer-Rachamimov, m.d., of Massachusetts General Hospital in Boston.

Source:
Greg Lester
The Wistar Institute

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