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Cancer cells spread by releasing 'bubbles', according to an MUHC study
April 22, 2008A new fundamental mechanism of how tumour cells communicate has just been discovered by the team of Dr. Janusz Rak at the Research Institute of the McGill University Health Centre (MUHC) in collaboration with Dr Guha from the University of Toronto. The cancer cells are able to communicate with their more healthy counter-parts by releasing vesicles. These bubble-like structures contain cancer-causing (oncogenic) proteins that can trigger specific mechanisms when they merge into non or less-malignant cells. These findings could change our view on how cancerous tissues work and lead to major clinical innovations. They were published on April 20 in the on-line edition of Nature Cell Biology.
The surface of some brain tumour cells has long been known to express a mutated version of what is called the variant III epidermal growth factor receptor (EGFRvIII). Although this factor is expressed only in a fraction of tumour cells, it has a major impact on the malignancy of the whole tumor. How could this cellular minority have such an important impact" This mechanism was still unknown- until now.
This study shows that the mutated EGFRvIII triggers production of small vesicles that project from the cell membrane and that carry mutated copies of EGFRvIII on their surfaces. They were baptised "oncosomes." Surprisingly enough, this shows that oncoproteins are not always confined to the cell that produced them. In this case they even migrate!
Oncosomes will migrate until they fuse with another cell, either healthy or benign tumoral. Oncogenic protein AGFRvIII then becomes integrated in the membrane of the "recipient" cell and starts stimulating specific metabolic pathways to make it act in an aberrant and malignant way. Although this may be a transient event, the changes could impact tumor behaviour by more rapid increases in cell numbers and by stimulation of blood vessel growth, hallmarks of malignant brain tumors.
"With this information we can imagine that many mutant proteins are not necessarily confined to the cells that make them, but rather can migrate and spread around as cargo of oncosomes, a process that could be referred to as formation of the "oncogenic field effect," explained Dr. Rak. "It demonstrates that cancer is a multi-cell process, where the cells talk to one another extensively. This goes against the traditional view that a single 'mutated' cell will simply multiply uncontrollably to the point of forming a tumour. This discovery opens exciting new research avenues, but we also hope that it will lead to positive outcomes for patients."
Indeed, the presence of oncosomes (containing EGFRvIII or other proteins) in blood of cancer patients could become a clinical marker, meaning that doctors could screen for a tumour's molecular characteristics instead of having to perform invasive surgery or biopsy. Currently, in the case of brain cancer, this very precise assessment cannot be performed without removing the tumour and therefore opening a patient's skull. However, the assay and analysis of oncosomes would potentially only require taking a small sample of blood or cerebrospinal fluid. This would be a step in ensuring patient comfort and choosing the best therapeutic strategy for them, factors that are key in the journey towards personalized medicine in a hopefully not-too-distant future.
McGill University Health Centre
Oncosomes will migrate until they fuse with another cell, either healthy or benign tumoral. Oncogenic protein AGFRvIII then becomes integrated in the membrane of the "recipient" cell and starts stimulating specific metabolic pathways to make it act in an aberrant and malignant way. Although this may be a transient event, the changes could impact tumor behaviour by more rapid increases in cell numbers and by stimulation of blood vessel growth, hallmarks of malignant brain tumors.
"With this information we can imagine that many mutant proteins are not necessarily confined to the cells that make them, but rather can migrate and spread around as cargo of oncosomes, a process that could be referred to as formation of the "oncogenic field effect," explained Dr. Rak. "It demonstrates that cancer is a multi-cell process, where the cells talk to one another extensively. This goes against the traditional view that a single 'mutated' cell will simply multiply uncontrollably to the point of forming a tumour. This discovery opens exciting new research avenues, but we also hope that it will lead to positive outcomes for patients."
Indeed, the presence of oncosomes (containing EGFRvIII or other proteins) in blood of cancer patients could become a clinical marker, meaning that doctors could screen for a tumour's molecular characteristics instead of having to perform invasive surgery or biopsy. Currently, in the case of brain cancer, this very precise assessment cannot be performed without removing the tumour and therefore opening a patient's skull. However, the assay and analysis of oncosomes would potentially only require taking a small sample of blood or cerebrospinal fluid. This would be a step in ensuring patient comfort and choosing the best therapeutic strategy for them, factors that are key in the journey towards personalized medicine in a hopefully not-too-distant future.
McGill University Health Centre
Cancer Cell Current Events and Cancer Cell News RSSBisphenol A linked to chemotherapy resistance
Exposure to bisphenol A (BPA) may reduce the effectiveness of chemotherapy treatments, say University of Cincinnati (UC) scientists.
Burnham Researchers Turn Cancer Friend into Cancer Foe
Burnham Institute for Medical Research today announced that scientists have created a peptide that binds to Bcl-2, a protein that protects cancer cells from programmed cell death, and converts it into a cancer cell killer.
Vitamin C supplements may reduce benefit from wide range of anti-cancer drugs
In pre-clinical studies, vitamin C appears to substantially reduce the effectiveness of anticancer drugs, say researchers at Memorial Sloan-Kettering Cancer Center.
Researchers identify mechanism used by gene to promote metastasis in human cancer cells
Virginia Commonwealth University Institute of Molecular Medicine and VCU Massey Cancer Center researchers have discovered how a gene, melanoma differentiation associated gene-9/syntenin (mda-9/syntenin), interacts with an important signaling protein to promote metastasis in human melanoma cells, a discovery that could one day lead to the development of the next generation of anti-metastatic drugs for melanoma and other cancers.
Penn researchers identify natural tumor suppressor
Researchers from the University of Pennsylvania School of Medicine have identified a key step in the formation - and suppression - of esophageal cancers and perhaps carcinomas of the breast, head, and neck.
Early stage colon cancer characterized by inactivation of gatekeeper gene
The absence or inactivation of the RUNX3 gatekeeper gene paves the way for the growth and development of colon cancer, Singapore scientists report in the Sept. issue of the journal Cancer Cell. Previous studies have shown that RUNX3 plays a role in gastric, breast, lung and bladder cancers.
New studies on the Mediterranean diet confirm its effectiveness for chronic disease prevention
Scientists of the Instituto de Nutrición y Tecnología de los Alimentos (Institute of Nutrition and Food Technology) of the University of Granada (UGR, Spain) have been doing research into the positive effects of Mediterranean diet's ingredients on health.
Variation of normal protein could be key to resistance to common cancer drug
Researchers at the Moores Cancer Center at the University of California, San Diego (UC SD) in La Jolla have found evidence explaining why a common chemotherapy drug, cisplatin, may not always work for every cancer patient. They have shown that when a variant version of a key protein that normally causes cell death is active, patients may be resistant to the cancer-killing drug.
Dense tissue promotes aggressive cancers
New research may explain why breast cancer tends to be more aggressive in women with denser breast tissue. Breast cancer cells grown in dense, rigid surroundings step up their invasive activities, Vanderbilt-Ingram Cancer Center investigators report in the Sept. 9 issue of Current Biology.
Anti-tumor effects are enhanced by inhibiting 2 pathways rather than 1
Two independent research groups have found that simultaneous inhibition of two signaling pathways resulted in substantially enhanced antitumor effects in mouse models of prostate and breast cancer. In an accompany commentary, Steven Grant, at Virginia Commonwealth University Health Science Center, Richmond, discusses the clinical importance of these studies and highlights some of the questions that still need to be answered.
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