Genes Set Scene For Metastasis
Main Category: Breast CancerAlso Included In: Genetics; Lung Cancer; Biology / Biochemistry
Article Date: 16 Apr 2007 - 21:00 PDT
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Biologists at Memorial Sloan-Kettering Cancer Center (MSKCC) have identified a set of genes expressed in human breast cancer cells that work together to remodel the network of blood vessels at the site of the primary tumor. These genes were also found to promote the spread of breast cancer to the lungs. The study, conducted in mice and reported in Nature, helps to explain how cancer metastasis can occur and highlights targets for therapeutic treatment.
Metastasis - the leading cause of mortality in cancer patients - entails numerous biological functions that collectively enable cancerous cells from a primary site to disseminate and overtake distant organs. A number of genes are already known to contribute to the spread of breast cancer cells to the lungs.
Using genetic and pharmacological approaches, Joan Massagué, PhD, Chair of MSKCC's Cancer Biology and Genetics Program and a Howard Hughes Medical Institute Investigator, and colleagues showed how four genes facilitate the formation of new tumor blood vessels, the release of cancer cells into the bloodstream, and the penetration of tumor cells from the bloodstream into the lung. The gene set comprises EREG (an epidermal growth factor receptor ligand), the cyclooxygenase COX2, and MMP1 and MMP2 (matrix enzymes that are expressed in human breast cancer cells).
The researchers conclude that drug combinations that target one or more of the proteins encoded by these genes may prove useful for treating metastatic breast cancer.
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The following Memorial Sloan-Kettering Cancer Center investigators contributed to the work: Gaorav P. Gupta, Don X. Nguyen, Anne C. Chiang, Paula D. Bos, Juliet Y. Kim, Cristina Nadal, Roger R. Gomis, Katia Todorova-Manova, and Joan Massagué.
Contact: Esther Napolitano
Memorial Sloan-Kettering Cancer Center
Visit our breast cancer section for the latest news on this subject.
MLA
15 Feb. 2012. <http://www.medicalnewstoday.com/releases/67639.php>
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http://www.medicalnewstoday.com/releases/67639.php.
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A Microvascular Viability Assay For Anti-angiogenesis-related Drugs
posted by Gregory D. Pawelski on 17 Apr 2007 at 2:57 pmThe ability of various agents to kill tumor and/or microvascular cells (anti-angiogenesis) in the same tumor specimen is highly variable among the different agents. There are so many agents out there now, doctors have a confusing array of choices. They don't know how to mix them together in the right order.
A major modification of the DISC (cell death) assay allows for the study of anti-microvascular drug effects of standard and targeted agents. The Microvascularity Viability Assay is based upon the principle that microvascular (endothelial and associated) cells are present in tumor cell microclusters obtained from solid tumor specimens. The assay which has a morphological endpoint, allows for visualization of both tumor and microvascular cells and direct assessment of both anti-tumor and anti-microvascular drug effect.
The principles and methods used in the Microvascularity Viability Assay include: 1. Obtaining a tissue, blood, bone marrow or malignant fluid specimen from an individual cancer patient. 2. Exposing viable tumor cells to anti-neoplastic drugs. 3. Measuring absolute in vitro drug effect. 4. Finding a statistical comparision of in vitro drug effect to an index standard, yielding an individualized pattern of relative drug activity. 5. Information obtained is used to aid in selecting from among otherwise qualified candidate drugs.
It is the only assay which involves direct visualization of the cancer cells at endpoint, allowing for accurate assessment of drug activity, discriminating tumor from non-tumor cells, and providing a permanent archival record, which improves quality, serves as control, and assesses dose response in vitro. Photomicrographs in the assay can show that some clones of tumor cells don't accumulate the drug. These cells won't get killed by it. The Assay measures the net effect of everything which goes on (Functional Profiling). Are the cells ultimately killed, or aren't they?
Each of these new targeted drugs are not for everybody. According to the National Cancer Institute, those who benefit substantially from "targeted" drugs is approximately 10% to 20%. What if you are one of those few? This kind of technique exists today and might be very valuable, especially when active chemoagents are limited in a particular disease, giving more credence to testing the tumor first.
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