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A longer lasting tumor blocker
April 28, 2009On the heels of dismaying reports that a promising antitumor drug could, in theory, shorten patients' long-term survival, comes a promising study by a Japanese team of researchers that suggests a potentially better option. The study appears in the May 11 issue of the Journal of Experimental Medicine (online April 27).
Many cancer treatments work by disrupting the formation of new blood vessels that feed growing tumors. Agents that block a vessel-promoting factor called VEGF have shown promise in human clinical trials. But recent studies in mice show that when treatment stops, tumor growth rapidly resumes. Now, Yoshiaki Kubota and colleagues find that blocking a different molecule, called M-CSF, suppressed tumor growth even after treatment was stopped.
Kubota and his team compared the efficacy of inhibitors against M-CSF and VEGF in mice with a certain kind of bone tumor. Three weeks of anti-VEGF treatment suppressed tumor growth but, similar to other recent reports, the tumors bounced back when the drug treatment was curtailed. Tumor growth in mice on a similar regiment of an M-CSF inhibitor remained suppressed in the absence of drug.
Another distinction between the two inhibitors was the type of vessel growth that was blocked. Blocking VEGF prevented dangerous vessels from growing such as those that feed tumors. But it also stopped beneficial vessels from growing, such as those that help injured tissues heal. Blocking M-CSF, on the other hand, only impeded bad vessel growth.
Most likely, the anti-M-CSF treatment had a lasting effect because it resulted in damage to the scaffolding that surrounds cancerous vessels, robbing the tumors of the structural support they need to grow. Meanwhile, the scaffold of mice treated with anti-VEGF remained intact.
M-CSF levels soar in patients with osteosarcoma (a malignant bone cancer), breast cancer and prostate cancer, making these cancers potentially the most responsive to M-CSF-blocking drugs Whether or not other types of cancer rely more on M-CSF than on VEGF for their blood supply remains unknown.
Rockefeller University Press
Another distinction between the two inhibitors was the type of vessel growth that was blocked. Blocking VEGF prevented dangerous vessels from growing such as those that feed tumors. But it also stopped beneficial vessels from growing, such as those that help injured tissues heal. Blocking M-CSF, on the other hand, only impeded bad vessel growth.
Most likely, the anti-M-CSF treatment had a lasting effect because it resulted in damage to the scaffolding that surrounds cancerous vessels, robbing the tumors of the structural support they need to grow. Meanwhile, the scaffold of mice treated with anti-VEGF remained intact.
M-CSF levels soar in patients with osteosarcoma (a malignant bone cancer), breast cancer and prostate cancer, making these cancers potentially the most responsive to M-CSF-blocking drugs Whether or not other types of cancer rely more on M-CSF than on VEGF for their blood supply remains unknown.
Rockefeller University Press
Tumor Growth Current Events and Tumor Growth News RSSCancer metabolism discovery uncovers new role of IDH1 gene mutation in brain cancer
Agios Pharmaceuticals today announced that its scientists have established, for the first time, that the mutated IDH1 gene has a novel enzyme activity consistent with a cancer-causing gene, or oncogene.
Laser therapy can aggravate skin cancer
High irradiances of low-level laser therapy (LLLT) should not be used over melanomas.
Common pain relief medication may encourage cancer growth
Although morphine has been the gold-standard treatment for postoperative and chronic cancer pain for two centuries, a growing body of evidence is showing that opiate-based painkillers can stimulate the growth and spread of cancer cells.
Cancers' Sweet Tooth May Be Weakness
The pedal-to-the-metal signals driving the growth of several types of cancer cells lead to a common switch governing the use of glucose, researchers at Winship Cancer Institute of Emory University have discovered.
Researchers 'notch' a victory toward new kind of cancer drug
Scientists have devised an innovative way to disarm a key protein considered to be "undruggable," meaning that all previous efforts to develop a drug against it have failed.
New mechanism explains how the body prevents formation of blood vessels
Researchers at Uppsala University, in collaboration with colleagues in Sweden and abroad, have identified an entirely new mechanism by which a specific protein in the body inhibits formation of new blood vessels.
CSHL study shows that some malignant tumors can be shut down after all
Oncologists have had their hands tied because more than half of all human cancers have mutations that disable a protein called p53.
Hundreds of genes distinguish patients likely to survive advanced melanoma
Although the chances of surviving advanced melanoma aren't very good with current therapies, some patients can live for years with cancer that has spread beyond the skin to other organs.
1930s drug slows tumor growth
Drugs sometimes have beneficial side effects. A glaucoma treatment causes luscious eyelashes. A blood pressure drug also aids those with a rare genetic disease.
Early-stage, HER2-positive breast cancer patients at increased risk of recurrence
Early-stage breast cancer patients with HER2 positive tumors one centimeter or smaller are at significant risk of recurrence of their disease, compared to those with early-stage disease who do not express the aggressive protein, according to a study led by researchers at The University of Texas M. D. Anderson Cancer Center.
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Growth Factors and Tumor Promotion: Implications for Risk Assessment by Tex.) International Conference on Carcinogenesis and Risk Assessment (7th : 1993 : Austin (Author), Thomas J. Slaga (Editor), Robert Leboeuf (Editor), Henry Pitot (Editor), R. Michael McClain (Editor) Hoffman LaRoche, Inc., Nutley, New Jersey. Proceedings of the Seventh International Conference on Carcinogenesis and Risk Assessment held December 1-4, 1993, in Austin, Texas. |
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No. 571(Tumors, Growths) 1 oz by PROGRESSIVE LABS | |
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Charlie Rose with Anthony Robbins (July 19, 2000) Motivational speaker Anthony Robbins on his unusual career advising everyone from Andre Agassi and President Clinton to the IBM Corporation and the United States Army and the launch of his new website, www.dreamlife.com. This product is manufactured on demand using DVD-R recordable media. Amazon.com's standard return policy will apply. |
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Intracranial Tumor Canvas Print - Canvas Art by FineArtAmerica.com This is a beautiful stretched-canvas art print wrapped on 2.5" thick stretcher bars. The print is professionally printed, assembled, and shipped within 2 - 3 business days from our production facility in North Carolina and arrives ready-to-hang on your wall. FineArtAmerica.com is home to more than 20,000 artists from all over the world who entrust us to fulfill their print orders online. We offer a 30-day money-back guarantee on every print that we sell and look forward to helping you select your next piece. |
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Olympian Labs Ip-6, Inositol Hexaphosphate by Olympian Labs Inositol hexaphosphate is a sugar molecule attached to six phosphate molecules. It is found throughout nature, in wheat and rice bran, legumes such as soybeans and virtually every kind of mammalian cell. It plays an important role in regulating vital cellular functions including cell proliferation and differentiation. There has been research on human liver cancer cells that were treated with inositol hexaphosphate and transplanted into mice. They found that inositol hexaphosphate slowed or stopped the growth of liver cancer cells and shrank existing tumors three- to four-fold. Inositol hexaphosphate does not kill cancer cells - it tames them and makes them behave like normal cells. Inositol hexaphosphate decreases proliferation of cancer cells and causes them to differentiate,... |
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Cancer Immunotherapy: Immune Suppression and Tumor Growth by George C. Prendergast (Editor), Elizabeth M. Jaffee (Editor) There has been major growth in understanding immune suppression mechanisms and its relationship to cancer progression and therapy. This book highlights emerging new principles of immune suppression that drive cancer and it offers radically new ideas about how therapy can be improved by attacking these principles. Following work that firmly establishes immune escape as an essential trait of cancer, recent studies have now defined specific mechanisms of tumoral immune suppression. It also demonstrates how attacking tumors with molecular targeted therapeutics or traditional chemotherapeutic drugs can produce potent anti-tumor effects in preclinical models. This book provides basic, translational, and clinical cancer researchers an indispensable overview of immune escape as a critical trait... |
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Peregrine's phospholipid-targeted antibodies fused wth cytokines reduce tumor growth.: An article from: BIOTECH Patent News by Gale Reference Team (Author) This digital document is an article from BIOTECH Patent News, published by Thomson Gale on September 1, 2006. The length of the article is 654 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser. Citation Details Title: Peregrine's phospholipid-targeted antibodies fused wth cytokines reduce tumor growth. Author: Gale Reference Team Publication: BIOTECH Patent News (Newsletter) Date: September 1, 2006 Publisher: Thomson Gale Volume: 20 Issue: 9 Distributed by Thomson... | |
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