New 'Targeted' Treatments Improve Colon Cancer Survival Rates
Main Category: Colorectal CancerAlso Included In: GastroIntestinal / Gastroenterology; Cancer / Oncology
Article Date: 04 Apr 2007 - 0:00 PDT
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People diagnosed with advanced colorectal cancer that has spread to distant organs, such as White House spokesman Tony Snow, are much more likely to survive today than even just a few years ago, due to the recent and continued emergence of improved therapies, say cancer experts.
"Anyone who looks at this as a death sentence is wrong," said Dr. Allyson Ocean, a gastrointestinal oncologist at Weill Cornell Medical College, quoted in a CBS News report, in reference to Snow's diagnosis just a few days ago of Stage IV (advanced) colon cancer.
The reason that statement can be made today -- when it would not have been true even five years ago -- is due mainly to the availability now of newer treatments known as "targeted" therapies that boost main therapies by hitting specific molecular targets driving the origin and growth of tumors, say cancer experts.
Snow has the option of adding the targeted therapy bevacuzimab (trade name Avastin) to one of the chemotherapy regimens most often used in Stage IV colon cancer. Doing so is more effective than using the chemotherapy alone, according to the American Cancer Society (ACS).
Such adjunctive treatments are one reason treatment of advanced colon cancer today can be curative, notes the ACS website.
Some New Targeted Compounds Are Natural
Not all the new targeted compounds are pharmaceutical products, or even drugs per se.
A naturally-occurring extract of fermented wheat germ (FWGE, trade name Avemar, Ave in the US), has been shown to substantially boost the efficacy of conventional therapies against a wide range of cancers, while lessening side effects of those drugs.
Researchers at UCLA found Avemar targets the transketolase (TK) pathway, a biochemical pathway that cancer cells -- but not normal cells -- preferentially use to rapidly make DNA for the fast cell division that makes cancer such a threat. It leaves normal cells unaffected.
Other studies found eight additional molecular targets the compound addresses, preventing the development of cancerous and precancerous lesions, reducing risk of cancer spread, stimulating cancer cell suicide and improving the anticancer effects of chemotherapy drugs.
In Hungary, where Avemar is approved as a medical nutriment in support of cancer therapy, colorectal cancer patients using Avemar along with conventional therapy had less metastases, fewer recurrences, and lived significantly longer. (A medical nutriment has supportive value in the treatment of colorectal cancer, Br J Cancer 2003 Aug 4;89(3):465-9.) Avemar became available in 2005 in the US as a nutritional supplement, Ave, from American BioSciences, Inc., http://www.americanbiosciences.com.
In childhood cancer patients, Avemar reduced incidences of febrile neutropenia -- low white blood cell count resulting in infection and high fever that can be life threatening. (Fermented Wheat Germ Extract Reduces Chemotherapy-Induced Febrile Neutropenia in Pediatric Cancer Patients, J Pediatr Hematol Oncol 26 (10), October 2004.) It showed none of the side effects of conventional drugs meant to boost blood cell count, and "has the safety profile of bread" according to expert toxicologists who reviewed toxicology test data on the compound.
Additional studies showed the extract improved physical condition and quality of life of late stage and other cancer patients during and following conventional treatment, partly by preventing immunosuppressive side-effects; making cancer related cachexia ("wasting" and weight loss) less likely to occur; reducing fatigue, and enhancing the ability of the immune system's natural killer (NK) cells to identify and kill cancer cells, among other effects.
See more information on cancer at http://www.cancer.org & more information specifically about Avemar at http://www.americanbiosciences.com/.
American BioSciences, Inc.
http://www.americanbiosciences.com/
Visit our colorectal cancer section for the latest news on this subject.
MLA
11 Feb. 2012. <http://www.medicalnewstoday.com/releases/67040.php>
APA
http://www.medicalnewstoday.com/releases/67040.php.
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Do "targeted" Treatments Work For Everyone?
posted by Gregory D. Pawelski on 4 Apr 2007 at 5:01 pmTargeted cancer therapies use drugs that block the growth and spread of cancer by interfering with specific molecules involved in carcinogenesis (the process by which normal cells become cancer cells) and tumor growth. The "targets" that the new "smart drugs" go after can be located on the "inside" or "outside" of a cancer cell. The most common targets on the outside are receptors, proteins that help relay chemical messages. And many targets on the inside are enzymes, proteins that help speed up chemical reactions in the body.
Monoclonal antibodies are "large" molecules that attach to specific proteins on the "outside" of cancer cells but not having a convenient way of getting access to a large majority of the targeted cells. There is multicellular resistance, the drugs affecting only the cells on the outside may not kill these cells if they are in contact with cells on the inside, which are protected from the drug. The cells may pass small molecules back and forth. "Small" molecules act on multiple receptors in the cancerous cells.
Angiogenesis is essential for the growth and metastasis of cancer. A growing tumor requires nutrients and oxygen, which helps it grow, invade nearby tissue, and metastasize. To reach these nutrients, the tumor builds new blood vessels. In fact, growing tumors can become inactive if they can't find a new supply of nutrients.
Angiogenesis starts when cancer cells produce a variety of growth factors and other activators (biologic molecules that begin a process). Growth factors cause endothelial cells (the cells that line blood vessels) to produce chemicals that break down the nearby tissue and the extracellular matrix (the spaces between cells). Then, the endothelial cells divide into more cells and begin building new blood vessels. Other elements, such as stromal cells (cells that form connective tissue), provide structural support for the new blood vessels.
Because angiogenesis is necessary in the growth and spread of cancer, each part of the angiogenesis process is a potential target for new cancer therapies. The assumption is that if a drug can stop the tumor from receiving the supply of nutrients, the tumor will "starve" and die.
Anti-angiogenesis drugs work by blocking the activity of vascular endothelial growth factor (VEGF) to prevent the growth of new capillaries into the tumor and thereby sustain tumor growth. VEGF causes angiogenesis by attaching to special receptors (proteins on the outside of cancer cells that act like doorways), and this action starts a series of chemical reactons inside the cell.
Avastin directly binds to VEGF to directly inhibit angiogenesis. Within 24 hours of VEGF inhibition, endothelial cells have been shown to shrivel, retract, fragment and die by apoptosis. Tumors which secrete relatively low levels of VEGF might be more susceptible to an agent like Avastin which works by blocking VEGF (Avastin "sensitive" tumors). It potently inhibits the formation of new blood vessels.
Avastin (bevacizumab) is a monoclonal antibody, a type of genetically engineered protein. Monoclonal antibodies are "large" molecules. These very large molecules don't have a convenient way of getting access to the large majority of cells. Plus, there is multicellular resistance, the drugs affecting only the cells on the outside may not kill these cells if they are in contact with cells on the inside which are protected from the drug. The cells may pass small molecules back and forth.
Does the drug even enter the cell? Once entered, does it immediately get metabolized or pumped out, or does it accumulate? In some cases, these and other drugs, kill tumor cells without killing microvascular cells in the same time frame. In other cases they kill microvascular cells without killing tumor cells. In yet other cases they kill both types of cells or neither type of cells. The ability of these agents to kill tumor and/or microvascular cells in the same tumor specimen is highly variable among the different agents.
A major modification of the DISC (cell death) assay allows for the study of anti-microvascular drug effects of standard and targeted agents, such as Avastin, Nexavar and vatalanib. 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 (Whole Cell 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.
Source: Cell Function Analysis
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