Doctors Try Suffocating Stubborn Tumors - Cutting Off Blood Supply, Nutrients May Help In Pancreatic Cancer
Main Category: Pancreatic CancerArticle Date: 12 May 2008 - 9:00 PDT
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Over the last 30 years, researchers have made some impressive strides in battling certain types of cancer. It's estimated, for example, that 99% of prostate cancer patients will survive at least five years and 9 out of 10 breast cancer patients will too.* While the numbers may not be quite as big when it comes to pancreatic cancer, the numbers are significant.
Having bought and rebuilt dozens of vintage juke boxes, Dr. Steve Qualman has an appreciation for just how much technology has changed when it comes to music. The same goes for his health. Diagnosed with pancreas cancer last summer, Steve knew what he was up against. Survival rates have barely changed in decades, but in his case...
"Right now they can't find my primary tumor on a CT scan, nor the original metastatic disease. I do have other areas that look like there's residual, but it's a very small amount of residual disease right now," says Qualman.
What's making the difference for these patients is a new approach that personalizes cancer treatments. Doctor Tanios Saab with Ohio State University's James Cancer Hospital says survival rates are still low, around 5%, but that number is nearly triple what it was a generation ago.
"For some of these patients, we actually see significant improvements in survival and, more importantly, in the quality of life," says Saab.
Dr. Saab says technology has lead to a better understanding of pancreas tumors and a better class of drugs to attack them. But the newest drugs don't attack the tumors themselves, instead they settle into the tissue around the tumor and starve it.
"The tumor needs blood and blood supply to grow. If you cut that off, then the tumor will be unlikely to grow and that's in the later stages," says Saab. These advances aren't lost on Steve. He was a doctor who worked around cancer most of his career. Knowing the small but sure steps that researchers are taking against this disease is music to his ears.
More than 100 times a day, someone is diagnosed with pancreatic cancer in the U.S.** Doctors say it can be hard to treat because there are few symptoms that allow them to catch it early. If you have dramatic and sudden weight loss or if your skin begins to appear yellow, those could be signs of trouble and you should see your doctor.
*Cancer Statistics 2008:Trends in Five-Year Survival (%) Rates, US, 1975-2003, American Cancer Society, retrieved April 2008 from http://www.cancer.org keywords: cancer statistics 2008
**Overview: Pancreatic Cancer, American Cancer Society, retrieved April 2008 from http://www.cancer.org
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What Is Targeted Therapy?
posted by Gregory D. Pawelski on 13 May 2008 at 4:16 pmFor the last two decades, the hallmark of medical treatment for cancer has been intravenous cytotoxic chemotherapy. The drugs targeted rapidly dividing cells, including cancer cells and, of course, certain normal cells (cancer cells and healthy cells). Traditional chemotherapy does not have any mechanism to distinguish between them.
In the last few years, 'targeted' therapies are becoming a component of treatment. 'Targeted' therapy is designed to block a specific gene or protein that has a critical role in the survival, growth, invasion, or metatasis of a specific cancer cell. It takes advantage of the biologic differences between cancer cells and healthy cells by 'targeting' faulty genes or proteins that contribute to the growth and development of cancer.
In other words, 'targeted' treatments fight cancer by correcting or modifying defective 'pathways' in a cancer cell. In healthy cells, each 'pathway' is tightly controlled. For instance, healthy cells are allowed to divide into new cells, and damaged cells are destroyed. However, in cancerous cells, certain points in the 'pathway' become disrupted, usually through a genetic mutation (change in form).
Designing "targeted" anticancer drugs begins with identifying the genes or proteins that are specific to the development of cancer and testing whether blocking those genes or proteins gets rid of the cancer. Genetic (molecular) tests are instrumental in accomplishing this task.
However, understanding 'targeted' treatments begins with understanding the cancer cell. Every tissue and organ in the body is made of cells. In order for cells to grow, divide, or die, they send and receive chemical messages. These messages are transmitted along specific 'pathways' that involve various genes and proteins in a cell.
Genetic testing examines a single process within the cell or a relatively small number of process. The aim is to tell if there is a theoretical predispostion to drug response. Cell-based testing not only examines for the presence of genes and proteins but also for their 'functionality' (their interaction with other genes, proteins, and processes occurring within the cell, and for their response to 'targeted' drugs).
Genetic testing involves the use of dead, formaldehyde preserved cells that are never exposed to 'targeted' drugs. Genetic tests cannot tells us anything about uptake of a certain drug into the cell or if the drug will be excluded before it can act or what changes will take place within the cell if the drug successfully enters the cell.
Genetic tests cannot discriminate among the activities of different drugs within the same class. Instead, it assumes that all drugs within a class will produce precisely the same effect, even though from clinical experience, this is not the case. Nor can Genetic tests tell us anything about drug combinations.
Cell-based testing looks at 'fresh' living cancer cells. It assesses the net result of all cellular processes, including interactions, occurring in real time when cancer cells actually are exposed to specific anti-cancer drugs. It can discriminate differing anti-tumor effects of different drugs within the same class. It can also identify synergies in drug combinations.
When considering a 'targeted' cancer drug which is believed to act only upon cancer cells that have a specific genetic defect, it is useful to know if a patient's cancer cells do or do not have precisely that defect. Although presence of a 'targeted' defect does not necessarily mean that a drug will be effective, absence of the targeted defect may rule out use of the drug.
As you can see, just selecting the right test to perform in the right situation is a very important step on the road to personalizing cancer therapy. Sometimes a drug will inhibit the 'target' but not stop the growth of cancer. Not all genes and proteins have a critical role in the survival and growth of cancer cells.
The are many pathways to altered cellular (forest) function, hence all the different 'trees' which correlate in different situations. Improvement can be made by measuring what happens at the end of all processes (the effects on the forest), rather than the status of the individual trees (pathways/mechanisms). You still need to measure the net effect of all processes, not just the individual molecular (gene/protein) 'targets.'
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