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Lani
11-30-2006, 10:21 PM
Drug Fights Cancer And Tumors
Nov. 29 - When breast cancer spreads to other parts of the body, it can be deadly. But now a new drug that seems to be able to stop advanced breast cancer from progressing and even reduces the size of tumors.


About 10 years ago, Karen Pike got the news. The mother of two had breast cancer.
Karen Pike, Breast cancer survivor: "I don't have any history in my family, so at 37, it was pretty scary. Our kids are 5 and 7, and I just went numb."

Karen's faith - and family - helped her stay strong. She needed the strength when the cancer came back three more times.


Karen Pike: "I couldn't have done any of this without my family. I know that I couldn't."

Karen has also relied on a team of doctors - and is now part of a clinical trial on a drug called sutent. In a study, the pill shrank tumors by one-third or more in 15 percent of patients - significant because they had very advanced disease and didn't have any luck with other treatments.

Doctor George Sledge says Sutent could be used as a frontline treatment for breast cancer that has spread.

George Sledge, M.D., Oncologist: "This holds out so much promise that I think if you are a physician dealing with breast cancer research you can only be excited about this."

Karen's only been on the drug for a month, but the lump in her neck has already drastically gone down in size - keeping her optimistic for the future.

Karen Pike: "Seeing both of my kids graduate from college, get married, have children, live a long life and be healthy for the rest of my life."

A simple dream she hopes will come true.

Sutent is an interesting drug. It has also shown promise in treating gastrointestinal and kidney tumors when other treatments start to fail. Right now, right now, it's just under investigation but could become FDA approved for certain cancers in the next year.

Researchers say, this drug is part of an entirely new class of agents and is working through mechanisms that haven't been used before.


Copyright 2006, ABC7/KGO-TV/DT.

FOR MORE INFORMATION, CONTACT:

Patient Referral
Indiana University School of Medicine
(888) 660-IUCC

Sherryg683
11-30-2006, 10:45 PM
Wow, I like this article, very uplifting...sherry

Jean
12-01-2006, 11:26 AM
Just love hearing positive, hopeful and exciting news such as this.

Jean

karenann
12-01-2006, 12:09 PM
This is a great article. It gives me hope.

Karen

gdpawel
10-05-2008, 09:31 PM
The short term future of cancer therapeutics is combinations of targeted drugs. Sutent could be one of those miracle targeted drugs. It is a "multi-targeted" kinase inhibitor. That means it inhibits several proteins involved in triggering replication in cancer cells.

Until Sutent, you had to take one type of drug for anti-tumor effects of human neoplasms, and another drug for anti-microvascular effects. With Sutent, multiple proteins are involved in both tumor proliferation (growth) and angiogenesis (blood vessels feeding a tumor). It has has both "anti-tumor" as well as "anti-angiogenic" properties. In addition, because it inhibits "multiple" kinases, it possesses activity against "multiple" types of tumors.

Sutent may directly bind to one of the proteins (VEGF) to directly inhibit angiogenesis (microvasculature regression). Within 24 hours of VEGF inhibition, endothelial cells have been shown to shrivel, retract, fragment and die by apoptosis (cell death). VEGF can cut off the supply of vessels that spring up to feed a tumor (angiogenesis).

How many days will Sutent take to respond on the tumors? No one really knows without testing the tumor first. Does the drug enter the cell? Once entered, does it immediately get metabolized of pumped out, or does it accumulate?

A couple of private laboratories have the abilities to take fresh "live" tumor specimens and be able to distinguish between susceptibility of the cell to different drugs in the same class and the susceptibility to combinations. They analyze the systems' response to drug treatments, not just one or a few targets or pathways.

If, by testing the tumor first, Sutent is "synergistic" (cooperative) to cancer cells, it could be a miracle drug. It will not cure, but it can prolong survival for some time (like the cronic diseases).

Cell-based functional profiling of tumor cells can measure the net effect of everything which goes on (the entire genome of a cancer cell). It can look at both the anti-tumor and anti-microvascular effects of cancer drugs. Are the cells ultimately killed, or aren't they?

http://weisenthalcancer.com

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Rich66
10-06-2008, 08:44 AM
Where is this at now? Loooks like the article is from 2006

gdpawel
10-06-2008, 05:07 PM
It was discovered that endothelial cells are present in tumor microclusters and it appears that drug effect of Sutent, and other anti-angiogenic drugs, upon these cells can be assessed in a microvascular viability assay.

Endothelial cells, the cells that form the walls of blood vessels, are the source of new blood vessels and have a remarkable ability to divide and migrate. The creation of new blood vessels occurs by a series of sequential steps. An endothelial cell forming the wall of an existing small blood vessel (capillary) becomes activated, secretes enzymes that degrade the extracellular matrix (the surrounding tissue), invades the matrix, and begins dividing. Eventually, strings of new endothelial cells organize into hollow tubes, creating new networks of blood vessels that make tissue growth and repair possible.

Most of the time endothelial cells lie dormant. But when needed, short bursts of blood vessel growth occur in localized parts of tissues. New capillary growth is tightly controlled by a finely tuned balance between factors that activate endothelial cell growth and those that inhibit it.

These new "targeted" drugs mostly need to be combined with active chemotherapy to provide any benefit. You had to take one type of drug for anti-tumor effects of human neoplams, and another drug for anti-microvascular effects. The nice thing about Sutent is that it is an inhibitor of multiple protein kinases involved in both anti-tumor effects and anti-microvascular effects.

Where are the predictive markers that are as useful as ER and Her2? The clinical applicaton of DNA or RNA content assays have been shown to correlate only with response and not survival. How about response and survival? And it would be nice to actually integrate all the gene expression into one convenient test result.

There will be a continuous parade of new "targeted" small and large molecule therapies that will continue to be introduced into the market virutally blind. There should be more use of integrated "targeted" testing to decrease the number of nonresponders (patients who do not benefit from a drug), and increase the number of responders (patients who benefit from a drug).

Joan M
10-07-2008, 05:51 AM
When I had the lung local recurrence, I was offered a Sutent trial through NY Presbyterian Hospital-Weill Cornell Medical Ctr:

A Phase 2 Efficacy and Safety Study of SU011248 in Combination with Trastuzumab as Treatment for Metastatic Disease in Patients with Breast Cancer

Joan

Lani
10-09-2008, 12:45 PM
There is, however, concern regarding the actual risk of heart failure with sunitinib, which may be higher in the real world than expected. Dr. Telli and colleagues from Stanford conducted a review of patients treated with sunitinib to further explore potential cardiotoxicity associated with the drug.

Previous studies that led to the FDA approval of sunitinib reported cardiotoxicity ranging from greater than 8% to more than 20%. For the most part, these cardiotoxicities were reversible and did not result in sustained, negative clinical effects. However, these trials typically did not include patients with pre-existing heart conditions. Conversely, in a “real world” setting, a significant portion of patients may indeed have comorbid cardiac conditions, a situation that needs to be addressed if sunitinib exacerbates their condition.

Researchers at Stanford noticed a higher-than-usual rate of cardiac complications among their patients on sunitinib, prompting analysis of data including 48 patients with kidney cancer or gastrointestinal stromal tumors (GIST) treated with sunitinib at Stanford between 2004 and 2007.[8]

15% of patients developed symptomatic and clinically significant heart failure.
Patients with coronary artery disease, low body mass index, or pre-existing heart failure were at a higher risk for developing subsequent heart failure on sunitinib.
The majority of patients who developed heart failure on sunitinib did so within the first three weeks of treatment.
The researchers suggested that cardiac monitoring should be routine among patients treated with sunitinib. Because this was a retrospective analysis including a small number of patients, the true incidence of heart failure associated with sunitinib may be greater or less than 15%.

gdpawel
10-09-2008, 01:12 PM
Very good point Lani. There are a number of issues about the use of Sutent, Herceptin, or any other targeted drug. In addition to taking them for a long time, these kind of individual, targeted oral drugs would be taken in addition to an existing repertoire of chemotherapy mixtures a cancer patient is already taking, instead of taking them alone. Adding even more potential toxicities and thousands of dollars to treatment.

Any cancer drug can cause potential heart damage, even death, and many doctors do not adequately monitor their patients or manage their care to minimize the health risk, according to a study by M. D. Anderson cardiologists.

Patients and doctors may not be aware of the spectrum of heart problems that can arise from cancer treatment, or know that many of these problems can be managed.

The study, published an issue of the journal Circulation, is the first large-scale review that details. Conducted with nine other M. D. Anderson cardiologists, the study reviews research on the cardiotoxicity of 29 anti-cancer drugs as well as 30 years of experience at M. D. Anderson.

Cardiotoxicity can occur in any patient. Generally speaking, patients most at risk are elderly and have other illnesses, such as diabetes and heart disease. Heart problems can occur during treatment or months and even years after treatment.

Even the newest targeted therapies like Sutent, a "multi-targeted kinase inhibitor" that inhibits several proteins involved in triggering replication in cancer cells.

Toxic effects of these drugs like Avastin, Erbitux, and Rituxin include: hypertension (high blood pressure) or hypotension (low blood pressure). The problems they produce usually involve changes in blood pressure, which can be easily treated if recognized.

The monoclonal antibody Herceptin is less toxic than generally believed, although it can cause chronic heart failure or dysfunction of the left ventricular, the main chamber of the heart that pumps blood to the body.

And the list goes on. Possible solutions include, avoiding certain drugs, lowering drug dosages, administering drugs slower and over a longer period of time, monitoring cardiac health more stringently, avoiding giving some drugs simultaneously, treating cardiac risk factors, use of an echocardiogram during and after cancer treatment, and treating patients with heart failure drugs.

The Anderson researchers found a profile of cardiotoxicity for the most often used anticancer drugs, but it is important to know that every patient has different risk factors that will determine how their hearts handle the treatment. Monitoring and management is key to surviving cancer with a good and lasting heart.

In addition to taking this drug for a long time, these kind of individual, targeted oral drugs would be taken in addition to an existing repertoire of chemotherapy mixtures a cancer patient is already taking, instead of taking them alone. Adding even more potential toxicities and thousands of dollars to treatment.

Overt congestive heart failure is a very late and serious manifestation of heart muscle damage. For every patient with frank congestive heart failure, there is probably another two, three, four or five patients with heart muscle damage short of congestive heart failure. The sort of heart muscle damage which can cause fatigue and/or shortness of breath with moderate or mild exertion, which otherwise wouldn't occur.

We don't know what will happen 10 or 20 years from now in women who didn't need any adjuvant therapy at all, who would have been cured by surgery alone. Only a minority of patients who receive adjuvant therapy benefit from it. Adjuvant therapy is worth it if the women have to suffer only short term, temporary toxicity, and if it even slightly reduces the probability that their cancers will come back. But if it produces permanent toxicity, whether "chemo brain" or "heart muscle damage," that is a whole different order of magnitude in terms of risk.