Tykerb Treatment for Breast Cancer
Tykerb Treatment for Breast Cancer(Lapatinib Treatment)
This weekend sees the first proper public presentation of the data from a study involving the newest drug for breast cancer - Tykerb or Lapatinib.
Tykerb better than Herceptin?
It's still early days of course but the manufacturers hope that the new Tykerb tablet will be at least as good or better than Herceptin in the treatment of breast cancer.
The research to be published in Atlanta will supposedly show that Tykerb works even after patients with advanced breast cancer no longer respond to Herceptin, and also that it has fewer side effects. The other advantage is that Tykerb or Lapatinib can be taken as a tablet where Herceptin needs to be given by injection.
Earlier studies seem to show that Tykerb works in some patients who no may not be responding to Herceptin treatment.
Some of the research has been done in the Edinburgh Cancer Centre and there are plans in Europe to subject Tykerb to it's largest clinical trial yet, involving 8,000 women with early breast cancer, before the end of the year.
The studies of Tykerb available at the moment have been done in women with metastatic breast cancer - or cancer that has already spread to other parts of their body. The new research with Tykerb is planned for those with early stage cancer.
This sound like more good news for breast cancer sufferers who are HER2 positive (or herceptin sensitive) - but lets remember that the research is still at a very early stage
Read more here
Gordon
posted by Marjory @ 8:55 AM
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Is Tykerb better than Herceptin? Maybe, for these reasons.
Cells are the most basic structure of the body. Cells make up tissues, and tissues make up organs, such as the lungs or liver. Each cell is surrounded by a membrane, a thin layer that separates the outside of the cell from the inside.
For a cell to perform necessary functions for the body and respond to its surroundings, it needs to communicate with other cells in the body. Communication occurs through chemical messages in a process called signal transduction. The purpose of these signals is to tell the cell what to do, such as when to grow, divide into two new cells, and die.
Targeted 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. By focusing on molecular and cellular changes that are specific to cancer, targeted cancer therapies may be more effective than current treatments and less harmful to normal cells.
However, the monoclonal antibodies like Herceptin and Erbitux 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.
Exciting results have come from studies of multitargeted tyrosine kinase inhibitors, "small" molecules that act on multiple receptors in the cancerous cells, like Tyberb and Sutent. Targeted "small-molecule" therapies ruled at the recent annual ASCO meeting of oncologists. The trend is away from the monoclonals to the small molecules, a trend in which a new predictive test may be able to hasten.
The EGRFx (TM) assay is able to test molecularly-targeted anti-cancer drug therapies like Iressa, Tarceva, Tykerb, Sutent and possibly Nexavar, because of being small molecules. The EGFRx (TM) assay relies upon a technique known as Whole Cell Profiling, in which living tumor cells are removed from an individual cancer patient and exposed in the laboratory to the new drugs.
A variety of metabolic and apoptotic measurements are then used to determine if a specific drug was successful at killing the patient's cancer cells. The whole cell profiling method differs from other tests in that it assesses the activity of a drug upon combined effect of all cellular processes, using several metabolic (cell metabolism) and morphologic (structure) endpoints, at the cell "population" level (rather than at the "single cell" level).
Other tests, such as those which identify DNA or RNA sequences or expression of individual proteins often examine only one component of a much larger, interactive process. Whole Cell Profiling measures 100,000 genes before and after drug exposure. Gene Expression Profiles measures the gene expression only in the "resting" state, prior to drug exposure.
So, will Tykerb be better than Herceptin? You be the judge.
Actually, its only about 23,000 genes in the human genome (not 100,000). Most people thought there would be 100,000, but it ended up being much less. This link describes the story behind determing the numbers.
http://www.ornl.gov/sci/techresources/Human_Genome/faq/genenumber.shtml
Basically, Whole Cell Profiling measures the response of the tumor cells to drug exposure. Following this exposure, it measures both cell metabolism and cell morphology. The effect of drugs on the whole cell, resulting in a cellular response to the drug, measures the interaction of the entire genome.
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