The company, GlaxoSmithKline, says patients who were given a combo of Tykerb and the drug Xeloda had a significant reduction in the size of measurable brain metastases, cancer that has spread from its site of origin.
This significant discovery was made in an extension of an earlier phase II study involving 49 patients where 20 percent of those receiving Tykerb and Xeloda experienced at least a 50 percent volume reduction in measurable brain metastases.
It is important because as many as one third of women with HER2-positive advanced breast cancer are likely to develop brain metastases.
Tykerb which is a once-daily pill, was approved by U.S. regulators in March and was given a conditional green light from the European Medicines Agency last week.
Tykerb is recommended as a treatment, in combination with Xeloda, for patients with advanced or metastatic breast cancer whose tumors over-express protein HER2.
Experts say the drug appears to prevent cancer from spreading in different ways and they are optimistic that it may signify a breakthrough in cancer treatment.
It is estimated that one third of advanced breast cancer patients who have the HER-2 gene also develop cancer in the central nervous system, including the brain; treatment options for such cancers include chemotherapy, radiation or surgery.
The results were presented at the San Antonio Breast Cancer Symposium in San Antonio, Texas.
To test the effects of permanent CnA 1 expression Enrique Lara-Pezzi from Rosenthal's lab overexpessed CnA 1 in muscle cells, and observed increased proliferation of muscle stem cells. Switching off the protein had the opposite effect; stem cells stopped dividing and differentiated into muscle cells instead. When CnA 1 was overexpressed in the muscles of transgenic mice, the animals were resistant to the destructive effects of muscle injury and regenerated the damage more efficiently.
Using sophisticated molecular techniques the scientists revealed that calcineurin accomplishes its effect on muscle by inhibiting another protein called FoxO. FoxO is a transcription factor, a protein that plays a crucial role in skeletal muscle atrophy through the induction of genes involved in cell cycle repression and protein degradation. Suppressing the effects of FoxO, calcineurin ensures that proliferating cells stay alive and keep dividing to produce enough cells to repair muscle damage.
Supplementary CnA 1 also reduces the formation of scars in damaged muscle, helps speed up the resolution of inflammation and protects muscle cells from atrophy under starvation, says Rosenthal. These effects make CnA 1 a promising candidate for new therapeutic approaches against muscle wasting.
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