News from IMIM
Trastuzumab-emtansin (T-DM1) is an innovative treatment for HER2 positive breast cancer, but in 50% of the cases it doesn’t work and the other 50% it stops after a while. Now a multicenter study led by Hospital del Mar and published in Clinical Cancer Research has described a mechanism that could explain the resistance to this treatment and predict which patients would benefit from it.
T-DM1 is a potentially very effective treatment because the trastuzumab antibody, which specifically recognizes the HER2 positive tumor cells, carries the DM1 chemotherapeutic agent selectively inside these cells. Once inside, the DM1 causes the tumor cell to generate the cyclin B1 enzyme, which at high levels causes the cell's death, thereby eliminating the tumor. Researchers have found that, in cases where resistance to this treatment is generated, the cell does not generate cyclin B1 in response to T-DM1.
"A pharmacodynamic study analyzing in each patient the induction of cyclin B1 after treatment with T-DM1 can help identify which ones will benefit from the treatment," explains the principal researcher of the study, Joan Albanell, head of the Oncology Department of the Hospital del Mar and director of the Cancer Research Program of the IMIM.
Scientists used four lines of HER2 positive cancer cells, and confirmed the results in 18 more samples of patients with this type of cancer. "We will further investigate this in a clinical prospective study with about 50 patients treated in different hospitals, and we will include genomic analyses in the tumour and in a liquid biopsy," adds Albanell.
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