(HealthDay News) — Trastuzumab emtansine (T-DM1) significantly improves progression-free survival (PFS) compared to treatment with capecitabine (Xeloda) and lapatinib (Tykerb) (referred to as XL) in women with HER2-positive (HER2+) locally advanced or metastatic breast cancer (MBC), according to a study being presented at the annual meeting of the American Society of Clinical Oncology, held from June 1 to 5 in Chicago.

Kimberly L. Blackwell, M.D., from Duke University in Durham, N.C., and colleagues randomized 978 T-refractory HER2+ MBC patients to receive T-DM1 or XL every three weeks until disease progression or unacceptable toxicity. Primary end points were PFS, overall survival, and safety.

The median follow-up was 12.9 months for the T-DM1 group and 12.4 months for the XL group. The researchers found that the T-DM1 patients had significantly improved PFS compared to the XL group (9.6 versus 6.4 months; hazard ratio, 0.650; 95 percent confidence interval, 0.549 to 0.771). Overall survival did not meet predetermined statistical significance. T-DM1 was well tolerated, with the most common grade ≥3 adverse events per treatment being thrombocytopenia (12.9 versus 0.2 percent), increased aspartate aminotransferase (4.3 versus 0.8 percent), and increased alanine aminotransferase (2.9 versus 1.4 percent). For XL, the most common adverse events were diarrhea (20.7 versus 1.6 percent), palmar-plantar erythrodysesthesia (16.4 versus 0 percent), and vomiting (4.5 versus 0.8 percent).

Continue Reading

“The drug worked. It was significantly better than a very effective approved therapy for HER2-overexpressing metastatic breast cancer,” Blackwell said in a statement. “Also, as a clinician who takes care of a lot of breast cancer patients, I’m pleased that this drug has very little dose-limiting toxicity. Patients don’t lose their hair from this drug. For patients facing metastatic breast cancer, this is a breakthrough.”

Several authors disclosed financial ties to pharmaceutical companies, including Roche, the developer of T-DM1.

More Information