Relapsed MCL means the disease has returned after an initial partial or total remission. Refractory MCL refers to cancer that does not respond to current treatment.Safety data were available for 111 patients in the trial. Patients treated with ibrutinib experienced treatment-emergent adverse events (AEs) that were consistent with previously reported data. Treatment-emergent AEs were mainly grade 1 or 2. Treatment-emergent AEs of all grades occurring in 20 percent or more patients were diarrhea, fatigue, nausea, upper respiratory tract infection and dyspnea (shortness of breath). Pneumonia was the only grade 3 or higher treatment-emergent AE occurring in 5 percent or more patients. "These results are encouraging because they suggest ibrutinib provided a durable response in the treatment of mantle cell lymphoma in this Phase 2 study," said Bob Duggan, CEO and Chairman of the Board of Directors of Pharmacyclics. "Pharmacyclics' overall mission is to improve the quality and duration of life for oncology patients." Study Details PCYC-1104-CA is an international, multicenter, open-label, Phase 2, single-agent study that treated 111 relapsed or refractory patients (63 bortezomib-naive and 48 bortezomib-exposed) with oral ibrutinib 560 mg daily for continuous dosing until disease progression. The primary endpoint of the study is ORR. Duration of response and safety evaluation are important secondary endpoints. About Mantle Cell Lymphoma MCL is an aggressive type of B-cell non-Hodgkin lymphoma (NHL) that usually occurs in middle-aged or older adults. The disease typically begins in the lymph nodes but can spread to other tissues, such as bone marrow and liver. In the United States, there are approximately 70,130 new cases of NHL and 4,600 new cases of MCL each year. About Ibrutinib Ibrutinib was designed to specifically target and selectively inhibit an enzyme called Bruton's tyrosine kinase (BTK). BTK is a key mediator of at least three critical B-cell pro-survival mechanisms occurring in parallel – regulating B-cell apoptosis, cell adhesion, and lymphocyte migration and homing. Data are consistent with a mechanistic model whereby ibrutinib blocks BCR signaling, which drives cells into apoptosis and/or disrupts cell migration and adherence to tumor-protective microenvironments.