Leukemia
Công bố khoa học tiêu biểu
* Dữ liệu chỉ mang tính chất tham khảo
Sắp xếp:
Chimeric receptors with 4-1BB signaling capacity provoke potent cytotoxicity against acute lymphoblastic leukemia
Leukemia - Tập 18 Số 4 - Trang 676-684 - 2004
Chimeric antigen receptor-modified T cells derived from defined CD8+ and CD4+ subsets confer superior antitumor reactivity in vivo
Leukemia - Tập 30 Số 2 - Trang 492-500 - 2016
Engineering CD19-specific T lymphocytes with interleukin-15 and a suicide gene to enhance their anti-lymphoma/leukemia effects and safety
Leukemia - Tập 24 Số 6 - Trang 1160-1170 - 2010
CS1-specific chimeric antigen receptor (CAR)-engineered natural killer cells enhance in vitro and in vivo antitumor activity against human multiple myeloma
Leukemia - Tập 28 Số 4 - Trang 917-927 - 2014
Perifosine and sorafenib combination induces mitochondrial cell death and antitumor effects in NOD/SCID mice with Hodgkin lymphoma cell line xenografts
Leukemia - Tập 27 Số 8 - Trang 1677-1687 - 2013
Nuclear transcription factor-κB as a target for cancer drug development
Leukemia - Tập 16 Số 6 - Trang 1053-1068 - 2002
Notch is an essential upstream regulator of NF-κB and is relevant for survival of Hodgkin and Reed–Sternberg cells
Leukemia - Tập 26 Số 4 - Trang 806-813 - 2012
Lymphopain, a cytotoxic T and natural killer cell-associated cysteine proteinase
Leukemia - Tập 12 Số 11 - Trang 1771-1781 - 1998
High-dose cytosine arabinoside and etoposide: an effective regimen without anthracyclines for refractory childhood acute non-lymphocytic leukemia
Leukemia - Tập 11 Số 2 - Trang 185-189 - 1997
Long-term findings from COMFORT-II, a phase 3 study of ruxolitinib vs best available therapy for myelofibrosis Abstract
Ruxolitinib is a Janus kinase (JAK) (JAK1/JAK2) inhibitor that has demonstrated superiority over placebo and best available therapy (BAT) in the Controlled Myelofibrosis Study with Oral JAK Inhibitor Treatment (COMFORT) studies. COMFORT-II was a randomized (2:1), open-label phase 3 study in patients with myelofibrosis; patients randomized to BAT could crossover to ruxolitinib upon protocol-defined disease progression or after the primary end point, confounding long-term comparisons. At week 48, 28% (41/146) of patients randomized to ruxolitinib achieved ⩾35% decrease in spleen volume (primary end point) compared with no patients on BAT (P <0.001). Among the 78 patients (53.4%) in the ruxolitinib arm who achieved ⩾35% reductions in spleen volume at any time, the probability of maintaining response was 0.48 (95% confidence interval (CI), 0.35–0.60) at 5 years (median, 3.2 years). Median overall survival was not reached in the ruxolitinib arm and was 4.1 years in the BAT arm. There was a 33% reduction in risk of death with ruxolitinib compared with BAT by intent-to-treat analysis (hazard ratio (HR)=0.67; 95% CI, 0.44–1.02; P =0.06); the crossover-corrected HR was 0.44 (95% CI, 0.18–1.04; P =0.06). There was no unexpected increased incidence of adverse events with longer exposure. This final analysis showed that spleen volume reductions with ruxolitinib were maintained with continued therapy and may be associated with survival benefits.
Leukemia - Tập 30 Số 8 - Trang 1701-1707 - 2016
Tổng số: 165
- 1
- 2
- 3
- 4
- 5
- 6
- 17