Results 11 to 20 of about 38,526 (184)

Nuclear translocation of B-cell-specific transcription factor, BACH2, modulates ROS mediated cytotoxic responses in mantle cell lymphoma.

open access: yesPLoS ONE, 2013
BACH2, a B-cell specific transcription factor, plays a critical role in oxidative stress-mediated apoptosis. Bortezomib (Velcade(TM)) is widely used to treat relapsed mantle cell lymphoma (MCL) patients despite varying clinical outcomes.
Zheng Chen   +8 more
doaj   +1 more source

Iron increases the susceptibility of multiple myeloma cells to bortezomib

open access: yesHaematologica, 2013
Multiple myeloma is a malignant still incurable plasma cell disorder. Pharmacological treatment based on proteasome inhibition has improved patient outcome; however, bortezomib-resistance remains a major clinical problem.
Alessandro Campanella   +8 more
doaj   +1 more source

Pirh2 mediates the sensitivity of myeloma cells to bortezomib via canonical NF-κB signaling pathway

open access: yesProtein & Cell, 2018
Clinical success of the proteasome inhibitor established bortezomib as one of the most effective drugs in treatment of multiple myeloma (MM). While survival benefit of bortezomib generated new treatment strategies, the primary and secondary resistance of
Li Yang   +13 more
doaj   +1 more source

Effective response with bortezomib retreatment in relapsed multiple myeloma

open access: yesSwiss Medical Weekly, 2012
Previous studies have shown that retreatment of relapsed/refractory multiple myeloma (MM) with a second course of bortezomib therapy could be effective in heavily pre-treated patients.
Christian Taverna   +4 more
doaj   +1 more source

Bortezomib with standard chemotherapy for children with acute myeloid leukemia does not improve treatment outcomes: a report from the Children’s Oncology Group

open access: yesHaematologica, 2020
New therapeutic strategies are needed for pediatric acute myeloid leukemia (AML) to reduce disease recurrence and treatment-related morbidity. The Children’s Oncology Group Phase III AAML1031 trial tested whether the addition of bortezomib to standard ...
Richard Aplenc   +16 more
doaj   +1 more source

Bortezomib cumulative dose, efficacy, and tolerability with three different bortezomib-melphalan-prednisone regimens in previously untreated myeloma patients ineligible for high-dose therapy

open access: yesHaematologica, 2014
Substantial efficacy has been demonstrated with bortezomib-melphalan-prednisone in phase III studies in transplant-ineligible myeloma patients using various twice-weekly and once-weekly bortezomib dosing schedules.
María-Victoria Mateos   +14 more
doaj   +1 more source

Selinexor Overcomes Hypoxia-Induced Drug Resistance in Multiple Myeloma

open access: yesTranslational Oncology, 2017
Increased levels of the nuclear export protein, exportin 1 (XPO1), were demonstrated in multiple myeloma (MM) patients. Targeting XPO1 with selinexor (the selective inhibitor of nuclear export; SINE compound KPT-330) demonstrates broad antitumor activity
Barbara Muz   +4 more
doaj   +1 more source

Cancer cell sensitivity to bortezomib is associated with survivin expression and p53 status but not cancer cell types

open access: yesJournal of Experimental & Clinical Cancer Research, 2010
Background Survivin is known playing a role in drug resistance. However, its role in bortezomib-mediated inhibition of growth and induction of apoptosis is unclear.
Chanan-Khan Asher A   +4 more
doaj   +1 more source

Proteasome inhibitors in the treatment of nonsmall cell lung cancer: A systematic review of clinical evidence

open access: yesHealth Science Reports, 2023
Background and Aims Nonsmall cell lung cancer accounts for over 85% of lung cancer incidences worldwide, and often has a poor prognosis. Proteasome inhibitors, such as bortezomib, have previously demonstrated evidence in preclinical and clinical models ...
Alethea Dasha Wenning Chua   +3 more
doaj   +1 more source

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

open access: yesMolecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto   +13 more
wiley   +1 more source

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