Results 161 to 170 of about 39,319 (333)

PI3Kδ Inhibitor Parsaclisib in Japanese Patients With Relapsed or Refractory Follicular Lymphoma

open access: yesCancer Science, EarlyView.
CITADEL‐213 evaluated the efficacy and safety of parsaclisib (PI3Kδ inhibitor) in Japanese patients with relapsed or refractory follicular lymphoma (R/R FL). The objective response rate was 88.1%, with 23.8% of patients experiencing a complete response and 64.3% experiencing a partial response; treatment‐emergent adverse events led to parsaclisib ...
Noriko Fukuhara   +15 more
wiley   +1 more source

Dialog between mantle cell lymphoma cells and lymphoma-associated macrophages underlies ibrutinib resistance

open access: yesJournal of Advanced Research
Introduction: Patients with mantle cell lymphoma (MCL) frequently develop resistance to ibrutinib. Lymphoma-associated macrophages (LAMs) may play a causal role in this resistance but remain underexplored in current literature.
Xiaoqing Sun   +10 more
doaj  

Durable Molecular Remissions in Chronic Lymphocytic Leukemia Treated With CD19-Specific Chimeric Antigen Receptor-Modified T Cells After Failure of Ibrutinib.

open access: yesJournal of Clinical Oncology, 2017
Purpose We evaluated the safety and feasibility of anti-CD19 chimeric antigen receptor-modified T (CAR-T) cell therapy in patients with chronic lymphocytic leukemia (CLL) who had previously received ibrutinib.
C. Turtle   +11 more
semanticscholar   +1 more source

Hypoxia Inhibitor Improves Iodine Uptake Disorder in Thyroid Cancer Through the hsa_circ_0023990/miR‐448/DNMT1/NIS Axis

open access: yesCancer Science, EarlyView.
Our study reveals that hypoxia inhibitors ameliorate iodine uptake dysfunction in thyroid cancer by acting on the hsa_circ_0023990/miR‐448/DNMT1/NIS signaling pathway. ABSTRACT This research seeks to investigate how hypoxia inhibitors enhance iodine uptake in thyroid cancer cells. Clinical samples were gathered and assessed for hsa_circ_0023990, DNMT1,
Ruiqin Gou   +5 more
wiley   +1 more source

Targeting BTK with ibrutinib in relapsed or refractory mantle-cell lymphoma.

open access: yesNew England Journal of Medicine, 2013
BACKGROUND Bruton's tyrosine kinase (BTK) is a mediator of the B-cell-receptor signaling pathway implicated in the pathogenesis of B-cell cancers. In a phase 1 study, ibrutinib, a BTK inhibitor, showed antitumor activity in several types of non-Hodgkin's
Michael L. Wang   +30 more
semanticscholar   +1 more source

Selinexor Reduces the Immunosuppression of Macrophages and Synergizes With CD19 CAR‐T Cells Against B‐Cell Lymphoma

open access: yesCancer Science, EarlyView.
In the tumor microenvironment, selinexor suppresses tumor cell growth and prevents macrophages from polarizing to M2 populations. The lower concentration of selinexor decreases CAR‐T cell exhaustion, enhances its cytotoxicity, and upregulates NGFR expression to prompt CAR‐T cell proliferation.
Wenjing Luo   +9 more
wiley   +1 more source

Ibrutinib Resistance in Chronic Lymphocytic Leukemia [PDF]

open access: bronze, 2014
Gustaaf Reurink   +7 more
openalex   +1 more source

Mechanistic Insights and Therapeutic Potentials of Ubiquitin‐Proteasome System in Non‐Small Cell Lung Cancer

open access: yesCell Proliferation, EarlyView.
Lung cancer development involves mechanisms like reduced EGFR/EGF ubiquitination driving cancer cell behaviors and immune evasion via loss of PD‐1/PD‐L1 ubiquitination. Balancing ubiquitination and deubiquitination may be a potential therapeutic strategy. ABSTRACT Non‐small cell lung cancer (NSCLC) remains a leading cause of cancer mortality.
Guangyao Zhou   +5 more
wiley   +1 more source

Classification of Platelet‐Activating Anti‐Platelet Factor 4 Disorders

open access: yesInternational Journal of Laboratory Hematology, EarlyView.
ABSTRACT Introduction The prototypic anti‐platelet factor 4 (PF4) disorder—heparin‐induced thrombocytopenia and thrombosis (HITT)—features immunoglobulin G (IgG) class antibodies that activate platelets, monocytes, and neutrophils in a mainly heparin‐dependent fashion via Fcγ receptor‐dependent cellular activation.
Theodore E. Warkentin
wiley   +1 more source

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