Role of Tyrosine Kinase Inhibitors in Indolent and Other Mature B-Cell Neoplasms

Kutsch, Nadine; Marks, Reinhard; Ratei, Richard; Held, T.; Schmidt‐Hieber, Martin

doi:10.4137/bmi.s22434

Cited by 2 publications

(2 citation statements)

References 92 publications

(109 reference statements)

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“…The activation (by tyrosine phosphorylation) of BTK may stimulate the nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) signaling pathways, and ultimately trigger a series of inflammatory reactions ( 14 – 18 ). Previous studies have reported that BTK inhibition may be efficient in controlling B cell malignancy and B cell-related autoimmune disorders ( 19 – 23 ); however, whether BTK participates in THS-induced lung injury remains to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of BTK protects lungs from trauma-hemorrhagic shock-induced injury in rats

Zhang

Han

et al. 2017

Molecular Medicine Reports

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The present study aimed to investigate the role of Bruton's tyrosine kinase (BTK) in the pathogenesis of lung injury induced by trauma-hemorrhagic shock (THS), and to examine the pulmonary protective effects of BTK inhibition. Male Sprague-Dawley rats were divided into four groups (n=12/group): i) A Sham group, which received surgery without induced trauma; ii) a THS-induced injury group; iii) a THS-induced injury group that also received treatment with the BTK inhibitor LFM-A13 prior to trauma induction; and iv) a Sham group that was pretreated with LFM-A13 prior to surgery but did not receive induced trauma. The expression of phosphorylated-BTK protein in the lungs was measured by immunohistochemistry and western blot analysis. The bronchoalveolar lavage fluid (BALF) protein concentration, total leukocyte and eosinophil numbers, and the expression levels of peripheral blood proinflammatory factors were measured. Morphological alterations in the lungs were detected by hematoxylin and eosin staining. Pulmonary nitric oxide (NO) concentration and inducible NO synthase (iNOS) expression were also assessed. Activities of the nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) signaling pathways were determined by western blotting or electrophoretic mobility shift assay. BTK was notably activated in lungs of THS rats. BALF protein concentration, total leukocytes and eosinophils, peripheral blood expression levels of tumor necrosis factor-α, interleukin (IL)-1β, IL-6 and monocyte chemotactic protein 1 were significantly upregulated after THS induction, and each exhibited decreased expression upon LFM-A13 treatment. THS-induced interstitial hyperplasia, edema and neutrophilic infiltration in lungs were improved by the inhibition of BTK. In addition, THS-induced NO release, iNOS overexpression, and NF-κB and MAPK signaling were suppressed by BTK inhibition. Results from the present study demonstrate that BTK may serve a pivotal role in the pathogenesis of THS-related lung injury, and the inhibition of BTK may significantly alleviate THS-induced lung damage. These results provide a potential therapeutic application for the treatment of THS-induced lung injury.

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Section: Introductionmentioning

confidence: 99%

Inhibition of BTK protects lungs from trauma-hemorrhagic shock-induced injury in rats

Zhang

Han

et al. 2017

Molecular Medicine Reports

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“…These mutations can dysregulate SYK activity, leading to aberrant proliferation, survival, and differentiation of B-cells, which play a pivotal role in the development and activation of these cells. Consequently, these alterations contribute to the development of hematological cancers ( Kutsch et al, 2015 ). Common tyrosine kinase inhibitors (TKIs) marketed or in the progress of clinical trials in HMs treatment are shown in Table 1 .…”

Section: The Clinical Regimens For the Treatment Of Hmsmentioning

confidence: 99%

The clinical regimens and cell membrane camouflaged nanodrug delivery systems in hematologic malignancies treatment

Liu,

Yu,

Chen

et al. 2024

Front. Pharmacol.

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Hematologic malignancies (HMs), also referred to as hematological or blood cancers, pose significant threats to patients as they impact the blood, bone marrow, and lymphatic system. Despite significant clinical strategies using chemotherapy, radiotherapy, stem cell transplantation, targeted molecular therapy, or immunotherapy, the five-year overall survival of patients with HMs is still low. Fortunately, recent studies demonstrate that the nanodrug delivery system holds the potential to address these challenges and foster effective anti-HMs with precise treatment. In particular, cell membrane camouflaged nanodrug offers enhanced drug targeting, reduced toxicity and side effects, and/or improved immune response to HMs. This review firstly introduces the merits and demerits of clinical strategies in HMs treatment, and then summarizes the types, advantages, and disadvantages of current nanocarriers helping drug delivery in HMs treatment. Furthermore, the types, functions, and mechanisms of cell membrane fragments that help nanodrugs specifically targeted to and accumulate in HM lesions are introduced in detail. Finally, suggestions are given about their clinical translation and future designs on the surface of nanodrugs with multiple functions to improve therapeutic efficiency for cancers.

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Role of Tyrosine Kinase Inhibitors in Indolent and Other Mature B-Cell Neoplasms

Cited by 2 publications

References 92 publications

Inhibition of BTK protects lungs from trauma-hemorrhagic shock-induced injury in rats

Inhibition of BTK protects lungs from trauma-hemorrhagic shock-induced injury in rats

The clinical regimens and cell membrane camouflaged nanodrug delivery systems in hematologic malignancies treatment

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