scholarly journals The First Reported Case of Neurotrophic Tyrosine Receptor Kinase Fusion-Positive Thymoma Treated Successfully With Entrectinib

Cureus ◽  
2021 ◽  
Author(s):  
Hassan Salame ◽  
Remy Mckey ◽  
Mohamad Ballout ◽  
Wajih Saad
Keyword(s):  
Receptor Kinase ◽  
Tyrosine Receptor Kinase

scholarly journals Fibrinogen-cellular prion protein complex formation on astrocytes

2020 ◽  
Vol 124 (2) ◽  
pp. 536-543 ◽  
Author(s):  
Mariam Charkviani ◽  
Nino Muradashvili ◽  
Nurul Sulimai ◽  
David Lominadze
Keyword(s):  
Prion Protein ◽  
Cellular Prion Protein ◽  
No Production ◽  
Oxygen Species ◽  
Receptor Kinase ◽  
Astrocyte Activation ◽  
Triggering Mechanism ◽  
Protein Complex Formation ◽  
Tyrosine Receptor Kinase ◽  
First Time

For the first time we showed that fibrinogen (Fg) can associate with cellular prion protein (PrPC) on the surface of cultured mouse brain astrocytes. At high levels, Fg causes upregulation of astrocyte PrPC and astrocyte activation accompanied with overexpression of tyrosine receptor kinase B (TrkB), which results in nitric oxide (NO) production and generation of reactive oxygen species (ROS). Fg/PrPC interaction can be a triggering mechanism for TrkB-NO-ROS axis activation and the resultant astrocyte-mediated neurodegeneration.

scholarly journals Tyrosine receptor kinase B receptor activation reverses the impairing effects of acute nicotine on contextual fear extinction

2018 ◽  
Vol 32 (3) ◽  
pp. 367-372 ◽  
Author(s):  
Munir Gunes Kutlu ◽  
Robert D Cole ◽  
David A Connor ◽  
Brendan Natwora ◽  
Thomas J Gould
Keyword(s):  
Receptor Activation ◽  
Fear Extinction ◽  
Receptor Kinase ◽  
Contextual Fear ◽  
Tyrosine Receptor Kinase

Tyrosine receptor kinase A expression in malignant and benign breast tumors

2017 ◽  
Vol 66 ◽  
pp. S29
Author(s):  
Aditi Dubey ◽  
Ritu Sehgal ◽  
Ashutosh Kumar ◽  
T.C. Nag ◽  
S. Anurag ◽  
...  
Keyword(s):  
Breast Tumors ◽  
Receptor Kinase ◽  
Tyrosine Receptor Kinase ◽  
Benign Breast Tumors ◽  
Kinase A

scholarly journals Tyrosine receptor kinase B is a drug target in astrocytomas

2016 ◽  
Vol 19 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Jing Ni ◽  
Shaozhen Xie ◽  
Shakti H. Ramkissoon ◽  
Victor Luu ◽  
Yu Sun ◽  
...  
Keyword(s):  
Drug Target ◽  
Receptor Kinase ◽  
Tyrosine Receptor Kinase

scholarly journals Advances in Biomarker-Driven Targeted Therapies in Thyroid Cancer

Cancers ◽  
2021 ◽  
Vol 13 (24) ◽  
pp. 6194
Author(s):  
Prachi Mishra ◽  
Dipranjan Laha ◽  
Robert Grant ◽  
Naris Nilubol
Keyword(s):  
Thyroid Cancer ◽  
Targeted Therapies ◽  
Kinase Inhibitors ◽  
Mapk Pathway ◽  
Treatment Strategies ◽  
Disease Recurrence ◽  
Receptor Kinase ◽  
New Treatment ◽  
Tyrosine Receptor Kinase ◽  
Multiple Receptor

Thyroid cancer is the most common type of endocrine malignancy comprising 2–3% of all cancers, with a constant rise in the incidence rate. The standard first-line treatments for thyroid cancer include surgery and radioactive iodine ablation, and a majority of patients show a good response to these therapies. Despite a better response and outcome, approximately twenty percent of patients develop disease recurrence and distant metastasis. With improved knowledge of molecular dysregulation and biological characteristics of thyroid cancer, the development of new treatment strategies comprising novel targets has accelerated. Biomarker-driven targeted therapies have now emerged as a trend for personalized treatments in patients with advanced cancers, and several multiple receptor kinase inhibitors have entered clinical trials (phase I/II/III) to evaluate their safety and efficacy. Most extensively investigated and clinically approved targeted therapies in thyroid cancer include the tyrosine receptor kinase inhibitors that target antiangiogenic markers, BRAF mutation, PI3K/AKT, and MAPK pathway components. In this review, we focus on the current advances in targeted mono- and combination therapies for various types of thyroid cancer.

scholarly journals PU.1 and MYC transcriptional network defines synergistic drug responses to KIT and LSD1 inhibition in acute myeloid leukemia

2021 ◽  
Author(s):  
Brittany M. Smith ◽  
Jake VanCampen ◽  
Garth L. Kong ◽  
William Yashar ◽  
Yiu H. Tsang ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Treatment Options ◽  
Protein Abundance ◽  
Receptor Kinase ◽  
Activating Mutations ◽  
Synergistic Response ◽  
Early Phase Clinical Trials ◽  
Tyrosine Receptor Kinase ◽  
Acute Myeloid

AbstractActivating mutations in the KIT tyrosine receptor kinase confer an adverse prognosis for patients with acute myeloid leukemia (AML). Outside of bone marrow transplantation, treatment options are limited. Here we demonstrate combined KIT and LSD1 inhibition produces synergistic cell death against KIT mutant AML cells. This combination suppresses MYC expression to drive cell cycle exit and apoptosis. This decreased MYC expression results from a loss of PU.1 binding at downstream MYC enhancers. The drug combination also inactivates PI3K/AKT/GSK3a/b signaling to decrease MYC protein abundance. KIT-mutant AML cells rapidly adapt to KIT inhibitor monotherapy by restoring PI3K/AKT activity, but cannot when treated with combined KIT and LSD1 inhibitor. In addition, we validate MYC suppression as a mechanism of synergy in KIT-mutant AML patient samples. Collectively, this work provides rational for a clinical trial to assess the efficacy of KIT and LSD1 inhibition in patients with KIT-mutant AML.Statement of significanceEffective treatment options for AML are limited. We describe the synergistic response to combined KIT and LSD1 inhibition in KIT-mutant AML and identify key biomarkers of drug response. The specificity and efficacy of this combination in cell lines and patient samples provides rationale for investigation in early phase clinical trials.

scholarly journals Diverse distribution of tyrosine receptor kinase B isoforms in rat multiple tissues

2017 ◽  
Vol 79 (9) ◽  
pp. 1516-1523 ◽  
Author(s):  
Kosuke OTANI ◽  
Muneyoshi OKADA ◽  
Hideyuki YAMAWAKI
Keyword(s):  
Receptor Kinase ◽  
Tyrosine Receptor Kinase

Neural expression of sorting nexin 25 and its regulation of tyrosine receptor kinase B trafficking

2020 ◽  
Vol 225 (9) ◽  
pp. 2615-2642
Author(s):  
Shoko Takemura ◽  
Ayami Isonishi ◽  
Tatsuhide Tanaka ◽  
Hiroaki Okuda ◽  
Kouko Tatsumi ◽  
...  
Keyword(s):  
Receptor Kinase ◽  
Sorting Nexin ◽  
Tyrosine Receptor Kinase

scholarly journals NTRK Fusions Identified in Pediatric Tumors: The Frequency, Fusion Partners, and Clinical Outcome

2021 ◽  
pp. 204-214
Author(s):  
Xiaonan Zhao ◽  
Chelsea Kotch ◽  
Elizabeth Fox ◽  
Lea F. Surrey ◽  
Gerald B. Wertheim ◽  
...  
Keyword(s):  
Pediatric Cancer ◽  
Genomic Profiling ◽  
Pediatric Tumors ◽  
Receptor Kinase ◽  
Papillary Thyroid ◽  
Thyroid Carcinomas ◽  
Dna And Rna ◽  
Tumor Types ◽  
Tyrosine Receptor Kinase ◽  
Generation Sequencing

PURPOSE Neurotrophic tyrosine receptor kinase (NTRK) fusions have been described as oncogenic drivers in a variety of tumors. However, little is known about the overall frequency of NTRK fusion in unselected pediatric tumors. Here, we assessed the frequency, fusion partners, and clinical course in pediatric patients with NTRK fusion–positive tumors. PATIENTS AND METHODS We studied 1,347 consecutive pediatric tumors from 1,217 patients who underwent tumor genomic profiling using custom-designed DNA and RNA next-generation sequencing panels. NTRK fusions identified were orthogonally confirmed. RESULTS AND DISCUSSION NTRK fusions were identified in 29 tumors from 27 patients with a positive yield of 2.22% for all patients and 3.08% for solid tumors. Although NTRK2 fusions were found exclusively in CNS tumors and NTRK1 fusions were highly enriched in papillary thyroid carcinomas, NTRK3 fusions were identified in all tumor categories. The most canonical fusion was ETV6-NTRK3 observed in 10 patients with diverse types of tumors. Several novel NTRK fusions were observed in rare tumor types, including KCTD16-NTRK1 in ganglioglioma and IRF2BP2-NTRK3 in papillary thyroid carcinomas. The detection of an NTRK fusion confirmed the morphologic diagnosis including five cases where the final tumor diagnosis was largely based on the discovery of an NTRK fusion. In one patient, the diagnosis was changed because of the identification of an ETV6-NTRK3 fusion. One patient with infantile fibrosarcoma was treated with larotrectinib and achieved complete pathologic remission. CONCLUSION NTRK fusions are more frequently seen in pediatric tumors than in adult tumors and involve a broader panel of fusion partners and a wider range of tumors than previously recognized. These results highlight the importance of screening for NTRK fusions as part of the tumor genomic profiling for patients with pediatric cancer.

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