Evidence map›Paper›PMID 34071917›Full record

ReviewInternational journal of molecular sciences2021

Bruton's Tyrosine Kinase Targeting in Multiple Myeloma.

Max Von Suskil, Kazi Nasrin Sultana, Weam Othman Elbezanti, Omar S Al-Odat, Robert Chitren, Amit K Tiwari, Kishore B Challagundla, Sandeep Kumar Srivastava, Subash C Jonnalagadda, Tulin Budak-Alpdogan and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 6 institutions in 1 country.

Max Von SuskilDepartment of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ 08103, USA.
Kazi Nasrin SultanaDepartment of Biosciences, Manipal University Jaipur, Jaipur 303007, India.
Weam Othman ElbezantiDepartment of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ 08103, USA.
Omar S Al-OdatDepartment of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ 08103, USA.
Robert ChitrenDepartment of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ 08103, USA.
Amit K TiwariDepartment of Pharmacology and Experimental Therapeutics, The University of Toledo, Toledo, OH 43606, USA.ORCID 0000-0002-7427-7155
Kishore B ChallagundlaDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Sandeep Kumar SrivastavaDepartment of Biosciences, Manipal University Jaipur, Jaipur 303007, India.
Subash C JonnalagaddaDepartment of Chemistry and Biochemistry, College of Science and Mathematics, Rowan University, Glassboro, NJ 08028, USA.
Tulin Budak-AlpdoganDepartment of Hematology, MD Anderson Cancer Center at Cooper, Cooper Health University, Camden, NJ 08103, USA.
Manoj K PandeyDepartment of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ 08103, USA.
Cooper Medical School of Rowan University · USManipal University JaipurCooper University Health Care · USRowan University · USUniversity of Nebraska Medical Center · USUniversity of Toledo · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM), a clonal plasma cell disorder, disrupts the bones' hematopoiesis and microenvironment homeostasis and ability to mediate an immune response against malignant clones. Despite prominent survival improvement with newer treatment modalities since the 2000s, MM is still considered a non-curable disease. Patients experience disease recurrence episodes with clonal evolution, and with each relapse disease comes back with a more aggressive phenotype. Bruton's Tyrosine Kinase (BTK) has been a major target for B cell clonal disorders and its role in clonal plasma cell disorders is under active investigation. BTK is a cytosolic kinase which plays a major role in the immune system and its related malignancies. The BTK pathway has been shown to provide survival for malignant clone and multiple myeloma stem cells (MMSCs). BTK also regulates the malignant clones' interaction with the bone marrow microenvironment. Hence, BTK inhibition is a promising therapeutic strategy for MM patients. In this review, the role of BTK and its signal transduction pathways are outlined in the context of MM.

Indexed as

Molecular Targeted TherapyAgammaglobulinaemia Tyrosine KinaseBiomarkers, TumorBone MarrowDisease ManagementDisease SusceptibilityDrug Resistance, NeoplasmHumansMultiple MyelomaProtein Kinase InhibitorsSignal TransductionStructure-Activity RelationshipTumor MicroenvironmentAgammaglobulinaemia Tyrosine KinaseBiomarkers, TumorProtein Kinase InhibitorsBruton’s Tyrosine Kinase (BTK) inhibitorsdrug developmentmicroenvironmentmultiple myelomaresistance

Identifiers

PMID34071917
PMCPMC8198777
OpenAlexW3164019586

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.