Evidence map›Paper›PMID 31036508›Full record

ReviewClinical lymphoma, myeloma & leukemia2019

Future of Personalized Therapy Targeting Aberrant Signaling Pathways in Multiple Myeloma.

Faiz Anwer, Kevin Mathew Gee, Ahmad Iftikhar, Mirza Baig, Atlantis Dawn Russ, Sabina Saeed, Muhammad Abu Zar, Faryal Razzaq, Jennifer Carew, Steffan Nawrocki and 5 more

Open access · greenAbstract readReview
In one paragraph

Review in Clinical lymphoma, myeloma & leukemia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
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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

15 authors at 4 institutions in 1 country.

Faiz AnwerTaussig Cancer Center, Department of Hematology, Medical Oncology, Cleveland Clinic, Cleveland, OH. Electronic address: anwerf@ccf.org.
Kevin Mathew GeeDepartment of Molecular and Cellular Biology, The University of Arizona, Tucson, AZ.
Ahmad IftikharDepartment of Medicine, The University of Arizona, Tucson, AZ.
Mirza BaigDepartment of Medicine, Summit Medical Group, Summit, NJ.
Atlantis Dawn RussDepartment of Medicine, The University of Arizona, Tucson, AZ.
Sabina SaeedCollege of Public Health, The University of Arizona, Tucson, AZ.
Muhammad Abu ZarDepartment of Medicine, Division of Hematology & Oncology, The University of Arizona, Tucson, AZ.
Faryal RazzaqDepartment of Medicine, Division of Hematology & Oncology, The University of Arizona, Tucson, AZ.
Jennifer CarewDepartment of Medicine, Division of Hematology & Oncology, The University of Arizona, Tucson, AZ.
Steffan NawrockiDepartment of Medicine, Division of Hematology & Oncology, The University of Arizona, Tucson, AZ.
Hussam Al-KatebDivision of Human Genetics, Children's Hospital, Cincinnati, OH.
Nadia Nunes Cavalcante ParrDepartment of Medicine, The University of Arizona, Tucson, AZ.
Ali McBrideCollege of Pharmacy, The University of Arizona, Tucson, AZ.
Jason ValentTaussig Cancer Center, Department of Hematology, Medical Oncology, Cleveland Clinic, Cleveland, OH.
Christy SamarasTaussig Cancer Center, Department of Hematology, Medical Oncology, Cleveland Clinic, Cleveland, OH.
University of Arizona · USCleveland Clinic · USCincinnati Children's Hospital Medical Center · USSummit Medical Group (United States) · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
Development of lysosome targeted therapeuticsR41CA271967 · NCI · MAJESTIC THERAPEUTICS, LLC · PI CAREW, JENNIFER S, NAWROCKI, STEFFAN T · 2022 to 2022
$258k
NCI NIH HHS P30 CA023074NCI NIH HHS R41 CA271967
6 · The paper itself

Abstract

Multiple myeloma (MM) is a genetically complex disease. Identification of mutations and aberrant signaling pathways that contribute to the progression of MM and drug resistance has potential to lead to specific targets and personalized treatment. Aberrant signal pathways include RAS pathway activation due to RAS or BRAF mutations (targeted by vemurafenib alone or combined with cobimetinib), BCL-2 overexpression in t(11:14) (targeted by venetoclax), JAK2 pathway activation (targeted by ruxolitinib), NF-κB pathway activation (treated with DANFIN combined with bortezomib), MDM2 overexpression, and PI3K/mTOR pathway activation (targeted by BEZ235). Cyclin D1 (CCND1) and MYC are also emerging as key potential targets. In addition, histone deacetylase inhibitors are already in use for the treatment of MM in combination therapy, and targeted inhibition of FGFR3 (AZD4547) is effective in myeloma cells with t(4;14) translocation. Bromodomain and extra terminal (BET) protein antagonists decrease the expression of MYC and have displayed promising antimyeloma activity. A better understanding of the alterations in signaling pathways that promote MM progression will further inform the development of precision therapy for patients.

Indexed as

BiomarkersMolecular Targeted TherapyPrecision MedicineClinical Trials as TopicDisease ManagementDisease SusceptibilityHumansMultiple MyelomaSignal TransductionBiomarkersIntracellular pathwayMMMutationsPrecision medicineTargeted therapy

Identifiers

PMID31036508
PMCPMC6626550
OpenAlexW2922878699

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.