Evidence map›Paper›PMID 33014834›Full record

ReviewFrontiers in oncology2020

Targeting CXCR4 in AML and ALL.

Daniel Cancilla, Michael P Rettig, John F DiPersio

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 106 citations in OpenAlex.

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  13. Disruption of constitutive CXCR4 oligomers impairs oncogenic properties in lymphoid neoplasms.Proceedings of the National Academy of Sciences of the United States of America · 2025
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3 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Daniel CancillaDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States.
Michael P RettigDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States.
John F DiPersioDivision of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States.
Washington University in St. Louis · US

Funding

Optimizing Hematopoietic Stem Cell Transplantation For The Treatment Of Hematological MalignanciesR35CA210084 · NCI · WASHINGTON UNIVERSITY · PI John F. Dipersio · 2017 to 2026
$7.8M
BM NICHE DISRUPTION AND IMMUNOTHERAPY IN HEMATOLOGICAL MALIGNANCIESR50CA211466 · NCI · WASHINGTON UNIVERSITY · PI Michael Rettig · 2016 to 2026
$2.3M
NCI NIH HHS R35 CA210084NCI NIH HHS R50 CA211466
6 · The paper itself

Abstract

The interaction of acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) blasts with the bone marrow microenvironment regulates self-renewal, growth signaling, as well as chemotherapy resistance. The chemokine receptor, CXC receptor 4 (CXCR4), with its ligand chemokine ligand 12 (CXCL12), plays a key role in the survival and migration of normal and malignant stem cells to the bone marrow. High expression of CXCR4 on AML and ALL blasts has been shown to be a predictor of poor prognosis for these diseases. Several small molecule inhibitors, short peptides, antibodies, and antibody drug conjugates have been developed for the purposes of more effective targeting and killing of malignant cells expressing CXCR4. In this review we will discuss recent results and strategies in targeting CXCR4 with these agents in patients with AML or ALL.

Indexed as

ALLAMLchemosensitizationCXCL12CXCR4

Identifiers

PMID33014834
PMCPMC7499473
OpenAlexW3083620184

What Socratic 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 Socratic graph.