Evidence map›Paper›PMID 28923207›Full record

ReviewSeminars in oncology2017

Eviction from the sanctuary: Development of targeted therapy against cell adhesion molecules in acute lymphoblastic leukemia.

Sonali P Barwe, Anthony Quagliano, Anilkumar Gopalakrishnapillai

Abstract readReview
In one paragraph

Review in Seminars in oncology, 2017. 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
2.0field-weighted citation impact, top 13% 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, 15 citations in OpenAlex.

  1. Epithelial-Mesenchymal Transition in Acute Leukemias.International journal of molecular sciences · 2024
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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

3 authors at 1 institution in 1 country.

Sonali P BarweNemours Center for Childhood Cancer Research, A.I. DuPont Hospital for Children, Wilmington, DE. Electronic address: barwe@medsci.udel.edu.
Anthony QuaglianoNemours Center for Childhood Cancer Research, A.I. DuPont Hospital for Children, Wilmington, DE.
Anilkumar GopalakrishnapillaiNemours Center for Childhood Cancer Research, A.I. DuPont Hospital for Children, Wilmington, DE. Electronic address: anil.g@nemours.org.
Community Health Systems - Dupont Hospital · US

Funding

Predictive Modeling & Optimal Control Framework for Model-Based Epidemic Response in DelawareP20GM103446 · NIGMS · UNIVERSITY OF DELAWARE · PI MELINDA K DUNCAN · 2012 to 2026
$67.2M
Subproject Title: Clinical Research Education, Mentoring and Career Development CoreU54GM104941 · NIGMS · UNIVERSITY OF DELAWARE · PI Gregory E Hicks · 2013 to 2026
$60.5M
Center for Pediatric Research Pilot ProgramP30GM114736 · NIGMS · NEMOURS CHILDREN'S HOSPITAL, DELAWARE · PI SHAFFER, THOMAS H · 2015 to 2019
$5.1M
NIGMS NIH HHS P20 GM103446NIGMS NIH HHS P30 GM114736NIGMS NIH HHS U54 GM104941
6 · The paper itself

Abstract

Acute lymphoblastic leukemia (ALL) is a malignant hematological disease afflicting hematopoiesis in the bone marrow. While 80%-90% of patients diagnosed with ALL will achieve complete remission at some point during treatment, ALL is associated with high relapse rate, with a 5-year overall survival rate of 68%. The initial remission failure and the high rate of relapse can be attributed to intrinsic chemoprotective mechanisms that allow persistence of ALL cells despite therapy. These mechanisms are mediated, at least in part, through the engagement of cell adhesion molecules (CAMs) within the bone marrow microenvironment. This review assembles CAMs implicated in protection of leukemic cells from chemotherapy. Such studies are limited in ALL. Therefore, CAMs that are associated with poor outcomes or are overexpressed in ALL and have been shown to be involved in chemoprotection in other hematological cancers are also included. It is likely that these molecules play parallel roles in ALL because the CAMs identified to be a factor in ALL chemoresistance also work similarly in other hematological malignancies. We review the signaling mechanisms activated by the engagement of CAMs that provide protection from chemotherapy. Development of targeted therapies against CAMs could improve outcome and raise the overall cure rate in ALL.

Indexed as

Drug Resistance, NeoplasmCell Adhesion MoleculesHumansMolecular Targeted TherapyPrecursor Cell Lymphoblastic Leukemia-LymphomaSignal TransductionCell Adhesion MoleculesAcute lymphoblastic leukemiaBone marrowCell adhesion moleculesChemoresistanceTargeted therapy

Identifiers

PMID28923207
PMCPMC5657583
OpenAlexW2735950082

What OpenQuestion 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 OpenQuestion graph.