Evidence map›Paper›PMID 30115759›Full record

ArticleMolecular cancer research : MCR2018

Impeding Circulating Tumor Cell Reseeding Decelerates Metastatic Progression and Potentiates Chemotherapy.

Chen Qian, Asurayya Worrede-Mahdi, Fei Shen, Anthony DiNatale, Ramanpreet Kaur, Qiang Zhang, Massimo Cristofanilli, Olimpia Meucci, Alessandro Fatatis

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

6 citing papers in PubMed, 7 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

9 authors at 4 institutions in 1 country.

Chen QianDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania.
Asurayya Worrede-MahdiDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania.
Fei ShenOncology Discovery, Janssen Pharmaceuticals, Spring House, Pennsylvania.
Anthony DiNataleDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania.
Ramanpreet KaurDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania.
Qiang ZhangDepartment of Medicine-Hematology and Oncology, Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Chicago, Illinois.
Massimo CristofanilliDepartment of Medicine-Hematology and Oncology, Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Chicago, Illinois.
Olimpia MeucciDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania.ORCID 0000-0001-8333-4804
Alessandro FatatisDepartment of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania. af39@drexel.edu.
Drexel University · USRobert H. Lurie Comprehensive Cancer Center of Northwestern UniversitySidney Kimmel Cancer Center · USSpringhouse · US

Funding

Role of CX3CR1 in breast cancer metastasisR01CA202929 · NCI · DREXEL UNIVERSITY · PI FATATIS, ALESSANDRO, MEUCCI, OLIMPIA · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA202929
6 · The paper itself

Abstract

Circulating tumor cells (CTCs) are commonly detected in the systemic blood of patients with cancer with metastatic tumors. However, the mechanisms controlling the viability of cancer cells in blood and length of time spent in circulation, as well as their potential for generating additional tumors are still undefined. Here, it is demonstrated that CX3CR1, a chemokine receptor, drives reseeding of breast CTCs to multiple organs. Antagonizing this receptor dramatically impairs the progression of breast cancer cells in a relevant model of human metastatic disease, by affecting both tumor growth and numerical expansion. Notably, therapeutic targeting of CX3CR1 prolongs CTC permanence in the blood, both promoting their spontaneous demise by apoptosis and counteracting metastatic reseeding. These effects lead to containment of metastatic progression and extended survival. Finally, targeting CX3CR1 improves blood exposure of CTCs to doxorubicin and in combination with docetaxel shows synergistic effects in containing overall tumor burden. IMPLICATIONS: The current findings shed light on CTCs reseeding dynamics and support the development of CX3CR1 antagonism as a viable strategy to counteract metastatic progression.

Indexed as

AnimalsAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCell SurvivalCX3C Chemokine Receptor 1Disease ProgressionDocetaxelDoxorubicinDrug SynergismFemaleHumansNeoplasm MetastasisNeoplasm TransplantationNeoplastic Cells, CirculatingPrognosisAntineoplastic AgentsCX3C Chemokine Receptor 1CX3CR1 protein, humanDocetaxelDoxorubicinSmall Molecule Libraries

Identifiers

PMID30115759
PMCPMC6279516
OpenAlexW2887707436

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.