Evidence map›Paper›PMID 34666995›Full record

ArticleCancer research2022

T Cells Promote Metastasis by Regulating Extracellular Matrix Remodeling following Chemotherapy.

Jozafina Haj-Shomaly, Avital Vorontsova, Tamar Barenholz-Cohen, Oshrat Levi-Galibov, Mahesh Devarasetty, Michael Timaner, Ziv Raviv, Tim J Cooper, Shay Soker, Peleg Hasson and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 65 citations in OpenAlex.

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  19. Integrins as Key Mediators of Metastasis.International journal of molecular sciences · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 2 countries.

Jozafina Haj-ShomalyRappaport Technion Integrated Cancer Center, Cell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Avital VorontsovaRappaport Technion Integrated Cancer Center, Cell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Tamar Barenholz-CohenFaculty of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa, Israel.
Oshrat Levi-GalibovDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel.
Mahesh DevarasettyWake Forest University School of Medicine, Wake Forest Institute for Regenerative Medicine, Winston-Salem, North Carolina.
Michael TimanerRappaport Technion Integrated Cancer Center, Cell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Ziv RavivRappaport Technion Integrated Cancer Center, Cell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Tim J CooperRappaport Technion Integrated Cancer Center, Cell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Shay SokerWake Forest University School of Medicine, Wake Forest Institute for Regenerative Medicine, Winston-Salem, North Carolina.
Peleg HassonDepartment of Genetics and Developmental Biology, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Daphne WeihsFaculty of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa, Israel.ORCID 0000-0002-9670-3418
Ruth Scherz-ShouvalDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel.ORCID 0000-0002-4570-121X
Yuval ShakedRappaport Technion Integrated Cancer Center, Cell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. yshaked@technion.ac.il.
Technion – Israel Institute of Technology · ILWake Forest University · USWeizmann Institute of Science · IL

Funding

European Research Council 771112
6 · The paper itself

Abstract

Metastasis is the main cause of cancer-related mortality. Despite intense efforts to understand the mechanisms underlying the metastatic process, treatment of metastatic cancer is still challenging. Here we describe a chemotherapy-induced, host-mediated mechanism that promotes remodeling of the extracellular matrix (ECM), ultimately facilitating cancer cell seeding and metastasis. Paclitaxel (PTX) chemotherapy enhanced rapid ECM remodeling and mechanostructural changes in the lungs of tumor-free mice, and the protein expression and activity of the ECM remodeling enzyme lysyl oxidase (LOX) increased in response to PTX. A chimeric mouse model harboring genetic LOX depletion revealed chemotherapy-induced ECM remodeling was mediated by CD8

Indexed as

Adoptive TransferAnimalsAntineoplastic Agents, PhytogenicBreast NeoplasmsCD8-Positive T-LymphocytesExtracellular MatrixExtracellular Matrix ProteinsFemaleHumansLung NeoplasmsMammary Neoplasms, ExperimentalMCF-7 CellsMiceMice, Inbred BALB CMice, KnockoutMice, SCIDAntineoplastic Agents, PhytogenicExtracellular Matrix ProteinsLOX protein, humanLox protein, mousePaclitaxelProtein-Lysine 6-Oxidase

Identifiers

PMID34666995
PMCPMC7612244
OpenAlexW3207821904

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.