Evidence map›Paper›PMID 28590032›Full record

ReviewMolecular oncology2017

Epithelial-mesenchymal transition in cancer metastasis through the lymphatic system.

Mikael C Karlsson, Santiago F Gonzalez, Josefin Welin, Jonas Fuxe

Open access · goldAbstract readReview
In one paragraph

Review in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
7.8field-weighted citation impact, top 2% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.

  1. Pooled it
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  16. Targeting FAPActa pharmaceutica Sinica. B · 2024
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17 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

4 authors at 2 institutions in 3 countries.

Mikael C KarlssonDepartment of Microbiology, Tumor Biology and Cell Biology (MTC), Karolinska Institutet, Stockholm, Sweden.
Santiago F GonzalezInstitute for Research in Biomedicine (IRB), Bellinzona, Switzerland.
Josefin WelinDepartment of Microbiology, Tumor Biology and Cell Biology (MTC), Karolinska Institutet, Stockholm, Sweden.
Jonas FuxeDepartment of Microbiology, Tumor Biology and Cell Biology (MTC), Karolinska Institutet, Stockholm, Sweden.
Karolinska Institutet · SEInstitute for Research in Biomedicine · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It was already in the 18th century when the French surgeon LeDran first noted that breast cancer patients with spread of tumor cells to their axillary lymph nodes had a drastically worse prognosis than patients without spread (LeDran et al., ). Since then, metastatic spread of cancer cells to regional lymph nodes has been established as the most important prognostic factor in many types of cancer (Carter et al., ; Elston and Ellis, ). However, despite its clinical importance, lymph metastasis remains an underexplored area of tumor biology. Fundamental questions, such as when, how, and perhaps most importantly, why tumor cells disseminate through the lymphatic system, remain largely unanswered. Accordingly, no treatment strategies exist that specifically target lymph metastasis. The identification of epithelial-mesenchymal transition (EMT) as a mechanism, which allows cancer cells to dedifferentiate and acquire enhanced migratory and invasive properties, has been a game changer in cancer research. Conceptually, EMT provides an explanation for why epithelial cancers with poor differentiation status are generally more aggressive and prone to metastasize than more differentiated cancers. Inflammatory cytokines, such as TGF-β, which are produced and secreted by tumor-infiltrating immune cells, are potent inducers of EMT. Thus, reactivation of EMT also links cancer-related inflammation to invasive and metastatic disease. Recently, we found that breast cancer cells undergoing TGF-β-induced EMT acquire properties of immune cells allowing them to disseminate in a targeted fashion through the lymphatic system similar to activated dendritic cells during inflammation. Here, we review our current understanding of the mechanisms by which cancer cells spread through the lymphatic system and the links to inflammation and the immune system. We also emphasize how imaging techniques have the potential to further expand our knowledge of the mechanisms of lymph metastasis, and how lymph nodes serve as an interface between cancer and the immune system.

Indexed as

AnimalsEpithelial-Mesenchymal TransitionHumansLymphatic MetastasisLymph NodesNeoplasm ProteinsNeoplasmsTransforming Growth Factor betaNeoplasm ProteinsTransforming Growth Factor betachemokinesEMTimmune cell propertieslymph metastasistargeted migrationTGF-β

Identifiers

PMID28590032
PMCPMC5496496
OpenAlexW2621577071

What OpenQuestion holds

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LicenceCC BY
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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.