Evidence map›Paper›PMID 29669530›Full record

ArticleBMC cancer2018

Small cell and non small cell lung cancer form metastasis on cellular 4D lung model.

Dhruva K Mishra, Ross A Miller, Kristi A Pence, Min P Kim

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. 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
2.4field-weighted citation impact, top 12% 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, 22 citations in OpenAlex.

  1. Article
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  6. The microRNA-520a-3p inhibits invasion and metastasis by targeting NF-kappaB signaling pathway in non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
  7. Article
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  11. Acellular and Cellular Lung Model to Study Tumor Metastasis.Journal of visualized experiments : JoVE · 2018
    Article
  12. Review
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 3 institutions in 1 country.

Dhruva K MishraDepartment of Surgery, Houston Methodist Hospital Research Institute, Houston, TX, USA.
Ross A MillerDepartment of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, TX, USA.
Kristi A PenceDivision of Thoracic Surgery, Department of Surgery, Weill Cornell Medical College, Houston Methodist Hospital, 6550 Fannin Street, Suite 1661, Houston, TX, 77030, USA.
Min P KimDepartment of Surgery, Houston Methodist Hospital Research Institute, Houston, TX, USA. mpkim@houstonmethodist.org.
Methodist Hospital · USCornell University · USMethodist Hospital · US

Funding

American Association for Thoracic Surgery (US) Second John W. Kirklin Research ScholarshipHouston Methodist Specialty Physician Group GrantMichael M. And Joan H. Cone Research Award Grant
6 · The paper itself

Abstract

backgroundMetastasis is the main cause of death for lung cancer patients. The ex vivo 4D acellular lung model has been shown to mimic this metastatic process. However, the main concern is the model's lack of cellular components of the tumor's microenvironment. In this study, we aim to determine if the intact lung microenvironment will still allow lung cancer metastasis to form.

methodsWe harvested a heart-lung block from a rat and placed it in a bioreactor after cannulating the pulmonary artery, trachea and tying the right main bronchus for 10-15 days without any tumor cells as a control group or with NSCLC (A549, H1299 or H460), SCLC (H69, H446 or SHP77) or breast cancer cell lines (MCF7 or MDAMB231) through the trachea. We performed lobectomy, H&E staining and IHC for human mitochondria to determine the primary tumor's growth and formation of metastatic lesions. In addition, we isolated circulating tumor cells (CTC) from the model seeded with GFP tagged cells.

resultsIn the control group, no gross tumor nodules were found, H&E staining showed hyperplastic cells and IHC showed no staining for human mitochondria. All of the models seeded with cancer cell lines formed gross primary tumor nodules that had microscopic characteristics of human cancer cells on H&E staining with IHC showing staining for human mitochondria. CTC were isolated for those cells labeled with GFP and they were viable in culture. Finally, all cell lines formed metastatic lesions with cells stained for human mitochondria.

conclusionThe cellular ex vivo 4D model shows that human cancer cells can form a primary tumor, CTC and metastatic lesions in an intact cellular environment. This study suggests that the natural matrix scaffold is the only necessary component to drive metastatic progression and that cellular components play a role in modulating tumor progression.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCarcinoma, Small CellCell Line, TumorDisease Models, AnimalDisease ProgressionHumansLung NeoplasmsMaleNeoplasm MetastasisNeoplastic Cells, CirculatingRatsTumor Burden4D cellular modelBreast cancerLung Cancer

Identifiers

PMID29669530
PMCPMC5907356
OpenAlexW2799449613

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.