Evidence map›Paper›PMID 25152705›Full record

ArticleCurrent signal transduction therapy2014

Metastasis-Initiating Cells in Renal Cancer.

Mohammed I Khan, Anna M Czarnecka, Renata Duchnowska, Wojciech Kukwa, Cezary Szczylik

Open access · hybridAbstract read
In one paragraph

Article in Current signal transduction therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  4. Involvement of the CBBMC cancer · 2018
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  7. Antcin-H Isolated fromEvidence-based complementary and alternative medicine : eCAM · 2017
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  10. Review
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  12. Review
  13. Protein interactions of cortactin in relation to invadopodia formation in metastatic renal clear cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
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

5 authors at 1 institution in 1 country.

Mohammed I KhanMolecular Oncology Laboratory, Clinic of Oncology, Military Institute of Medicine, ul. Szaserów 128, 04-141 Warsaw, Poland.
Anna M CzarneckaMolecular Oncology Laboratory, Clinic of Oncology, Military Institute of Medicine, ul. Szaserów 128, 04-141 Warsaw, Poland.
Renata DuchnowskaMolecular Oncology Laboratory, Clinic of Oncology, Military Institute of Medicine, ul. Szaserów 128, 04-141 Warsaw, Poland.
Wojciech KukwaDepartment of Otolaryngology, Czerniakowski Hospital, Medical University of Warsaw, ul. Stepinska 19/25, Warsaw, Poland.
Cezary SzczylikMolecular Oncology Laboratory, Clinic of Oncology, Military Institute of Medicine, ul. Szaserów 128, 04-141 Warsaw, Poland.
Medical University of Warsaw · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis is a complex process that propagates cells from the primary or initial site of the cancer occurrence to distant parts of the body. Cancer cells break from the cancer site and circulate through the bloodstream or lymph vessels, allowing them to reach nearly all parts of the body. These circulating tumour cells (CTCs) contain specialized metastasis-initiating cells (MICs) that reside in the biological heterogeneous primary tumour. Researchers have hypothesized that metastasis of renal cell carcinoma is initiated by circulation of MICs in patients' blood and bone marrow. Based on the cancer stem/progenitor cell concept of carcinogenesis, understanding the molecular phenotypes of metastasis-initiating cells (MICs) in renal cancer could play a vital role in developing strategies for therapeutic interventions in renal cancer. Existence of MICs among CTCs in renal carcinoma has not been proven in large scale. However, some studies have reported that specialized markers are found on the surface of circulating cells from the primary tumour. In mice, MICs have been isolated from CTCs using such markers, which have then been transplanted into xenograft model to show whether they give rise to metastasis in different organs. Considering these findings, in this review we have attempted to summarize the studies connected with MICs and their gene expression profiles that are responsible for metastasis in renal cancer.

Indexed as

Circulating tumour cellsmetastasis-initiating cellsrenal cell carcinomatumour-initiating cells.

Identifiers

PMID25152705
PMCPMC4141324
OpenAlexW2031229530

What OpenQuestion holds

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Registered trials

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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.