Evidence map›Paper›PMID 26040280›Full record

ArticleBreast cancer research : BCR2015

CD24(+) cells fuel rapid tumor growth and display high metastatic capacity.

Ran Rostoker, Sagi Abelson, Inna Genkin, Sarit Ben-Shmuel, Ravi Sachidanandam, Eyal J Scheinman, Keren Bitton-Worms, Zila Shen Orr, Avishay Caspi, Maty Tzukerman and 1 more

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-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

21 citing papers in PubMed, 33 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

11 authors at 4 institutions in 2 countries.

Ran RostokerDiabetes and Metabolism Clinical Research Center of Excellence, Clinical Research Institute at Rambam (CRIR) and the Faculty of Medicine, Technion, Rambam Medical Center, P.O.B 9602, Haifa, 31096, Israel. ranrosto@gmail.com.
Sagi AbelsonLaboratory of Molecular Medicine, Rambam Health Care Campus and Rappaport Faculty of Medicine and Research Institute, Technion, Haifa, 31096, Israel. sagiab@tx.technion.ac.il.
Inna GenkinDiabetes and Metabolism Clinical Research Center of Excellence, Clinical Research Institute at Rambam (CRIR) and the Faculty of Medicine, Technion, Rambam Medical Center, P.O.B 9602, Haifa, 31096, Israel. inna.genkin@mail.utoronto.ca.
Sarit Ben-ShmuelDiabetes and Metabolism Clinical Research Center of Excellence, Clinical Research Institute at Rambam (CRIR) and the Faculty of Medicine, Technion, Rambam Medical Center, P.O.B 9602, Haifa, 31096, Israel. saritbe9@gmail.com.
Ravi SachidanandamDepartment of Oncological Science, Icahn School of Medicine at Mt Sinai and the James J Peters VA Medical Center, New York, USA. ravi.sachidanandam@mssm.edu.
Eyal J ScheinmanDiabetes and Metabolism Clinical Research Center of Excellence, Clinical Research Institute at Rambam (CRIR) and the Faculty of Medicine, Technion, Rambam Medical Center, P.O.B 9602, Haifa, 31096, Israel. eyal.scheinman@gmail.com.
Keren Bitton-WormsDiabetes and Metabolism Clinical Research Center of Excellence, Clinical Research Institute at Rambam (CRIR) and the Faculty of Medicine, Technion, Rambam Medical Center, P.O.B 9602, Haifa, 31096, Israel. kerenworms@gmail.com.
Zila Shen OrrDiabetes and Metabolism Clinical Research Center of Excellence, Clinical Research Institute at Rambam (CRIR) and the Faculty of Medicine, Technion, Rambam Medical Center, P.O.B 9602, Haifa, 31096, Israel. z_shenorr@rambam.health.gov.il.
Avishay CaspiDiabetes and Metabolism Clinical Research Center of Excellence, Clinical Research Institute at Rambam (CRIR) and the Faculty of Medicine, Technion, Rambam Medical Center, P.O.B 9602, Haifa, 31096, Israel. avishaycaspi@walla.com.
Maty TzukermanLaboratory of Molecular Medicine, Rambam Health Care Campus and Rappaport Faculty of Medicine and Research Institute, Technion, Haifa, 31096, Israel. bimaty@tx.technion.ac.il.
Derek LeRoithDiabetes and Metabolism Clinical Research Center of Excellence, Clinical Research Institute at Rambam (CRIR) and the Faculty of Medicine, Technion, Rambam Medical Center, P.O.B 9602, Haifa, 31096, Israel. derek.leroith@mssm.edu.
Technion – Israel Institute of Technology · ILRambam Health Care Campus · ILIcahn School of Medicine at Mount Sinai · USJames J. Peters VA Medical Center · US

Funding

Mechanisms for the pro-metastatic effects of hyperinsulinemia on breast cancerR01CA128799 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEROITH, DEREK · 2008 to 2018
$3.7M
NCI NIH HHS 2R01CA128799-06A1NCI NIH HHS R01 CA128799
6 · The paper itself

Abstract

introductionBreast tumors are comprised of distinct cancer cell populations which differ in their tumorigenic and metastatic capacity. Characterization of cell surface markers enables investigators to distinguish between cancer stem cells and their counterparts. CD24 is a well-known cell surface marker for mammary epithelial cells isolation, recently it was suggested as a potential prognostic marker in a wide variety of malignancies. Here, we demonstrate that CD24(+) cells create intra-tumor heterogeneity, and display highly metastatic properties.

methodsThe mammary carcinoma Mvt1 cells were sorted into CD24(-) and CD24(+) cells. Both subsets were morphologically and phenotypically characterized, and tumorigenic capacity was assessed via orthotopic inoculation of each subset into the mammary fat pad of wild-type and MKR mice. The metastatic capacity of each subset was determined with the tail vein metastasis assay. The role of CD24 in tumorigenesis was further examined with shRNA technology. GFP-labeled cells were monitored in vivo for differentiation. The genetic profile of each subset was analyzed using RNA sequencing.

resultsCD24(+) cells displayed a more spindle-like cytoplasm. The cells formed mammospheres in high efficiency and CD24(+) tumors displayed rapid growth in both WT and MKR mice, and were more metastatic than CD24- cells. Interestingly, CD24-KD in CD24+ cells had no effect both in vitro and in vivo on the various parameters studied. Moreover, CD24(+) cells gave rise in vivo to the CD24(-) that comprised the bulk of the tumor. RNA-seq analysis revealed enrichment of genes and pathways of the extracellular matrix in the CD24(+) cells.

conclusionCD24(+) cells account for heterogeneity in mammary tumors. CD24 expression at early stages of the cancer process is an indication of a highly invasive tumor. However, CD24 is not a suitable therapeutic target; instead we suggest here new potential targets accounting for early differentiated cancer cells tumorigenic capacity.

Indexed as

AnimalsBiomarkersBreast NeoplasmsCD24 AntigenCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalExtracellular MatrixFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockout TechniquesImmunophenotypingMiceNeoplasm MetastasisNeoplastic Stem CellsBiomarkersCD24 Antigen

Identifiers

PMID26040280
PMCPMC4479226
OpenAlexW2132744824

What OpenQuestion holds

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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.