Evidence map›Paper›PMID 24762141›Full record

ArticleEndocrinology2014

Combination of 13-Cis retinoic acid and lovastatin: marked antitumor potential in vivo in a pheochromocytoma allograft model in female athymic nude mice.

Svenja Nölting, Alessio Giubellino, Yasin Tayem, Karen Young, Michael Lauseker, Petra Bullova, Jan Schovanek, Miriam Anver, Stephanie Fliedner, Márta Korbonits and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

10 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Metastatic Phaeochromocytoma: Spinning Towards More Promising Treatment Options.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2019
    Review
  7. Article
  8. Article
  9. Article
  10. 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

14 authors at 10 institutions in 5 countries.

Svenja NöltingEunice Kennedy Shriver National Institute of Child Health and Human Development (S.N., A.Gi., Y.T., P.B., J.S., K.P.), National Institutes of Health, Bethesda, Maryland 20892; Department of Endocrinology (S.N., K.Y., M.K.), William Harvey Research Institute, Barts and the London School of Medicine, Queen Mary University of London, London EC1M 6BQ, United Kingdom; Department of Internal Medicine II (S.N., B.G., G.V.), Campus Grosshadern, University-Hospital of the Ludwig-Maximilians-University of Munich, and Institute of Medical Informatics, Biometry, and Epidemiology (M.L.), University of Munich, Munich 81377, Germany; Department of Molecular Medicine (P.B.), Institute of Virology, Slovak Academy of Sciences, Bratislava 84505, Slovakia; Department of Internal Medicine III (J.S.), Nephrology, Rheumatology, and Endocrinology, Faculty of Medicine and Dentistry, Palacky University, Olomouc 77520, Czech Republic; Leidos Biomedical Research, Inc (M.A.), Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702; First Medical Department (S.F.), University Medical Center Schleswig-Holstein, Campus Lübeck, Lübeck 23538, Germany; and Oxford Centre for Diabetes, Endocrinology and Metabolism (A.Gr.), University of Oxford, Oxford OX3 7LE, United Kingdom.
Alessio Giubellino
Yasin Tayem
Karen Young
Michael Lauseker
Petra Bullova
Jan Schovanek
Miriam Anver
Stephanie Fliedner
Márta Korbonits
Burkhard Göke
George Vlotides
Ashley Grossman
Karel Pacak
National Institutes of Health · USLudwig-Maximilians-Universität München · DEEunice Kennedy Shriver National Institute of Child Health and Human Development · USLeidos (United States) · USOxford Centre for Diabetes, Endocrinology and Metabolism · GBPalacký University Olomouc · CZQueen Mary University of London · GBSlovak Academy of Sciences · SKWilliam Harvey Research Institute · GBZimmer Biomet (Germany) · DE

Funding

Diagnosis, Pathophysiology And Molecular Biology of Pheochromocytoma and ParagangliomaZIAHD008735 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI PACAK, KAREL · 2009 to 2024
$28.4M
PHS HHS HSN261200800001E
6 · The paper itself

Abstract

Currently, there are no reliably effective therapeutic options for metastatic pheochromocytoma (PCC) and paraganglioma. Moreover, there are no therapies that may prevent the onset or progression of tumors in patients with succinate dehydrogenase type B mutations, which are associated with very aggressive tumors. Therefore, we tested the approved and well-tolerated drugs lovastatin and 13-cis-retinoic acid (13cRA) in vitro in an aggressive PCC mouse cell line, mouse tumor tissue-derived (MTT) cells, and in vivo in a PCC allograft nude mouse model, in therapeutically relevant doses. Treatment was started 24 hours before sc tumor cell injection and continued for 30 more days. Tumor sizes were measured from outside by caliper and sizes of viable tumor mass by bioluminescence imaging. Lovastatin showed antiproliferative effects in vitro and led to significantly smaller tumor sizes in vivo compared with vehicle treatment. 13cRA promoted tumor cell growth in vitro and led to significantly larger viable tumor mass and significantly faster increase of viable tumor mass in vivo over time compared with vehicle, lovastatin, and combination treatment. However, when combined with lovastatin, 13cRA enhanced the antiproliferative effect of lovastatin in vivo. The combination-treated mice showed slowest tumor growth of all groups with significantly slower tumor growth compared with the vehicle-treated mice and significantly smaller tumor sizes. Moreover, the combination-treated group displayed the smallest size of viable tumor mass and the slowest increase in viable tumor mass over time of all groups, with a significant difference compared with the vehicle- and 13cRA-treated group. The combination-treated tumors showed highest extent of necrosis, lowest median microvessel density and highest expression of α-smooth muscle actin. The combination of high microvessel density and low α-smooth muscle actin is a predictor of poor prognosis in other tumor entities. Therefore, this drug combination may be a well-tolerated novel therapeutic or preventive option for malignant PCC.

Indexed as

ActinsAdrenal Gland NeoplasmsAnimalsAntigens, CD34Antineoplastic Combined Chemotherapy ProtocolsCell Line, TumorCell SurvivalChromogranin AFemaleImmunohistochemistryIsotretinoinLovastatinLung NeoplasmsMiceMice, NudeMuscle, SmoothActinsAntigens, CD34Chromogranin AIsotretinoinLovastatinTyrosine 3-Monooxygenase

Identifiers

PMID24762141
PMCPMC4060189
OpenAlexW1975407113

What OpenQuestion holds

Textmetadata
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.