Evidence map›Paper›PMID 27363025›Full record

ArticleOncotarget2016

Regression of experimental NIS-expressing breast cancer brain metastases in response to radioiodide/gemcitabine dual therapy.

Corinne Renier, John Do, Andrea Reyna-Neyra, Deshka Foster, Abhijit De, Hannes Vogel, Stefanie S Jeffrey, Victor Tse, Nancy Carrasco, Irene Wapnir

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

Corinne RenierDepartment of Surgery, Stanford University School of Medicine, Stanford, CA, USA.
John DoDepartment of Surgery, Stanford University School of Medicine, Stanford, CA, USA.
Andrea Reyna-NeyraDepartment of Cellular and Molecular Physiology, Yale University, New Haven, CT, USA.
Deshka FosterDepartment of Surgery, Stanford University School of Medicine, Stanford, CA, USA.
Abhijit DeDepartment of Radiology and Molecular Imaging Program at Stanford, Stanford, CA, USA.
Hannes VogelDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Stefanie S JeffreyDepartment of Surgery, Stanford University School of Medicine, Stanford, CA, USA.
Victor TseDepartment of Neurosurgery, Stanford University School of Medicine, Stanford, CA, USA.
Nancy CarrascoDepartment of Cellular and Molecular Physiology, Yale University, New Haven, CT, USA.
Irene WapnirDepartment of Surgery, Stanford University School of Medicine, Stanford, CA, USA.

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI MEGAN C KING · 1985 to 2026
$85.0M
THYROID SODIUM I/ SYMPORTERR01DK041544 · NIDDK · YESHIVA UNIVERSITY · PI ABBOTT, GEOFFREY W, CARRASCO, NANCY · 1989 to 2017
$5.6M
NCATS NIH HHS UL1 TR001863NCI NIH HHS P30 CA016359NIDDK NIH HHS R01 DK041544
6 · The paper itself

Abstract

Treating breast cancer brain metastases (BCBMs) is challenging. Na+/I- symporter (NIS) expression in BCBMs would permit their selective targeting with radioiodide (131I-). We show impressive enhancement of tumor response by combining131I- with gemcitabine (GEM), a cytotoxic radiosensitizer. Nude mice mammary fat-pad (MFP) tumors and BCBMs were generated with braintropic MDA-MB-231Br cells transduced with bicistronically-linked NIS and firefly luciferase cDNAs. Response was monitored in vivo via bioluminescent imaging and NIS tumor expression.131I-/GEM therapy inhibited MFP tumor growth more effectively than either agent alone. BCBMs were treated with: high or low-dose GEM (58 or 14.5 mg/Kg×4); 131I- (1mCi or 2×0.5 mCi 7 days apart); and 131I-/GEM therapy. By post-injection day (PID) 25, 82-86% of controls and 78-83% of 131I--treated BCBM grew, whereas 17% low-dose and 36% high-dose GEM regressed. The latter tumors were smaller than the controls with comparable NIS expression (~20% of cells). High and low-dose 131I-/ GEM combinations caused 89% and 57% tumor regression, respectively. High-dose GEM/131I- delayed tumor growth: tumors increased 5-fold in size by PID45 (controls by PID18). Although fewer than 25% of cells expressed NIS, GEM/131I- caused dramatic tumor regression in NIS-transduced BCBMs. This effect was synergistic, and supports the hypothesis that GEM radiosensitizes cells to 131I-.

Indexed as

AnimalsAntimetabolites, AntineoplasticBrain NeoplasmsBreast NeoplasmsCell Line, TumorCombined Modality TherapyDeoxycytidineFemaleGemcitabineHEK293 CellsHumansIodine RadioisotopesMice, NudeSodium-Iodide SymportersSymportersTransfectionAntimetabolites, AntineoplasticDeoxycytidineGemcitabineIodine RadioisotopesSodium-Iodide SymportersSymportersbreast cancer brain metastases (BCBMs)radioiodide therapysodium/iodide symporter (NIS)

Identifiers

PMID27363025
PMCPMC5342383

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.