Evidence map›Paper›PMID 22454149›Full record

ArticleEndocrinology2012

Dietary vitamin D₃ and 1,25-dihydroxyvitamin D₃ (calcitriol) exhibit equivalent anticancer activity in mouse xenograft models of breast and prostate cancer.

Srilatha Swami, Aruna V Krishnan, Jennifer Y Wang, Kristin Jensen, Ronald Horst, Megan A Albertelli, David Feldman

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 3 pooled it
10.7field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 3 syntheses or guidelines pooled it, 163 citations in OpenAlex.

  1. Pooled it
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  9. The double disparity: Vitamin D deficiency and lethal prostate cancer in black men.The Journal of steroid biochemistry and molecular biology · 2025
    Review
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27 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Srilatha SwamiDepartment of Medicine-Endocrinology, Stanford University School of Medicine, Stanford, California 94305-5103, USA.
Aruna V Krishnan
Jennifer Y Wang
Kristin Jensen
Ronald Horst
Megan A Albertelli
David Feldman
Stanford Medicine · USStanford University · US

Funding

The Development of Vitamin D as a Therapy for Breast CancerR01CA130991 · NCI · STANFORD UNIVERSITY · PI FELDMAN, DAVID · 2008 to 2011
$1.2M
NCI NIH HHS CA130991NCI NIH HHS R01 CA130991
6 · The paper itself

Abstract

1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3) or calcitriol], the hormonally active vitamin D metabolite, exhibits anticancer actions in models of breast cancer and prostate cancer. Because CYP27B1 (1α-hydroxylase), the enzyme catalyzing 1,25(OH)(2)D(3) formation in the kidney, is also expressed in extrarenal tissues, we hypothesize that dietary vitamin D(3) will be converted to 25(OH)D(3) in the body and then to 1,25(OH)(2)D(3) locally in the cancer microenvironment in which it will exert autocrine/paracrine anticancer actions. Immunocompromised mice bearing MCF-7 breast cancer xenografts showed significant tumor shrinkage (>50%) after ingestion of a vitamin D(3)-supplemented diet (5000 IU/kg) compared with a control diet (1000 IU/kg). Dietary vitamin D(3) inhibition of tumor growth was equivalent to administered calcitriol (0.025, 0.05, or 0.1 μg/mouse, three times a week). Both treatments equivalently inhibited PC-3 prostate cancer xenograft growth but to a lesser extent than the MCF-7 tumors. Calcitriol at 0.05 μg and 0.1 μg caused modest but statistically significant increases in serum calcium levels indicating that the dietary vitamin D(3) comparison was to a maximally safe calcitriol dose. Dietary vitamin D(3) did not increase serum calcium, demonstrating its safety at the concentration tested. The vitamin D(3) diet raised circulating 1,25 dihydroxyvitamin D levels and did not alter CYP27B1 mRNA in the kidney but increased it in the tumors, suggesting that extrarenal sources including the tumors contributed to the elevated circulating 1,25 dihydroxyvitamin D(3). Both calcitriol and dietary vitamin D(3) were equipotent in suppressing estrogen synthesis and signaling and other proinflammatory and growth signaling pathways. These preclinical data demonstrate the potential utility of dietary vitamin D(3) supplementation in cancer prevention and therapy.

Indexed as

Xenograft Model Antitumor Assays25-Hydroxyvitamin D3 1-alpha-HydroxylaseAnimalsBody WeightBreast NeoplasmsCalcitriolCalciumCell Line, TumorCholecalciferolDietary SupplementsEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHumansImmunohistochemistryMale25-Hydroxyvitamin D3 1-alpha-HydroxylaseCalcitriolCalciumCholecalciferolEstrogen Receptor alphaReceptors, CalcitriolSteroid HydroxylasesVitamin D3 24-HydroxylaseVitamins

Identifiers

PMID22454149
PMCPMC3359605
OpenAlexW2085491680

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.