Evidence map›Paper›PMID 25223561›Full record

ArticleThe pharmacogenomics journal2015

Genetic polymorphisms in the mevalonate pathway affect the therapeutic response to alendronate treatment in postmenopausal Chinese women with low bone mineral density.

C Wang, H Zheng, J-W He, H Zhang, H Yue, W-W Hu, J-M Gu, C Shao, W-Z Fu, Y-Q Hu and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in The pharmacogenomics journal, 2015. 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
1.5field-weighted citation impact, top 20% 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, 26 citations in OpenAlex.

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  7. Pharmacogenomics and personalized medicine · 2021
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  10. Observational
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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

13 authors at 3 institutions in 1 country.

C Wang1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
H Zheng1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
J-W He1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
H Zhang1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
H Yue1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
W-W Hu1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
J-M Gu1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
C Shao1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
W-Z Fu1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
Y-Q Hu1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
M Li1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
Y-J Liu1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
Z-L Zhang1] Metabolic Bone Disease and Genetics Research Unit, Department of Osteoporosis and Bone Diseases, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China [2] Shanghai Key Clinical Center for Metabolic Disease, Shanghai, China.
Shanghai Sixth People's Hospital · CNShanghai Jiao Tong University · CNShanghai Clinical Research Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alendronate is an antiosteoporotic drug that targets the mevalonate pathway. To investigate whether the genetic variations in this pathway affect the clinical efficacy of alendronate in postmenopausal Chinese women with osteopenia or osteoporosis, 23 single-nucleotide polymorphisms (SNPs) in 7 genes were genotyped in 500 patients treated with alendronate for 12 months. Bone mineral density (BMD) was measured at baseline and after 12 months. The rs10161126 SNP in the 3' flanking region of MVK and the GTCCA haplotype in FDFT1 were significantly associated with therapeutic response. A 6.6% increase in BMD in the lumbar spine was observed in the GG homozygotes of rs10161126; AG heterozygotes and AA homozygotes experienced a 4.4 and 4.5% increase, respectively. The odds ratio (95% confidence interval) of G allele carriers to be responders in lumbar spine BMD was 2.06 (1.08-6.41). GTCCA haplotype in FDFT1 was more frequently detected in the group of responders than in the group of non-responders at the total hip (2.6 vs 0.5%, P=0.009). Therefore, MVK and FDFT1 polymorphisms are genetic determinants for BMD response to alendronate therapy in postmenopausal Chinese women.

Indexed as

AgedAlendronateAllelesAsian PeopleBone DensityBone Density Conservation AgentsBone Diseases, MetabolicFemaleHaplotypesHumansLumbar VertebraeMevalonic AcidOsteoporosisPhosphotransferases (Alcohol Group Acceptor)Polymorphism, Single NucleotidePostmenopauseAlendronateBone Density Conservation Agentsmevalonate kinaseMevalonic AcidPhosphotransferases (Alcohol Group Acceptor)

Identifiers

PMID25223561
OpenAlexW2001865334

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.