Evidence map›Paper›PMID 26732077›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2016

Altered Lamin A/C splice variant expression as a possible diagnostic marker in breast cancer.

Ahmad Aljada, Joseph Doria, Ayman M Saleh, Shahad H Al-Matar, Sarah AlGabbani, Heba Bani Shamsa, Ahmad Al-Bawab, Altayeb Abdalla Ahmed

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-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

18 citing papers in PubMed, 31 citations in OpenAlex.

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  14. Quantification of theInternational journal of molecular sciences · 2019
    Article
  15. Alternative Splicing as a Target for Cancer Treatment.International journal of molecular sciences · 2018
    Review
  16. The Emerging Role of Lamin C as an ImportantFrontiers in cell and developmental biology · 2018
    Article
  17. Article
  18. Review
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

8 authors at 3 institutions in 2 countries.

Ahmad AljadaDepartment of Basic Medical Sciences, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Kingdom of Saudi Arabia. aljadaa@ksau-hs.edu.sa.
Joseph DoriaDepartment of Neurology, Virginia Commonwealth University Medical Center, Richmond, VA, USA.
Ayman M SalehDepartment of Basic Medical Sciences, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Kingdom of Saudi Arabia.
Shahad H Al-MatarDepartment of Basic Medical Sciences, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Kingdom of Saudi Arabia.
Sarah AlGabbaniDepartment of Basic Medical Sciences, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Kingdom of Saudi Arabia.
Heba Bani ShamsaKing Abdullah International Medical Research Center (KAIMRC), National Guard Health Affairs, Riyadh, Kingdom of Saudi Arabia.
Ahmad Al-BawabDepartment of Basic Medical Sciences, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Kingdom of Saudi Arabia.
Altayeb Abdalla AhmedDepartment of Basic Medical Sciences, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Kingdom of Saudi Arabia.
King Saud bin Abdulaziz University for Health Sciences · SAKing Abdullah International Medical Research Center · SAVirginia Commonwealth University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLamin A/C alternative splice variants (Lamin A, Lamin C, Lamin AΔ10 and Lamin AΔ50) have been implicated in cell cycle regulation, DNA replication, transcription regulation, cellular differentiation, apoptosis and aging. In addition, loss of Lamin A/C expression has been observed in several cancers, including breast cancer, and it has been found that Lamin A/C suppression may lead to cancer-like aberrations in nuclear morphology and aneuploidy. Based on these observations, we hypothesized that Lamin A/C transcript variant quantification might be employed for the diagnosis of breast cancer.

methodsNewly designed TaqMan qRT-PCR assays for the analysis of Lamin A/C splice variants were validated and their use as biomarkers for the diagnosis of breast cancer was assessed using 16 normal breast tissues and 128 breast adenocarcinomas. In addition, the expression levels of the Lamin A/C transcript variants were measured in samples derived from seven other types of cancer.

resultsWe found that the expression level of Lamin C was significantly increased in the breast tumors tested, whereas the expression levels of Lamin A and Lamin AΔ50 were significantly decreased. No significant change in Lamin AΔ10 expression was observed. Our data also indicated that the Lamin C : Lamin A mRNA ratio was increased in all clinical stages of breast cancer. Additionally, we observed increased Lamin C : Lamin A mRNA ratios in liver, lung and thyroid carcinomas and in colon, ovary and prostate adenocarcinomas.

conclusionsFrom our data we conclude that the Lamin C : Lamin A mRNA ratio is increased in breast cancer and that this mRNA ratio may be of diagnostic use in all clinical stages of breast cancer and, possibly, also in liver, lung, thyroid, colon, ovary and prostate cancers.

Indexed as

Gene Expression Regulation, NeoplasticAlternative SplicingBiomarkers, TumorBreast NeoplasmsFemaleGene Expression ProfilingHumansLamin Type AOrgan SpecificityReal-Time Polymerase Chain ReactionRNA, MessengerBiomarkers, Tumorlamin CLamin Type ARNA, MessengerBreast cancerLamin A/CMetastasisProgerinTumor marker

Identifiers

PMID26732077
PMCPMC13001873
OpenAlexW2227469241

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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.