Evidence map›Paper›PMID 38670588›Full record

ArticleCancer genomics & proteomics

Genomic Frequencies of Dynamic DNA Sequences and Mammalian Lifespan.

Marianna Martella, Nadia Carlesso, Zoë A E Waller, Guido Marcucci, Flavia Pichiorri, Steven S Smith

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer genomics & proteomics. 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
1.1field-weighted citation impact, top 21% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

6 authors at 3 institutions in 2 countries.

Marianna MartellaJudy and Bernard Briskin Center for Multiple Myeloma Research, City of Hope, Duarte, CA, U.S.A.
Nadia CarlessoJudy and Bernard Briskin Center for Multiple Myeloma Research, City of Hope, Duarte, CA, U.S.A.
Zoë A E WallerUniversity College London School of Pharmacy, London, U.K.
Guido MarcucciDepartment of Hematological Malignancies and Translational Science, City of Hope, Duarte, CA, U.S.A.
Flavia PichiorriJudy and Bernard Briskin Center for Multiple Myeloma Research, City of Hope, Duarte, CA, U.S.A.
Steven S SmithBeckman Research Institute of the City of Hope, Duarte, CA, U.S.A.; ssmith@coh.org.
City Of Hope National Medical Center · USCity of Hope · USUniversity of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimDynamic DNA sequences (i.e. sequences capable of forming hairpins, G-quadruplexes, i-motifs, and triple helices) can cause replication stress and associated mutations. One example of such a sequence occurs in the RACK7 gene in human DNA. Since this sequence forms i-motif structures at neutral pH that cause replication stress and result in spontaneous deletions in prostate cancer cells, our initial aim was to determine its potential utility as a biomarker of prostate cancer. MATERIALS AND

methodsWe cloned and sequenced the region in RACK7 where i-motif deletions often occur in DNA obtained from eight individuals. Expressed prostatic secretions were obtained from three individuals with a positive biopsy for prostate cancer and two with individuals with a negative biopsy for prostate cancer. Peripheral blood specimens were obtained from two control healthy bone marrow donors and a marrow specimen was obtained from a third healthy marrow donor. Follow-up computer searches of the genomes of 74 mammalian species available at the NCBI ftp site or frequencies of 6 dynamic sequences known to produce mutations or replication stress using a program written in Mathematica were subsequently performed.

resultsDeletions were found in RACK7 in specimens from both older normal adults, as well as specimens from older patients with cancer, but not in the youngest normal adult. The deletions appeared to show a weak trend to increasing frequency with patient age. This suggested that endogenous mutations associated with dynamic sequences might accumulate during aging and might serve as biomarkers of biological age rather than direct biomarkers of cancer. To test that hypothesis, we asked whether or not the genomic frequencies of several dynamic sequences known to produce replication stress or mutations in human DNA were inversely correlated with maximum lifespan in mammals.

conclusionOur results confirm this correlation for six dynamic sequences in 74 mammalian genomes studied, thereby suggesting that spontaneously induced replication stress and mutations linked to dynamic sequence frequency may limit lifespan by limiting genome stability.

Indexed as

Prostatic NeoplasmsAdultAgedAnimalsHumansLongevityMaleMammalsMiddle AgedMutationReceptors, Cell SurfaceReceptors, Cell Surfacecruciformendogenous mutagenesisG-Quadruplexi-motiflifespanTriplex

Identifiers

PMID38670588
PMCPMC11059594
OpenAlexW4395684742

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.