Evidence map›Paper›PMID 37397663›Full record

ArticleCureus2023

Mitochondrial Deoxyribonucleic Acid (mtDNA), Maternal Inheritance, and Their Role in the Development of Cancers: A Scoping Review.

Sabitha Vadakedath, Venkataramana Kandi, Jayashankar Ca, Swapna Vijayan, Kushal C Achyut, Shivani Uppuluri, Praveen Kumar K Reddy, Monish Ramesh, P Pavan Kumar

Abstract readScoping Review
In one paragraph

Article in Cureus, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Review
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  4. Review
  5. Review
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  7. 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

9 authors.

Sabitha VadakedathBiochemistry, Prathima Institute of Medical Sciences, Karimnagar, IND.
Venkataramana KandiClinical Microbiology, Prathima Institute of Medical Sciences, Karimnagar, IND.
Jayashankar CaInternal Medicine, Vydehi Institute of Medical Sciences and Research Centre, Bengaluru, IND.
Swapna VijayanPediatrics, Sir CV Raman General Hospital, Bengaluru, IND.
Kushal C AchyutInternal Medicine, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, IND.
Shivani UppuluriInternal Medicine, Vydehi Institute of Medical Sciences and Research Centre, Bengaluru, IND.
Praveen Kumar K ReddyGeneral Medicine, Vydehi Institute of Medical Sciences and Research Centre, Bengaluru, IND.
Monish RameshInternal Medicine, Vydehi Institute of Medical Sciences and Research Centre, Bengaluru, IND.
P Pavan KumarGeneral Medicine, Vydehi Institute of Medical Sciences and Research Centre, Bengaluru, IND.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial DNA (mtDNA) is a small, circular, double-stranded DNA inherited from the mother during fertilization. Evolutionary evidence supported by the endosymbiotic theory identifies mitochondria as an organelle that could have descended from prokaryotes. This may be the reason for the independent function and inheritance pattern shown by mtDNA. The unstable nature of mtDNA due to the lack of protective histones, and effective repair systems make it more vulnerable to mutations. The mtDNA and its mutations could be maternally inherited thereby predisposing the offspring to various cancers like breast and ovarian cancers among others. Although mitochondria are considered heteroplasmic wherein variations among the multiple mtDNA genomes are noticed, mothers can have mitochondrial populations that are homoplasmic for a given mitochondrial mutation. Homoplasmic mitochondrial mutations may be transmitted to all maternal offspring. However, due to the complex interplay between the mitochondrial and nuclear genomes, it is often difficult to predict disease outcomes, even with homoplasmic mitochondrial populations. Heteroplasmic mtDNA mutations can be maternally inherited, but the proportion of mutated alleles differs markedly between offspring within one generation. This led to the genetic bottleneck hypothesis, explaining the rapid changes in allele frequency witnessed during the transmission of mtDNA from one generation to the next. Although a physical reduction in mtDNA has been demonstrated in several species, a comprehensive understanding of the molecular mechanisms is yet to be demonstrated. Despite initially thought to be limited to the germline, there is evidence that blockages exist in different cell types during development, perhaps explaining why different tissues in the same organism contain different levels of mutated mtDNA. In this review, we comprehensively discuss the potential mechanisms through which mtDNA undergoes mutations and the maternal mode of transmission that contributes to the development of tumors, especially breast and ovarian cancers.

Indexed as

cancerendosymbiotic theoryinheritancemitochondrial dnamtdna

Identifiers

PMID37397663
PMCPMC10314188

What Socratic holds

Textmetadata
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 Socratic graph.