Evidence map›Paper›PMID 24140413›Full record

ReviewBiochimica et biophysica acta2013

Mitochondrial DNA mutations and breast tumorigenesis.

Neelu Yadav, Dhyan Chandra

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

55 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. The Genomic and Biologic Landscapes of Breast Cancer and Racial Differences.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Omics-Based Investigations of Breast Cancer.Molecules (Basel, Switzerland) · 2023
    Review
  10. Analysis of Mitochondrial Transfer RNA Mutations in Breast Cancer.Balkan journal of medical genetics : BJMG · 2023
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. PeerJ · 2022
    Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Neelu YadavDepartment of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.
Dhyan Chandra
Roswell Park Comprehensive Cancer Center · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI Dean G. Tang · 1985 to 2026
$116.6M
Hsp60 regulation of apoptosis in prostate cancerR01CA160685 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI CHANDRA, DHYAN · 2013 to 2018
$1.1M
Novel Insight on Nucleotide Regulation of Apoptosome ActivationK01CA123142 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI CHANDRA, DHYAN · 2007 to 2010
$588k
NCI NIH HHS K01 CA123142NCI NIH HHS K01CA123142NCI NIH HHS P30 CA016056NCI NIH HHS R01 CA160685NCI NIH HHS R01CA160685
6 · The paper itself

Abstract

Breast cancer is a heterogeneous disease and genetic factors play an important role in its genesis. Although mutations in tumor suppressors and oncogenes encoded by the nuclear genome are known to play a critical role in breast tumorigenesis, the contribution of the mitochondrial genome to this process is unclear. Like the nuclear genome, the mitochondrial genome also encodes proteins critical for mitochondrion functions such as oxidative phosphorylation (OXPHOS), which is known to be defective in cancer including breast cancer. Mitochondrial DNA (mtDNA) is more susceptible to mutations due to limited repair mechanisms compared to nuclear DNA (nDNA). Thus changes in mitochondrial genes could also contribute to the development of breast cancer. In this review we discuss mtDNA mutations that affect OXPHOS. Continuous acquisition of mtDNA mutations and selection of advantageous mutations ultimately leads to generation of cells that propagate uncontrollably to form tumors. Since irreversible damage to OXPHOS leads to a shift in energy metabolism towards enhanced aerobic glycolysis in most cancers, mutations in mtDNA represent an early event during breast tumorigenesis, and thus may serve as potential biomarkers for early detection and prognosis of breast cancer. Because mtDNA mutations lead to defective OXPHOS, development of agents that target OXPHOS will provide specificity for preventative and therapeutic agents against breast cancer with minimal toxicity.

Indexed as

Oxidative PhosphorylationAnimalsBreast NeoplasmsCell Transformation, NeoplasticDNA, MitochondrialFemaleHumansMutationDNA, MitochondrialBreast cancerHomoplasmy and heteroplasmyMitochondrial DNAmtDNA mutationsOXPHOSWarburg effect

Identifiers

PMID24140413
PMCPMC3891589
OpenAlexW2014569996

What OpenQuestion holds

Textmetadata
LicenceTDM
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.