Evidence map›Paper›PMID 34298989›Full record

ReviewInternational journal of molecular sciences2021

Mitochondrial Heteroplasmy Shifting as a Potential Biomarker of Cancer Progression.

Carlos Jhovani Pérez-Amado, Amellalli Bazan-Cordoba, Alfredo Hidalgo-Miranda, Silvia Jiménez-Morales

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

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  7. The Multifaceted Role of Mitochondria in Angiogenesis.International journal of molecular sciences · 2025
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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

4 authors.

Carlos Jhovani Pérez-AmadoLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Mexico City 14610, Mexico.ORCID 0000-0002-7594-9224
Amellalli Bazan-CordobaLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Mexico City 14610, Mexico.
Alfredo Hidalgo-MirandaLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Mexico City 14610, Mexico.ORCID 0000-0003-2315-3977
Silvia Jiménez-MoralesLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Mexico City 14610, Mexico.ORCID 0000-0002-6590-9712

Funding

Instituto Nacional de Medicina Genómica 24/2016/I
6 · The paper itself

Abstract

Cancer is a serious health problem with a high mortality rate worldwide. Given the relevance of mitochondria in numerous physiological and pathological mechanisms, such as adenosine triphosphate (ATP) synthesis, apoptosis, metabolism, cancer progression and drug resistance, mitochondrial genome (mtDNA) analysis has become of great interest in the study of human diseases, including cancer. To date, a high number of variants and mutations have been identified in different types of tumors, which coexist with normal alleles, a phenomenon named heteroplasmy. This mechanism is considered an intermediate state between the fixation or elimination of the acquired mutations. It is suggested that mutations, which confer adaptive advantages to tumor growth and invasion, are enriched in malignant cells. Notably, many recent studies have reported a heteroplasmy-shifting phenomenon as a potential shaper in tumor progression and treatment response, and we suggest that each cancer type also has a unique mitochondrial heteroplasmy-shifting profile. So far, a plethora of data evidencing correlations among heteroplasmy and cancer-related phenotypes are available, but still, not authentic demonstrations, and whether the heteroplasmy or the variation in mtDNA copy number (mtCNV) in cancer are cause or consequence remained unknown. Further studies are needed to support these findings and decipher their clinical implications and impact in the field of drug discovery aimed at treating human cancer.

Indexed as

AllelesBiomarkersDisease ProgressionDNA Restriction EnzymesEpigenesis, GeneticGenetic TherapyHeteroplasmyHumansMitochondriaNeoplasmsTumor MicroenvironmentBiomarkersDNA Restriction Enzymescancerheteroplasmyheteroplasmy shiftingmitochondrial DNAmitochondrial mutations

Identifiers

PMID34298989
PMCPMC8304746

What OpenQuestion holds

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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.