ReviewBiochimica et biophysica acta2012
The awakening of an advanced malignant cancer: an insult to the mitochondrial genome.
Review in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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.
Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Busulfan resistance in AML is associated with changes in mitochondrial copy number and lipid metabolism.Scientific reports · 2026Article
- Combinatorial therapy regimens targeting preclinical models of melanoma resistant to immune checkpoint blockade.The Journal of clinical investigation · 2025Article
- DNAJA3/Tid1 Is Required for Mitochondrial DNA Maintenance and Regulates Migration and Invasion of Human Gastric Cancer Cells.Cancers · 2020Article
- Review
- Role of the mitochondrial stress response in human cancer progression.Experimental biology and medicine (Maywood, N.J.) · 2020Review
- Metabolic Plasticity in Chemotherapy Resistance.Frontiers in oncology · 2020Review
- Mitochondrial DNA content in breast cancer: Impact on in vitro and in vivo phenotype and patient prognosis.Oncotarget · 2016Article
- Article
- Altered regulation of PDK4 expression promotes antiestrogen resistance in human breast cancer cells.SpringerPlus · 2015Article
- Putative role of adipose tissue in growth and metabolism of colon cancer cells.Frontiers in oncology · 2014Review
- Inheritance of the fittest mitochondria in yeast.Trends in cell biology · 2014Review
- When numbers matters: mitochondrial DNA and gliomagenesis.Cell death and differentiation · 2013Article
- Association of decreased mitochondrial DNA content with the progression of colorectal cancer.BMC cancer · 2013Article
- Secreted human adipose leptin decreases mitochondrial respiration in HCT116 colon cancer cells.PloS one · 2013Article
- RecQL4 cytoplasmic localization: implications in mitochondrial DNA oxidative damage repair.The international journal of biochemistry & cell biology · 2012Article
- Roles of Mitochondrial DNA Changes on Cancer Initiation and Progression.Cell biology : research & therapy · 2012Article
- Dynamin-related protein 1 heterozygote knockout mice do not have synaptic and mitochondrial deficiencies.Biochimica et biophysica acta · 2012Article
- Abnormal mitochondrial dynamics and synaptic degeneration as early events in Alzheimer's disease: implications to mitochondria-targeted antioxidant therapeutics.Biochimica et biophysica acta · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIn only months-to-years a primary cancer can progress to an advanced phenotype that is metastatic and resistant to clinical treatments. As early as the 1900s, it was discovered that the progression of a cancer to the advanced phenotype is often associated with a shift in the metabolic profile of the disease from a state of respiration to anaerobic fermentation - a phenomenon denoted as the Warburg Effect. SCOPE OF REVIEW: Reports in the literature strongly suggest that the Warburg Effect is generated as a response to a loss in the integrity of the sequence and/or copy number of the mitochondrial genome content within a cancer. MAJOR
conclusionsMultiple studies regarding the progression of cancer indicate that mutation, and/or, a flux in the copy number, of the mitochondrial genome content can support the early development of a cancer, until; the mutational load and/or the reduction-to-depletion of the copy number of the mitochondrial genome content induces the progression of the disease to an advanced phenotype. GENERAL SIGNIFICANCE: Collectively, evidence has revealed that the human cell has incorporated the mitochondrial genome content into a cellular mechanism that, when pathologically actuated, can de(un)differentiate a cancer from the parental tissue of origin into an autonomous disease that disrupts the hierarchical structure-and-function of the human body. This article is part of a Special Issue entitled: Biochemistry of Mitochondria.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.