Evidence map›Paper›PMID 36292613›Full record

ArticleGenes2022

Targeted Anti-Mitochondrial Therapy: The Future of Oncology.

Farzad Taghizadeh-Hesary, Hassan Akbari, Moslem Bahadori, Babak Behnam

Abstract read
In one paragraph

Article in Genes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed.

  1. Trial
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  4. Mitochondrial Metabolism and Dynamics in Cancer Cells.Cancer treatment and research · 2026
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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.

Farzad Taghizadeh-HesaryENT and Head and Neck Research Center and Department, The Five Senses Health Institute, School of Medicine, Iran University of Medical Sciences, Tehran 1445613131, Iran.ORCID 0000-0002-6195-2203
Hassan AkbariDepartment of Pathology, Shahid Beheshti University of Medical Sciences, Tehran P.O. Box 4739-19395, Iran.
Moslem BahadoriFaculty of Medicine, Tehran University of Medical Sciences, Tehran P.O. Box 14155-6559, Iran.
Babak BehnamDepartment of Regulatory Affairs, Amarex Clinical Research, Germantown, MD 20874, USA.ORCID 0000-0002-1266-1602

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Like living organisms, cancer cells require energy to survive and interact with their environment. Mitochondria are the main organelles for energy production and cellular metabolism. Recently, investigators demonstrated that cancer cells can hijack mitochondria from immune cells. This behavior sheds light on a pivotal piece in the cancer puzzle, the dependence on the normal cells. This article illustrates the benefits of new functional mitochondria for cancer cells that urge them to hijack mitochondria. It describes how functional mitochondria help cancer cells' survival in the harsh tumor microenvironment, immune evasion, progression, and treatment resistance. Recent evidence has put forward the pivotal role of mitochondria in the metabolism of cancer stem cells (CSCs), the tumor components responsible for cancer recurrence and metastasis. This theory highlights the mitochondria in cancer biology and explains how targeting mitochondria may improve oncological outcomes.

Indexed as

MitochondriaNeoplasmsHumansNeoplastic Stem CellsTumor MicroenvironmentATPcancer cellcancer stem cellcancer treatmentmitochondriaT cell

Identifiers

PMID36292613
PMCPMC9602426

What OpenQuestion holds

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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.