ReviewApoptosis : an international journal on programmed cell death2026
Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.
Review in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Inhibition of PGC1β-dependent mitochondrial biogenesis enhances EGFR-targeted therapy in lung cancer.EMBO molecular medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial transcription factor A (TFAM) is indispensable for mitochondrial DNA (mtDNA) maintenance and transcription, governing cellular bioenergetics. Despite its known physiological importance, TFAM plays a complex and often paradoxical role in cancer biology. This study integrates pan-cancer bioinformatics analyses with experimental evidence to comprehensively elucidate TFAM's multifaceted impact on tumorigenesis. We systematically investigated the heterogeneity of TFAM across diverse cancer types, specifically focusing on its regulatory mechanisms in metabolic reprogramming, signal transduction, and immune microenvironment remodeling. Our analysis reveals that TFAM functions as a critical node connecting mitochondrial integrity to tumor progression, balancing tumor-promoting and tumor-suppressive roles depending on the context. Finally, we discuss the challenges of targeting TFAM, such as off-target toxicity, and highlight emerging precision oncology strategies, including mitochondria-targeted delivery systems, that aim to exploit these mitochondrial vulnerabilities.
Indexed as
Identifiers
What Socratic 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 Socratic graph.