ReviewSeminars in cancer biology2019
Metabolic and epigenetic reprogramming in the arsenic-induced cancer stem cells.
Review in Seminars in cancer biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Comorbidity of hypertension and lung cancer: interplay of genetics and environment.Discover oncology · 2025Review
- Chronic arsenic exposure-provoked biotoxicity involved in liver-microbiota-gut axis disruption in chickens based on multi-omics technologies.Journal of advanced research · 2025Article
- Metabolic reprogramming and therapeutic targeting in non-small cell lung cancer: emerging insights beyond the Warburg effect.Frontiers in oncology · 2025Review
- Arsenic disrupts H3K9me3 and H3K27me3 balance by biasing PRC2.1 and PRC2.2 activity via PALI1 inhibition in carcinogenesis.International journal of biological sciences · 2025Article
- Multiple roles of arsenic compounds in phase separation and membraneless organelles formation determine their therapeutic efficacy in tumors.Journal of pharmaceutical analysis · 2024Review
- Mechanistic understanding of the toxic effects of arsenic and warfare arsenicals on human health and environment.Cell biology and toxicology · 2023Review
- Disruption of the tumor suppressor-like activity of aryl hydrocarbon receptor by arsenic in epithelial cells and human lung cancer.International journal of biological sciences · 2023Article
- Profiling of histone H3 trimethylation and distinct epigenetic pattern of chromosome Y in the transformed bronchial epithelial cells induced by consecutive arsenic treatment.Genes & diseases · 2022Article
- Arsenic Exposure through Dietary Intake and Associated Health Hazards in the Middle East.Nutrients · 2022Review
- Arsenic Activates the ER Stress-Associated Unfolded Protein Response via the Activating Transcription Factor 6 in Human Bronchial Epithelial Cells.Biomedicines · 2022Article
- Article
- Abnormal lipid synthesis as a therapeutic target for cancer stem cells.World journal of stem cells · 2022Review
- Metabolomic dynamics of the arsenic-transformed bronchial epithelial cells and the derived cancer stem-like cells.International journal of biological sciences · 2022Article
- Fbw7 Inhibits the Progression of Activated B-Cell Like Diffuse Large B-Cell Lymphoma by Targeting the Positive Feedback Loop of the LDHA/lactate/miR-223 Axis.Frontiers in oncology · 2022Article
- Arsenic exposure increases susceptibility toAmerican journal of translational research · 2022Article
- New Discoveries and Ambiguities of Nrf2 and ATF3 Signaling in Environmental Arsenic-Induced Carcinogenesis.Antioxidants (Basel, Switzerland) · 2021Review
- Mechanisms of the synergistic lung tumorigenic effect of arsenic and benzo(a)pyrene combined- exposure.Seminars in cancer biology · 2021Review
- Connections between endoplasmic reticulum stress-associated unfolded protein response, mitochondria, and autophagy in arsenic-induced carcinogenesis.Seminars in cancer biology · 2021Review
- Cooperation between NRF2-mediated transcription and MDIG-dependent epigenetic modifications in arsenic-induced carcinogenesis and cancer stem cells.Seminars in cancer biology · 2021Review
- p62 functions as a signal hub in metal carcinogenesis.Seminars in cancer biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
At present, the belief that genetic mutations control every aspect of tumorigenesis is still very popular. Even for the highly debated "bad luck" theory of cancers, it ascertained that random mutation of genes during the self-renewal of somatic stem cells is responsible for cancer initiation. Logically, most of the new therapeutic strategies so far, from molecular targeting to precision medicine or personalized medicine, are genome-obsessed and focused on identifying and targeting these mutated genes. Accordingly, a rather simplified therapeutic regimen was formulated: cancers with the same mutations, e.g., lung cancer, pancreatic cancer, breast cancer, ovarian cancer, etc, were managed with the same chemo or targeting medicine, whereas for a particular cancer, such as breast cancer or lung cancer, with different mutational spectrums was treated with different, so-called personalized medicine. The outcomes of this strategy, however, are mixed with encouraging and disappointing findings. In this review article, we will address the importance of non-genetic factors, the metabolic and epigenetic reprogramming, during the induction of cancer stem cells in response to arsenic, a major environmental human carcinogen. The information provided may not only advance our understanding of carcinogenic mechanism to a new level but also help in designing new strategies through targeting the metabolic and epigenetic signaling pathways for cancer therapy.
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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.