ReviewThoracic cancer2018
Therapeutic targeting of cellular stress responses in cancer.
Review in Thoracic cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 59 citations in OpenAlex.
- Chronic stress and myeloid immunosuppression in cancer: A neuroimmune link to behavioral dysfunction.Brain, behavior, & immunity - health · 2026Review
- Learning from plants: is it possible to make an animal organism a non-host for cancer?Frontiers in oncology · 2026Article
- Therapeutic Potential of Sodium Selenite Application for Promoting Radioactive Iodine Avidity in Papillary Thyroid Cancer.Bioinorganic chemistry and applications · 2026Article
- eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by small molecules.Cell reports · 2025Article
- eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by novel small molecules.bioRxiv : the preprint server for biology · 2025Article
- Cancer stem cell populations are resistant to 5-aminolevulinic acid-photodynamic therapy (5-ALA-PDT).Scientific reports · 2025Article
- A systems biology approach to unveil shared therapeutic targets and pathological pathways across major human cancers.Computational and structural biotechnology journal · 2025Article
- AGR2 knockdown induces ER stress and mitochondria fission to facilitate pancreatic cancer cell death.Biochimica et biophysica acta. Molecular cell research · 2025Article
- WTAP and mCellular and molecular life sciences : CMLS · 2024Article
- OGA mutant aberrantly hydrolyzes O-GlcNAc modification from PDLIM7 to modulate p53 and cytoskeleton in promoting cancer cell malignancy.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mapping the tumor stress network reveals dynamic shifts in the stromal oxidative stress response.Cell reports · 2024Article
- HSF1 at the crossroads of chemoresistance: from current insights to future horizons in cell death mechanisms.Frontiers in cell and developmental biology · 2024Review
- Multikinase inhibitors modulate non-constitutive proteasome expression in colorectal cancer cells.Frontiers in molecular biosciences · 2024Article
- HSP110 Inhibition in Primary Effusion Lymphoma Cells: One Molecule, Many Pro-Survival Targets.Cancers · 2023Article
- Cell-Type-Specific Signalling Networks Impacted by Prostate Epithelial-Stromal Intercellular Communication.Cancers · 2023Article
- Doxorubicin-sensitive and -resistant colorectal cancer spheroid models: assessing tumor microenvironment features for therapeutic modulation.Frontiers in cell and developmental biology · 2023Article
- Current research status of tumor cell biomarker detection.Microsystems & nanoengineering · 2023Review
- Molecular relation between biological stress and carcinogenesis.Molecular biology reports · 2022Review
- Cytosolic Hsp90 Isoform-Specific Functions and Clinical Significance.Biomolecules · 2022Review
- The Role of HDACs in the Response of Cancer Cells to Cellular Stress and the Potential for Therapeutic Intervention.International journal of molecular sciences · 2022Review
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
No grant is acknowledged in the PubMed record.
Abstract
Similar to bacteria, yeast, and other organisms that have evolved pathways to respond to environmental stresses, cancer cells develop mechanisms that increase genetic diversity to facilitate adaptation to a variety of stressful conditions, including hypoxia, nutrient deprivation, exposure to DNA-damaging agents, and immune responses. To survive, cancer cells trigger mechanisms that drive genomic instability and mutation, alter gene expression programs, and reprogram the metabolic pathways to evade growth inhibition signaling and immune surveillance. A deeper understanding of the molecular mechanisms that underlie the pathways used by cancer cells to overcome stresses will allow us to develop more efficacious strategies for cancer therapy. Herein, we overview several key stresses imposed on cancer cells, including oxidative, metabolic, mechanical, and genotoxic, and discuss the mechanisms that drive cancer cell responses. The therapeutic implications of these responses are also considered, as these factors pave the way for the targeting of stress adaption pathways in order to slow cancer progression and block resistance to therapy.
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.