ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012
Molecular pathways: involving microenvironment damage responses in cancer therapy resistance.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 72 citations in OpenAlex.
- A new perspective on prostate cancer treatment: the interplay between cellular senescence and treatment resistance.Frontiers in immunology · 2024Review
- Effect of Proton Therapy on Tumor Cell Killing and Immune Microenvironment for Hepatocellular Carcinoma.Cells · 2023Article
- Combination treatment with hENT1 and miR-143 reverses gemcitabine resistance in triple-negative breast cancer.Cancer cell international · 2022Article
- A positive feedback loop: RAD18-YAP-TGF-β between triple-negative breast cancer and macrophages regulates cancer stemness and progression.Cell death discovery · 2022Article
- Role of Base Excision Repair in Innate Immune Cells and Its Relevance for Cancer Therapy.Biomedicines · 2022Review
- Immune cells regulate matrix metalloproteinases to reshape the tumor microenvironment to affect the invasion, migration, and metastasis of pancreatic cancer.American journal of translational research · 2022Article
- SOX1 Is a Backup Gene for Brain Neurons and Glioma Stem Cell Protection and Proliferation.Molecular neurobiology · 2021Review
- Effect of 1α,25-Dihydroxyvitamin D3 on the Radiation Response in Prostate Cancer: Association With IL-6 Signaling.Frontiers in oncology · 2021Article
- EB virus-induced ATR activation accelerates nasopharyngeal carcinoma growth via M2-type macrophages polarization.Cell death & disease · 2020Article
- Correlation of APE1 with VEGFA and CD163Oncology letters · 2020Article
- Biomarkers in the path from cellular senescence to frailty.Experimental gerontology · 2020Review
- Tissue specificity of DNA damage response and tumorigenesis.Cancer biology & medicine · 2019Article
- A Transient Pseudosenescent Secretome Promotes Tumor Growth after Antiangiogenic Therapy Withdrawal.Cell reports · 2018Article
- Tumor-Independent Host Secretomes Induced By Angiogenesis and Immune-Checkpoint Inhibitors.Molecular cancer therapeutics · 2018Article
- The senescence-associated secretory phenotype is potentiated by feedforward regulatory mechanisms involving Zscan4 and TAK1.Nature communications · 2018Article
- DNA Damage Induces a Secretory Program in the Quiescent TME that Fosters Adverse Cancer Phenotypes.Molecular cancer research : MCR · 2017Article
- Curcumin-Free Turmeric Exhibits Activity against Human HCT-116 Colon Tumor Xenograft: Comparison with Curcumin and Whole Turmeric.Frontiers in pharmacology · 2017Article
- Article
- Inhibition of STAT3 enhances the radiosensitizing effect of temozolomide in glioblastoma cells in vitro and in vivo.Journal of neuro-oncology · 2016Article
- SFRP2 augments WNT16B signaling to promote therapeutic resistance in the damaged tumor microenvironment.Oncogene · 2016Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The armamentarium of therapeutics used to treat cancer patients relies heavily on ionizing radiation and chemotherapeutic drugs that severely damage DNA. Tumor cells' responses to such treatments are heavily influenced by their environment: Physical contacts with structural elements such as the extracellular matrix, associations with resident and transitory benign cells such as fibroblasts and leukocytes, and interactions with numerous soluble endocrine and paracrine-acting factors all modulate tumor-cell behavior. Of importance, this complex tumor microenvironment is not static and dynamically responds to a variety of stimuli. Here, we describe emerging data indicating that genotoxic cancer treatments activate highly conserved damage response programs in benign constituents of the tumor microenvironment. These damage signals, transmitted via master regulators such as NF-κB, culminate in a powerful and diverse secretory program that generates a proangiogenic, proinflammatory microenvironment. Constituents of this program include interleukin (IL)-6, IL-8, hepatocyte growth factor, amphiregulin, matrix metalloproteinases, and other factors that have been shown to promote adverse tumor-cell phenotypes, such as enhanced resistance to treatment and rapid tumor repopulation. A detailed understanding of these survival signals induced in the context of genotoxic stress provides a platform for developing combinatorial treatment strategies that take into account malignant cells, the tumor microenvironment, and the dynamics exerted by the treatment itself.
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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.