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Nrf2 is a transcription factor that stimulates the expression of genes which have antioxidant response element-like sequences in their promoter. Nrf2 is a cellular protector, and this principle applies to both normal cells and malignant cells. While healthy cells are protected from DNA damage induced by reactive oxygen species, malignant cells are defended against chemo- or radiotherapy. Through our literature search, we found that Nrf2 activates several oncogenes unrelated to the antioxidant activity, such as Matrix metallopeptidase 9 (), B-cell lymphoma 2 (), B-cell lymphoma-extra large (), Tumour Necrosis Factor (), and Vascular endothelial growth factor A (). We also did a brief analysis of The Cancer Genome Atlas (TCGA) data of lung adenocarcinoma concerning the effects of radiation therapy and found that the therapy-induced Nrf2 activation is not universal. For instance, in the case of recurrent disease and radiotherapy, we observed that, for the majority of Nrf2-targeted genes, there is no change in expression level. This proves that the universal, axiomatic rationale that Nrf2 is activated as a response to chemo- and radiation therapy is wrong, and that each scenario should be carefully evaluated with the help of Nrf2-targeted genes. Moreover, there were nine genes involved in lipid peroxidation, which showed underexpression in the case of new radiation therapy: , , , , , , , , and . This may relate to the fact that, while some studies reported the co-activation of Nrf2 and other oncogenic signaling pathways such as Phosphoinositide 3-kinases (), mitogen-activated protein kinase (), and Notch1, other reported the inverse correlation between Nrf2 and the tumor-promoter Transcription Factor (TF), Nuclear factor kappa-light-chain-enhancer of activated B cells (). Lastly, Nrf2 establishes its activity through interactions at multiple levels with various microRNAs. MiR-155, miR-144, miR-28, miR-365-1, miR-93, miR-153, miR-27a, miR-142, miR-29-b1, miR-340, and miR-34a, either through direct repression of Nrf2 messenger RNA (mRNA) in a Kelch-like ECH-associated protein 1 (Keap1)-independent manner or by enhancing the Keap1 cellular level, inhibit the Nrf2 activity. Keap1-Nrf2 interaction leads to the repression of miR-181c, which is involved in the Nuclear factor kappa light chain enhancer of activated B cells (NF-κB) signaling pathway. Nrf2's role in cancer prevention, diagnosis, prognosis, and therapy is still in its infancy, and the future strategic planning of Nrf2-based oncological approaches should also consider the complex interaction between Nrf2 and its various activators and inhibitors.
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http://dx.doi.org/10.3390/cancers11111755 | DOI Listing |
J Appl Clin Med Phys
December 2024
Department of Radiotherapy, University Medical Center Utrecht, Utrecht, Netherlands.
Background: For the development and validation of dynamic treatment modalities and processes on the MR-linac, independent measurements should be performed that validate dose delivery and linac behavior at a high temporal resolution. To achieve this, a detector with both high temporal and spatial resolution is necessary.
Purpose: This study investigates the suitability of a Delta4 Phantom+ MR (Delta4) detector array for time-resolved dosimetry in the 1.
Phys Imaging Radiat Oncol
October 2024
Amsterdam UMC location Vrije Universiteit Amsterdam, Department of Radiation Oncology, De Boelelaan 1117, Amsterdam, the Netherlands.
Background And Purpose: Segmentation imperfections (noise) in radiotherapy organ-at-risk segmentation naturally arise from specialist experience and image quality. Using clinical contours can result in sub-optimal convolutional neural network (CNN) training and performance, but manual curation is costly. We address the impact of simulated and clinical segmentation noise on CNN parotid gland (PG) segmentation performance and provide proof-of-concept for an easily implemented auto-curation countermeasure.
View Article and Find Full Text PDFWorld J Clin Oncol
December 2024
Department of Pathology, Peking University People's Hospital, Beijing 100044, China.
Background: Primary squamous cell carcinoma (SCC) of the middle ear is rare, with non-keratinizing basaloid types being exceptionally uncommon. Distinguishing these cancers, often caused by viral factors (, human papillomavirus or Epstein-Barr virus), or specific genetic alterations (, bromodomain-containing protein 4-nuclear protein in or gene fused with FLI chromosomal rearrangement), from other cranial conditions, is difficult. The recently identified DEK::AFF2 non-keratinizing SCC (NKSCC) is a novel subtype, fitting the World Health Organization classification of head and neck neoplasms.
View Article and Find Full Text PDFWorld J Clin Oncol
December 2024
Oncology Operative Unit, Hospital of Frattamaggiore, ASL Napoli 2 Nord, Naples 80027, Italy.
Background: Squamous cell carcinoma of the head and neck (SCCHN) accounts for 3% of all malignant tumors in Italy. Immune checkpoint inhibitors combined with chemotherapy is first-line treatment for SCCHN; however, second-line treatment options are limited. Taxanes are widely used for combination therapy of SCCHN, as clinical trials have shown their efficacy in patients with this disease, particularly in patients with prior therapy.
View Article and Find Full Text PDFFront Oncol
December 2024
Radiotherapy Department, Montpellier Regional Cancer Institute, Montpellier, France.
Introduction: Following a preliminary work validating the technological feasibility of an adaptive workflow with Ethos for whole-breast cancer, this study aims to clinically evaluate the automatic segmentation generated by Ethos.
Material And Methods: Twenty patients initially treated on a TrueBeam accelerator for different breast cancer indications (right/left, lumpectomy/mastectomy) were replanned using the Ethos emulator. The adaptive workflow was performed using 5 randomly selected extended CBCTs per patient.
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