Cervical carcinoma is the most prevalent gynecology malignant tumor and ranks as the fourth most common cancer worldwide, thus posing a significant threat to the lives and health of women. Advanced and early-stage cervical carcinoma patients with high-risk factors require adjuvant treatment following surgery, with radiotherapy being the primary approach. However, the tolerance of cervical cancer to radiotherapy has become a major obstacle in its treatment. Recent studies have demonstrated that radiation resistance in cervical cancer is closely associated with DNA damage repair pathways, the tumor microenvironment, tumor stem cells, hypoxia, cell cycle arrest, and epigenetic mechanisms, among other factors. The development of tumor radiation resistance involves complex interactions between multiple genes, pathways, and mechanisms, wherein each factor interacts through one or more signaling pathways. This paper provides an overview of research progress on an understanding of the mechanism underlying radiation resistance in cervical cancer.
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http://dx.doi.org/10.3389/fonc.2024.1380448 | DOI Listing |
J Thorac Oncol
January 2025
Division of Medical Oncology, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, Republic of Korea. Electronic address:
Introduction: Treatment options for patients with epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer (NSCLC) with disease progression on/after osimertinib and platinum-based chemotherapy are limited.
Methods: CHRYSALIS-2 Cohort A evaluated amivantamab+lazertinib in patients with EGFR exon 19 deletion- or L858R-mutated NSCLC with disease progression on/after osimertinib and platinum-based chemotherapy. Primary endpoint was investigator-assessed objective response rate (ORR).
EMBO J
January 2025
Department of Oncology, The University of Oxford, Oxford, OX3 7DQ, UK.
Hypoxia is a common feature of solid tumors that has previously been linked to resistance to radiotherapy and chemotherapy, and more recently to immunotherapy. In particular, hypoxic tumors exclude T cells and inhibit their activity, suggesting that tumor cells acquire a mechanism to evade T-cell recognition and killing. Our analysis of hypoxic tumors indicates that hypoxia downregulates the expression of MHC class I and its bound peptides (i.
View Article and Find Full Text PDFCell Death Discov
January 2025
Department of Radiation Oncology, China-Japan Union Hospital of Jilin University, Changchun, China.
Cervical cancer (CC) is becoming a major health issue globally, and radiotherapy plays a crucial role in its treatment. However, the prognosis of some patients remains poor due to tumor resistance to the therapy. This study aimed to explore whether vitamin D could confer a more radiosensitive phenotype in CC based on our previous findings and detection using the database.
View Article and Find Full Text PDFPLoS One
January 2025
Division of Cell- and Neurobiology, Department of Biomedical and Clinical Sciences, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
Emerging evidence suggests that fusion of cancer cells with leucocytes, such as macrophages, plays a significant role in cancer metastasis and results in tumor hybrid cells that acquire resistance to chemo- and radiation therapy. However, the precise mechanisms behind the leukocyte-cancer cell fusion remain unclear. The present in vitro study explores the presence of fusion between the monocyte cell line (THP-1) and the breast cancer cell line (MCF-7) in relation to the expression of CD36 and phosphatidylserine with and without treatment of these cells with ionizing radiation.
View Article and Find Full Text PDFSci Adv
January 2025
Key Laboratory of Automobile Materials (Jilin University), Ministry of Education, Department of Materials Science and Engineering, Jilin University, Changchun 130022, China.
Vacancies are crucial for the radiation resistance, strength, and ductility of high-entropy alloys (HEAs). However, complex electronic interactions resulting from chemical disorder prohibit the quantification of vacancy formation energy () and migration barriers (). Herein, we propose an electronic descriptor χ (electronegativity χ and valence-electron number ) to quantify the bonding strength of constituents on the basis of the tight-binding model, which allows us to build analytical models to achieve the site-to-site quantification of and .
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