Female, young adult, Wistar rats were given a single inhalation exposure to a submicron sized aerosol of high-fired 239PuO2 and observed during their lifespan for primary lung tumours. Rats were distributed among sham-control (n = 1052) and exposed (n = 2105) groups. Survival was significantly reduced only in rats with lung doses > 30 Gy. A total of 99 primary lung tumours were found, of which 92% were malignant and 80% were carcinomas. Of malignant lung tumours, 49 were squamous cell carcinoma, 23 adenocarcinoma, nine hemangiosarcoma, seven adenosquamous carcinoma, and three fibrosarcoma. One adenocarcinoma was found in controls and only four adenomas were seen in the exposed rat at lung doses < 1.5 Gy. The lowest doses at which lung tumours appeared in exposed rats were 1.5 Gy for squamous cell carcinoma, 3.1 Gy for adenocarcinoma. 4.1 Gy for hemangiosarcoma, and about 9 Gy for adenosquamous carcinoma and fibrosarcoma. Pulmonary squamous metaplasia was not seen in controls and was first seen in exposed rats only at lung doses > 1 Gy. Primary lung tumours were the presumed cause of death (fatal) in 60% of rats with malignant lung tumours; causes of death were equally distributed among all tumour types and doses. The incidence of all lung tumours was 0.095% in control rats, 0.21% in 1877 rats with lung doses < 1 Gy, and 41% in 228 rats with doses > 1 Gy. Lung tumour incidence increased in a linear manner from 6.9% at 2.3 Gy to an incidence of 64-88% at 16-44 Gy. Absolute malignant lung tumour risk averaged 270 lung tumours per 10(4) rat-Gy above a lung dose of 1 Gy. All types of malignant lung tumours induced by inhaled 239PuO2 exhibited a threshold at a lung dose > 1 Gy.
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http://dx.doi.org/10.1080/09553009314551601 | DOI Listing |
Expert Rev Respir Med
January 2025
Division of Pulmonary & Critical Care Medicine, Mayo Clinic, Rochester MN, USA.
Introduction: Amyloidosis, a polymeric deposition disease classified according to protein subtype, may have varied pulmonary manifestations. Its anatomic-radiologic phenotypes include nodular, cystic, alveolar-septal, and tracheobronchial forms. Clinical presentation may range from asymptomatic parenchymal nodules to respiratory failure from diffuse parenchymal infiltration or diaphragmatic deposition.
View Article and Find Full Text PDFTechnol Cancer Res Treat
January 2025
Department of Radiation Oncology, Cancer Hospital of Shantou University Medical College, Shantou, Guangdong, PR China.
Purpose: To evaluate the impact of patient setup errors on the dosimetry and radiobiological models of intensity-modulated radiotherapy (IMRT) for esophageal cancer.
Methods And Materials: This retrospective study with 56 patients in thermoplastic mask (TM) and vacuum bag (VB) groups utilized real setup-error (RSE) data from cone-beam CT scans to generate simulated setup-error (SSE) data following a normal distribution. The SSE data were applied to simulate all treatment fractions per patient by shifting the plan isocenter and recalculating the dose.
Stat Med
February 2025
Department of Biostatistics, Yale School of Public Health, New Haven, Connecticut, USA.
With the increasing maturity of genetic profiling, an essential and routine task in cancer research is to model disease outcomes/phenotypes using genetic variables. Many methods have been successfully developed. However, oftentimes, empirical performance is unsatisfactory because of a "lack of information.
View Article and Find Full Text PDFThorac Cancer
January 2025
Department of Thoracic Surgery, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin, China.
Background: Our study aimed to explore the specific functions and potential mechanisms of miR-224-5p in non-small cell lung cancer (NSCLC).
Methods: We first analyzed the expression of miR-224-5p in NSCLC patients and cell lines through the GEO database and qRT-PCR analysis. Then, we used MTT assays, wound healing assays, Transwell assays, and western blotting to evaluate the effects of miR-224-5p on NSCLC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).
Thorac Cancer
January 2025
Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Background: The clinical implications of different EML4-ALK fusion variants remain poorly elucidated in the era of second-generation ALK inhibitors.
Methods: This was a retrospective cohort study, wherein patients diagnosed with locally advanced or metastatic non-small cell lung cancer harboring EML4-ALK fusion were stratified into two cohorts based on their first-line treatment: Cohort 1 received alectinib, while Cohort 2 received crizotinib. Statistical analysis was employed to investigate the impact of different EML4-ALK variants and TP53 status on the efficacy of first-line ALK-TKIs.
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