The “Polonium In Vivo” Study: Polonium-210 in Bronchial Lavages of Patients with Suspected Lung Cancer

Few studies have reported on polonium-210, a decay breakdown product of radon-222 and lead-210, in human lungs and there has been no study in patients with suspected lung cancer. The main aim of this “Polonium in vivo” study was to evaluate polonium-210 radioactivity in bronchopulmonary systems of smoker, ex-smoker and never smoker patients with suspected lung cancer. Alpha-spectrometric analyses were performed on bronchial lavage (BL) fluids from two Italian hospitals in 2013–2016. Socio-demographic, smoking, occupational and spirometric characteristics, lung cancer confirmation and histologic type and radon-222 concentration in patients’ homes were collected. Seventy BL samples from never (n = 13), former (n = 35) and current smokers (n = 22) were analyzed; polonium-210 was detected in all samples from current and former smokers and in 54% of samples from never smokers (p < 0.001; median values: 1.20, 1.43 and 0.40 mBq, respectively). Polonium-210 levels were significantly higher in COPD versus no COPD patients (median value: 3.60 vs. 0.97 mBq; p = 0.007); former and current smokers, without and with COPD, had significantly increased polonium-210 levels (p = 0.012); 96% of confirmed versus 69% of non-confirmed lung cancer patients recorded detectable polonium-210 levels (p = 0.018). A polonium-210 detectable activity was measured in BL samples from all current and former smokers. Polonium-210 in the lungs could be the result of lead-210 entrapment, which, with its half-life of 22 years, could provide a continuous emission of alpha radioactivity, even many years after quitting, thus proposing a possible explanation for the onset of lung cancer, particularly in former smokers.

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Cancer development in COPD patients: retrospective analysis of the National Health Insurance Service-National Sample Cohort in Korea

10.21203/rs.2.22947/v2 ◽

2020 ◽

Author(s):

Song Vogue Ahn ◽

Eunyoung Lee ◽

Bumhee Park ◽

Jin Hee Jung ◽

Ji Eun Park ◽

...

Keyword(s):

Colorectal Cancer ◽

Lung Cancer ◽

Risk Factor ◽

Health Insurance ◽

Smoking Status ◽

National Sample ◽

Factors Associated ◽

Copd Patients ◽

Former Smokers ◽

Never Smokers

Abstract Background: COPD is a well-known risk factor for lung cancer, independent of smoking behavior. By investigating the retrospective National Health Insurance Service-National Sample Cohort (NHIS-NSC) in Korea, this study attempted to prove the hypothesis that COPD is a risk factor for major cancers developing outside of the lungs. We also aimed to investigate the environmental factors associated with the development of lung cancer in COPD patients. Methods: This study analyzed data from the NHIS-NSC over a 12-year period. Among the 514,795 subjects in the NHIS-NSC, 16,757 patients who were diagnosed with any cancer from 2002 to 2003 were excluded. This cohort enrolled six arms consisting of never-smokers without COPD (N=313,553), former smokers without COPD (N=41,359), smokers without COPD (N=112,627), never-smokers with COPD (N=7,789), former smokers with COPD (N=1,085), and smokers with COPD (N=2,677). Results: Incident rate of lung cancer per 100,000 person-year was higher according to smoking and COPD (216 in non-COPD and 757 in COPD among never-smokers, 271 in non-COPD and 1266 in COPD among former smokers, 394 in non-COPD and 1560 in COPD among former smokers, p<0.01). Age, male gender, lower BMI, low exercise level, smoking, and COPD were independent factors associated with the development of lung cancer (p<0.01). Multi-variable analyses showed that COPD, regardless of smoking status, contributed to the development of lung cancer, and colorectal cancer and liver cancer among other major cancers (p < 0.01). Conclusion: Our data suggested that COPD was an independent risk factor for the development of lung cancer, and colorectal cancer and liver cancer among other major cancers in the Korean population, regardless of smoking status.

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Cancer development in COPD patients: retrospective analysis of the National Health Insurance Service-National Sample Cohort in Korea

10.21203/rs.2.22947/v1 ◽

2020 ◽

Author(s):

Song Vogue Ahn ◽

Bumhee Park ◽

Jin Hee Jung ◽

Eunyoung Lee ◽

Ji Eun Park ◽

...

Keyword(s):

Lung Cancer ◽

Risk Factor ◽

Smoking Status ◽

National Sample ◽

Control Group ◽

Factors Associated ◽

Copd Patients ◽

Healthy Control ◽

Former Smokers ◽

Never Smokers

Abstract Background COPD is a well-known risk factor for lung cancer, independent of smoking behavior. By investigating the retrospective National Health Insurance Service-National Sample Cohort (NHIS-NSC) in Korea, this study attempted to prove our hypothesis that COPD is a risk factor for major cancers developing outside of the lungs. We also aimed to investigate the environmental factors associated with the development of lung cancer in COPD patients. Methods This study analyzed data from the NHIS-NSC over a 12-year period. Among the 514,795 subjects in the NHIS-NSC, 20,837 patients who were diagnosed with any cancer from 2002 to 2003 were excluded. Finally, this cohort enrolled four arms, the healthy control group (N=127,884), never-smokers with COPD (N=29,799), former smokers with COPD (N=3,267), and smokers with COPD (N=8,335). Results Over a 12-year period, lung cancer developed in 1.27% of the never-smokers with COPD, 2.97% of the former smokers with COPD, and 4.79% of smokers with COPD much higher than in 0.63% of the healthy control group (p < 0.001). Multivariate analyses showed that COPD, regardless of smoking status, contributed to the development of lung cancer but was not linked with any other major cancers, including stomach cancer, colorectal cancer, liver cancer and acute myeloid leukemia (p < 0.01). Age, male gender, lower BMI, low exercise level, smoking, and COPD were independent factors associated with the development of lung cancer (p< 0.01) Conclusion Our data suggest that COPD was an independent risk factor for the development of lung cancer in the Korean population, regardless of smoking status but other major cancers were not linked with COPD.

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Cancer of the Lung, Larynx, and Pleura

10.1093/oso/9780190676827.003.0014 ◽

2018 ◽

Author(s):

Jyoti Malhotra ◽

Paolo Boffetta ◽

Lorelei Mucci

Keyword(s):

Lung Cancer ◽

Secondhand Smoke ◽

Lung Cancer Risk ◽

Occupational Exposures ◽

Men And Women ◽

Established Risk Factor ◽

Former Smokers ◽

Never Smokers ◽

Exposure To Secondhand Smoke ◽

Cancer Of The Lung

Lung cancer is the most commonly diagnosed cancer among men in most countries, and is the primary cause of cancer death in men and women. Its epidemic increase in incidence began in the first half of the twentieth century, paralleling the uptake of cigarette smoking that occurred 20 years before. A series of landmark studies beginning in 1950 established tobacco as the primary cause of lung cancer. Current smokers have a 10- to 20-fold higher lung cancer risk compared to never smokers. Important for prevention, former smokers substantially reduce this excess risk 5 years after smoking cessation. Exposure to secondhand smoke, a well-established risk factor for lung cancer, has a 20%–25% higher risk for those exposed. There are several occupational exposures associated with lung cancer, including asbestos. Despite the success in defining lung cancer’s etiology, this highly preventable disease remains among the most common and most lethal cancers globally.

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USP9X-mediated KDM4C deubiquitination promotes lung cancer radioresistance by epigenetically inducing TGF-β2 transcription

Cell Death and Differentiation ◽

10.1038/s41418-021-00740-z ◽

2021 ◽

Author(s):

Xiaohua Jie ◽

William Pat Fong ◽

Rui Zhou ◽

Ye Zhao ◽

Yingchao Zhao ◽

...

Keyword(s):

Lung Cancer ◽

Affinity Purification ◽

Smad Signaling ◽

Lung Cancer Patients ◽

Lysine Specific Demethylase ◽

Underlying Mechanisms ◽

H3k9me3 Level ◽

Critical Binding

AbstractRadioresistance is regarded as the main barrier to effective radiotherapy in lung cancer. However, the underlying mechanisms of radioresistance remain elusive. Here, we show that lysine-specific demethylase 4C (KDM4C) is overexpressed and correlated with poor prognosis in lung cancer patients. We provide evidence that genetical or pharmacological inhibition of KDM4C impairs tumorigenesis and radioresistance in lung cancer in vitro and in vivo. Moreover, we uncover that KDM4C upregulates TGF-β2 expression by directly reducing H3K9me3 level at the TGF-β2 promoter and then activates Smad/ATM/Chk2 signaling to confer radioresistance in lung cancer. Using tandem affinity purification technology, we further identify deubiquitinase USP9X as a critical binding partner that deubiquitinates and stabilizes KDM4C. More importantly, depletion of USP9X impairs TGF-β2/Smad signaling and radioresistance by destabilizing KDM4C in lung cancer cells. Thus, our findings demonstrate that USP9X-mediated KDM4C deubiquitination activates TGF-β2/Smad signaling to promote radioresistance, suggesting that targeting KDM4C may be a promising radiosensitization strategy in the treatment of lung cancer.

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Analysis of Erythrocyte Glycophorin-A Variants by Flow Cytometry in Lung Disease Patients Detects the Effect of Tobacco Smoke

Analytical Cellular Pathology ◽

10.1155/2000/512786 ◽

2000 ◽

Vol 21 (1) ◽

pp. 35-40 ◽

Cited By ~ 2

Author(s):

Monica Neri ◽

Elio Geido ◽

Rosangela Filiberti ◽

Roberto Orecchia ◽

Angela Di Vinci ◽

...

Keyword(s):

Lung Cancer ◽

Flow Cytometry ◽

Cancer Risk ◽

Tobacco Smoke ◽

Lung Cancer Risk ◽

Small Population ◽

Cancer Risk Assessment ◽

Lung Cancer Patients ◽

Increased Risk

The glycophoryn A (GPA) assay evaluates somaticin vivomutations. It is considered a cumulative biodosimeter for genotoxic exposures and is under evaluation in cancer risk assessment.GPA, a polymorphic membrane protein of the erythrocytes, determines the MN blood groups. The N0 and NN variant frequencies (VF) may be detected in MN subjects (about 50% of the population) by flow cytometry using two differently labelled antibodies.We explored if GPA N0 and NN VF might be relevant to the assessment of individual lung cancer risk and susceptibility, in a small population with a high prevalence of heavy tobacco smokers: 8 lung cancer patients and 16 subjects with non‐malignant lung diseases associated with increased risk of lung cancer.There was a wide interindividual variability and complete overlap between non‐neoplastic and neoplastic patients. A significant positive correlation was seen with smoking duration in N0 VF (p=0.04, age‐adjusted). Current smokers (n=12) displayed higher N0 values than never (n=1) or ex‐smokers (n=11), 36.3±18.2 and 21.0±13.2, respectively (p< 0:01). No association was shown with occupational exposure.The present exploratory study suggests that assessment of individual lung cancer risk and susceptibility by the GPA assay does not seem to be feasible. The assay appears to provide a biomarker of longterm exposure to tobacco smoke.

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Characterization of Lung Cancer by Amide Proton Transfer (APT) Imaging: An In-Vivo Study in an Orthotopic Mouse Model

PLoS ONE ◽

10.1371/journal.pone.0077019 ◽

2013 ◽

Vol 8 (10) ◽

pp. e77019 ◽

Cited By ~ 29

Author(s):

Osamu Togao ◽

Chase W. Kessinger ◽

Gang Huang ◽

Todd C. Soesbe ◽

Koji Sagiyama ◽

...

Keyword(s):

Lung Cancer ◽

Mouse Model ◽

Proton Transfer ◽

In Vivo Study ◽

Amide Proton ◽

Orthotopic Mouse Model ◽

Amide Proton Transfer ◽

Apt Imaging

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Acute Changes in Calcitonin Levels in Lung Cancer Patients Treated with C. Parvum: Do These Reflect in Vivo Killing of Tumour Cells?

Metastasis ◽

10.1007/978-94-009-8925-2_67 ◽

1980 ◽

pp. 346-350

Author(s):

H. D. Mitcheson ◽

C. J. Hillyard ◽

I. MacIntyre ◽

J. E. Castro

Keyword(s):

Lung Cancer ◽

Cancer Patients ◽

Tumour Cells ◽

Lung Cancer Patients ◽

Acute Changes

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Effect of Octreotide on Neuroenolase Levels in Patients with Small Cell Lung Cancer

Tumori Journal ◽

10.1177/030089169408000503 ◽

1994 ◽

Vol 80 (5) ◽

pp. 332-334 ◽

Cited By ~ 2

Author(s):

Enzo Soresi ◽

Giovanni Invernizzi ◽

Roberto Boffi ◽

Umberto Borghini ◽

Gianfranco Schiraldi ◽

...

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Cell Lung Cancer ◽

Serum Levels ◽

Small Cell ◽

Small Cell Lung ◽

Lung Cancer Patients ◽

Octreotide Treatment

Aims and Background The somatostatin analog octreotide has an antiproliferative effect on small cell lung cancer lines in vitro and in experimental xenograft transplantation systems in vivo. Thus it is worth investigating octreotide activity in the clinical setting. Methods We studied the effect of octreotide (200 μg three times a day subcutaneously for seven days) on serum levels of the tumor marker neuroenolase in 13 patients with small cell lung cancer. Results A decrease in neuroenolase levels was observed at day 7 during octreotide treatment, with a mean ± SD of 32.6 ± 42.0 ng/ml compared to basal values of 44.4 ± 57.7 ng/ml and to washout values of 50.3 ± 65.7 ng/ml ( P < 0.03). Conclusions Our results indicate that octreotide is effective in reducing neuroenolase levels in small cell lung cancer patients. These data suggest a possible role for octreotide in the treatment of this kind of tumor.

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