• Journal of Ginseng Research
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• v.18 no.2
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• pp.89-94
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• 1994

The authors have already shown that 6 year old red ginseng extract or its powder has remarkable anticarcinogenic effects. In this study, we further investigated whether fresh ginseng or white ginseng has similar anticarcinogenic effects and also if their anticarcinogenic effects are related to the types and ages of ginseng using Yun's anticarcinogenicity test (9 week medium term bioassay model). Dried fresh ginseng and red ginseng at 1.5, 3, 4, 5 and 6 years, and while ginseng at 3, 4, 5 and 6 years were used. The following results were obtained: 1) In the dried fresh ginseng treated groups, the incidence of lung adenoma induced by benzo(a)pyrene was 41.39) and its incidence was reduced to 31.2%, 30.0%, 31.3%, 30.7% and 27.8% after co-treatment with 1.5, 3, 4, 5 and 6 year-dried fresh ginseng, respectively. A significant effect was observed only in 6 Year-dried fresh ginseng. 2) In the white ginseng treated groups, the incidence of lung adenoma induced by benzo(a)pyrene was 45.0% and its incidence decreased to 41.3%, 38.0%, 31.6%, and 25.3% after co-treatment with 3, 4, 5 and 6 year-white ginseng, respectively. Five and 6 year-ginsengs showed significant inhibition of lung adenoma. 3) In the red ginseng treated groups, the incidence of lung adenoma induced by benzo(a) pyrene was 48.6% and its incidence diminished to 37.9%, 41.7%, 31.7%, 28.3% and 25.5% after co-treat-melt with 1.5, 3, 4, 5 and 6 year-red ginseng, respectively. In 4, 5 and 6 year-ginsengs, the anticarcinogenic effect was prominent. From the above results, we concluded that a significant anticarcinogenic effect was observed in 6 year-dried fresh ginseng, 5 and 6 year-white ginsengs, and 4, 5 and 6 year-red ginsengs.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.10
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• pp.4447-4450
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• 2015

Background: Nasopharyngeal cancer is a disease with distinct ethnic and geographical distribution. The aim of this review was to describe the epidemiological characteristics of nasopharyngeal cancer in Iran from 2004 to 2009 because no systematic study has been performed to evaluate the trends of its incidence yet. Materials and Methods: The data were derived from the databases of the National Cancer Data System Registry in the period of 2004-2009. Nasopharyngeal cancers were classified according to the International Classification of Diseases for Oncology. Incidence rates and trends were calculated and evaluated by gender, age decade, and histopathology types. Results: A total of 1,637 nasopharyngeal cancers were registered in Iran from 2004 to 2009 giving an incidence of 0.38 per 100,000. The male-to-female ratio was 2.08:1. The trend of incidence was found to have increased, with a significant increase observed in males. Undifferentiated carcinoma was the most common histopathology type in all the age decades. Conclusions: Because the incidence of nasopharyngeal cancers in Iran has increased, especially in males, further studies are recommended for understanding of the etiological factors involved in the rise of the disease.

• Biomedical Science Letters
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• v.29 no.4
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• pp.336-343
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• 2023

Lung cancer is one of the cancers with high mortality and incidence rates worldwide. Although, various anticancer research efforts are underway to completely treat cancer, the challenge against it remains in the inability to eliminate cancer stem cells (CSCs), leading to difficulties in curing the cancer and resulting in recurrence. As a result, there is a growing interest in the discovery of new biomarkers and therapeutic molecules that can simultaneously target both cancer cells and CSCs. From this point of view, we focused on fibronectin leucine rich transmembrane protein 3 (FLRT3), one of the genes known to be present in human lung cells and the discovery from our previous cancer proteomic analysis study. This study aimed to evaluate the potential of FLRT3 as a specific therapeutic biomarker for lung cancer and Lung Cancer-derived-Stem Cells (LCSC). Also, to estimate the biological function of FLRT3 in cancer and LCSC, short hairpin RNA (shRNA) was generated and showed the ability of the decreased-cell migration and cell proliferation of lung cancer through ERK signaling pathway when FLRT3 was knock-downed. In conclusion, our study is the first to report that FLRT3 has the potential as therapeutic biomarker for the treatment of lung cancer and LCSC.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.7
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• pp.2613-2617
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• 2015

Radiation induced lung injury has long been considered a treatment limiting factor for patients requiring thoracic radiation. This radiation induced lung injury happens early as well as late. Radiation induced lung injury can occur in two phases viz. early (< 6 months) when it is called radiation pneumonitis and late (>6 months) when it is called radiation induced lung fibrosis. There are multiple factors that can be patient, disease or treatment related that predict the incidence and severity of radiation pneumonitis. Radiation induced damage to the type I pneumocytes is the triggering factor to initiate such reactions. Over the years, radiation therapy has witnessed a paradigm shift in radiation planning and delivery and successfully reduced the incidence of lung injury. Radiation pneumonitis is usually a diagnosis of exclusion. Steroids, ACE inhibitors and pentoxyphylline constitute the cornerstone of therapy. Radiation induced lung fibrosis is another challenging aspect. The pathophysiology of radiation fibrosis includes continuing inflammation and microvascular changes due to pro-angiogenic and profibrogenic stimuli resembling those in adult bronchiectasis. General supportive management, mobilization of airway secretions, anti-inflammatory therapy and management of acute exacerbations remains the treatment option. Radiation induced lung injury is an inevitable accompaniment of thoracic radiation.

• Toxicological Research
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• v.24 no.2
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• pp.109-112
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• 2008

The G184C and G134A single nucleotide polymorphisms(SNPs) of the CYP1A1 gene result in Ala62Pro and Gly45Asp substitutions, respectively. Here, we tested whether these SNPs are associated with an alteration in lung cancer incidence. We examined 80 Korean subjects with lung cancer and 240 age- and sex-matched controls. For each subject, the CYP1A1 gene was PCR amplified and sequenced. We observed that the odds ratio(OR) for lung cancer was 3.37 higher in subjects with the G184C polymorphism than in controls(95% confidence interval(CI), $0.89{\sim}12.73$, P=0.07). In contrast, the OR for lung cancer was 1.23 in subjects with the G134A polymorphism compared to controls(95% CI, $0.68{\sim}2.20$, P=0.49). The G184C polymorphism exacerbated the effects of smoking on lung cancer development. Gene-smoking interaction analyses revealed that past or present smokers with the G184C polymorphism had a higher incidence of lung cancer(OR, 24.72; 95% CI, $4.48{\sim}136.31$; P<0.01) than control smokers(OR, 6.65; 95% CI, $2.72{\sim}16.28$; P<0.01). However, there was only a slight difference in the ORs for lung cancer between control smokers and smokers with the G134A polymorphism. These findings suggest that the G184C polymorphism, but not the G134A polymorphism, is associated with an increased risk of lung cancer.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.191-192
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• 2001

Although the incidence rates of gastric cancer and liver cancer, the most common cancers in Korea, are tending decrease, lung cancer is on the increase every year as cause of cancer death as well as incidence rate in Korea. And cigarette smoke is believed to be responsible for 90% of lung cancer. Many investigators have reported an association between genetic polymorphism of cytochromes P-450 (CYPs) or glutathoine S-transferase (GSTs) and susceptibility to lung cancer.(omitted)

• Tuberculosis and Respiratory Diseases
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• v.69 no.1
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• pp.1-15
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• 2010

Lung cancer remains the most common cause of cancer death in the United States and worldwide. About 80~90% of cases are smoking-related and smoking cessation programs are of great importance in reducing lung cancer risk. However, the lifetime risk for lung cancer remains elevated even in ex-smokers. Chemoprevention holds the promise to further reduce this risk and thus to decrease lung cancer incidence and mortality. Over the last decades, most chemoprevention trials for lung cancer have yielded negative outcomes. Population-based studies suggest that high intake of certain foods such as soy, red wine or green vegetables may be associated with decreased cancer risk. Because of these observations and their general safety, a plethora of natural compounds is currently being studied for the chemoprevention of cancer. In this review we discuss promising in vitro and in vivo data of novel natural compounds, their interference with molecular mechanisms responsible for lung cancer development and potential implications for their further preclinical and clinical investigation.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.5
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• pp.1993-1999
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• 2014

Background: This study aimed to explore the role of XRCC1 (Arg399Gln) and XPD (Lys751Gln) gene polymorphisms, lifestyle and environmental factors as well as their possible interactions in propensity to develop lung cancer in a population with high incidence from North East India. Materials and Methods: A total of 272 lung cancer cases and 544 controls were collected and XRCC1 (Arg399Gln) and XPD (Lys751Gln) genotypes were analyzed using a polymerase chain reaction based restriction fragment length polymorphism assay. Conditional multiple logistic regression analysis was used to calculate adjusted odds ratios and 95% confidence intervals after adjusting for confounding factors. Results: The combined Gln/Gln genotype of XRCC1 and XPD genes (OR=2.78, CI=1.05-7.38; p=0.040) was significantly associated with increased risk for lung cancer. Interaction of XRCC1Gln/Gln genotype with exposure of wood combustion (OR=2.56, CI=1.16-5.66; p=0.020), exposure of cooking oil fumes (OR=3.45, CI=1.39-8.58; p=0.008) and tobacco smoking (OR=2.54, CI=1.21-5.32; p=0.014) and interaction of XPD with betel quid chewing (OR=2.31, CI=1.23-4.32; p=0.009) and tobacco smoking (OR=2.13, CI=1.12-4.05; p=0.022) were found to be significantly associated with increased risk for lung cancer. Conclusions: Gln/Gln alleles of both XRCC1 and XPD genes appear to amplify the effects of household exposure, smoking and betel quid chewing on lung cancer risk in the study population.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.19
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• pp.8345-8349
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• 2014

Background: Cancer is an increasing cause of mortality and morbidity worldwide. Incidences of common cancers has been growing in different provinces of Iran in recent years but trends in Khuzestan which shares a border with Iraq and is located in south west of Iran have not been investigated. This study aimed to assess secular changes in incidences of common cancers in Khuzestan province from 2004 to 2008. Materials and Methods: Data were collected from Khuzestan cancer registry which is a branch of Iranian Ministry of Health Cancer Registry (http://ircancer.ir) for the period 2004-2008. Data were presented as incidence rates by site, sex, age, using the crude rate and age-standardized rate (ASR) per $10^5$ persons. A direct method of standardization was applied according to the WHO guideline and data analysis was performed using the SPSS package. Results: During the 2004-2008 period, 14,893 new cases of cancer were registered in Khuzestan cancer registry. The age-standardized incidence rate of all cancers was 153.7 per $10^5$ in males and 156.4 per $10^5$ in females. The incidence was increased over the period of five years. The most incident cancers among males were skin cancer ($ASR=18.7/10^5$), stomach cancer ($ASR13.8/10^5$), lung cancer ($ASR12.9/10^5$), leukemia ($ASR=12.6/10^5$) and prostate cancer ($ASR=12.4/10^5$). In females, the most incident cancers were breast cancer ($ASR=41/10^5$), skin cancer ($ASR=16.4/10^5$), colorectal cancer ($ASR=10.0/10^5$), leukemia ($ASR=8.1/10^5$) and lung cancer ($ASR=6.9/10^5$). Conclusions: Incidences of various cancers are rising in Khuzestan. It is necessary to develop and implement comprehensive cancer control programs in this region which could be monitored and evaluated by the future trend data from Khuzestan cancer registry.

• Journal of Ginseng Research
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• v.18 no.3
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• pp.160-164
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• 1994

In this study, we investigeated the anticarcinogenicity of various types and ages of ginseng extracts as an extended study using Yun's anticarcinogenicity test. Fresh ginseng at 1.5, 3, 4, 5 and 6 years was dried and powdered. And white ginseng was processed in the same way that of fresh ginseng after removal fo the ginseng cortex and fine root. For red ginsneg, fresh ginseng was steamed and dried. Each ginseng powder was extracted and extracts was freeze dried. Newborn N:GP(S) mice were given a single subcutaneous injection of 0.5 mg of benzo(a)pyrene(BP). Various types and ages of ginseng extracts at 2.5mg/ml were orally administered. All the mice were sacrificed at the 9th week. The following results were obtained. In the dried fresh ginseng extract treated group, the incidence of lung adenoma induced by BP was 63.9% and its incidence was reduced to 48.3%, 52.5%, 51.8%, 47.5% and 44.1% after co-treatment with 1.5, 3, 4, 5 and 6 year-dried fresh ginseng, respectively. The incidence of lung adenoma induced by BP on the white ginseng extract treated group was 41.3% and decreased to 31.0%, 46.0%, 44.0% and 26.5% after co-treatment with 3, 4, 5 and 6 year-white ginseng, respectively. In the red ginseng extract treated group, the incidence of lung adenoma induced by BP was 47.5% and its incidence diminished to 40.7%, 35.0%, 30.1%, 30.0% and 26.3% after co-treatment with 1.5, 3, 4, 5 and 6 year-red ginseng, respectively. From the above results, we concluded that a statistically significant anticarcinogenic effect was observed in extracts of 6 year-dried fresh ginseng, 6 year-white ginseng, and 4, 5 and 6 year-red ginseng and it is suggested that the anticarcinogenicity of ginseng varies according to the types and ages Key words Ginseng extract, types and ages. anticarcinogenic, newborn mice, lung tumor.