Asbestos ; adverse effects ; Humans ; Lung Neoplasms ; chemically induced ; Mesothelioma ; chemically induced ; Peritoneal Neoplasms ; chemically induced

Antineoplastic Agents ; adverse effects ; therapeutic use ; Diarrhea ; chemically induced ; Drug Delivery Systems ; methods ; Exanthema ; chemically induced ; Humans ; Leukopenia ; chemically induced ; Lung Diseases, Interstitial ; chemically induced ; Myocardial Infarction ; chemically induced ; Neoplasms ; drug therapy ; Tumor Lysis Syndrome ; etiology

The modifying potential of capsaicin (CAP) on lesion development was examined in a rat multiorgan carcinogenesis model. Groups 1 and 2 were treated sequentially with diethylnitrosamine (DEN) (100 mg/kg, ip, single dose at commencement), N-methylnitrosourea (MNU) (20 mg/kg, ip, 4 doses at days 2, 5, 8, and 11), and N,N-dibutylnitrosamine (DBN) (0.05% in drinking water during weeks 3 and 4). Group 3 received vehicles without carcinogens during the initiation period. Group 4 served as the untreated control. After this initiating procedure, Groups 2 and 3 were administered a diet containing 0.01% CAP. All surviving animals were killed 20 weeks after the beginning of the experiment and the target organs examined histopathologically. The induction of GST-P+ hepatic foci in rats treated with carcinogens was significantly inhibited by treatment with CAP. CAP treatment significantly decreased the incidence of adenoma of the lung but increased the incidence of papillary or nodular (PN) hyperplasia of the urinary bladder. The tumor incidence of other organs, such as the kidney and thyroid, was not significantly different from the corresponding controls. These results demonstrated that concurrent treatment with CAP not only can inhibit carcinogenesis but can also enhance it depending on the organ. Thus, this wide-spectrum initiation model could be used to confirm organ-specific modification potential and, in addition, demonstrate different modifying effects of CAP on liver, lung, and bladder carcinogenesis.
Animals ; Capsaicin/pharmacology/*toxicity ; Cocarcinogenesis ; Diethylnitrosamine ; Liver Neoplasms, Experimental/chemically induced/prevention & control ; Lung Neoplasms/chemically induced/prevention & control ; Male ; Methylnitrosourea ; Neoplasms, Experimental/*chemically induced/prevention & control ; Nitrosamines ; Rats ; Rats, Inbred F344 ; Urinary Bladder Neoplasms/chemically induced

Asbestos is a carcinogen that causes diseases such as mesothelioma and lung cancer in humans. There was a sharp increase in the use of asbestos in Korea in the 1970s as Korea's economy developed rapidly, and asbestos was only recently banned from use. Despite the ban of its use, previously applied asbestos still causes many problems. A series of asbestos-related events that recently occurred in Korea have caused the general public to become concerned about asbestos. Therefore, it is necessary to take proper action to deal with asbestos-related events, such as mass outbreaks of mesothelioma among residents who lived near asbestos textile factories or asbestos mines. Although there have been no rapid increases in asbestos-related illnesses in Korea to date, such illnesses are expected to increase greatly due to the amount of asbestos used and long latency period. Decreasing the asbestos exposure level to levels as low as possible is the most important step in preventing asbestos-related illnesses in the next few decades. However, there is a lack of specialized facilities for the analysis of asbestos and experts to diagnose and treat asbestos-related illnesses in Korea; therefore, national-level concern and support are required.
Asbestos/*toxicity ; Asbestosis/*epidemiology/etiology/mortality ; Environmental Exposure/prevention & control ; Humans ; Korea ; Lung Neoplasms/*chemically induced ; Mesothelioma/*chemically induced/epidemiology

Adult ; Bis(Chloromethyl) Ether ; poisoning ; Humans ; Lung Neoplasms ; chemically induced ; Male ; Middle Aged ; Occupational Diseases ; chemically induced

OBJECTIVETo explore prodromes of chemotherapy-induced vomiting (CIV) and their association with CIV in lung cancer patients.

METHODSThe prodromes of CIV in 250 lung cancer patients were analyzed. Logistic regression was used to determine the symptoms most likely correlated with CIV. One hundred fifty-seven patients received medical interventions. The development of correlative symptoms and occurrence of CIV between the intervention and non-intervention groups was analyzed.

RESULTSAmong the 250 patients with the prodromes of CIV, the incidence rate of CIV was 67.2%. Logistic regression indicated that nausea, constipation, insomnia, hiccups, anorexia, and history of drinking were correlated with CIV (P < 0.05 for all). Among the 20 symptoms observed in this study, the incidence rates of relatively common symptoms were nausea (72.0%), anorexia (68.4%), taste changes (48.8%), constipation (45.6%), abdominal distension (45.6%), stomach distension(40.4%), and insomnia (40.0%). The incidence rats of all symptoms except hiccups before and after intervention had significant difference (P < 0.05 for all). The incidence rates of CIV were 30.0% in the intervention group and 50.6% in the non-intervention group, with a significant difference between the two groups (P = 0.009).

CONCLUSIONSProdromes of CIV are closely related to the occurrence of CIV. Timely intervention for prodromes of CIV can reduce the incidence rate of CIV during chemotherapy in lung cancer patients.

Animals ; Antineoplastic Agents ; adverse effects ; Humans ; Lung Neoplasms ; epidemiology ; Nausea ; chemically induced ; diagnosis ; epidemiology ; Rats ; Vomiting ; chemically induced ; diagnosis ; epidemiology

OBJECTIVEAflatoxin G1 (AFG1) is a member of the carcinogenic aflatoxin family produced by aspergillus flavus. It is a major contaminating mycotoxin in food in areas of China with high cancer incidence. The purpose of this study is to explore the carcinogenic effects of AFG1 in NIH mice.

METHODSNIH mice were randomly divided into three groups. Two experimental groups were treated intragastrically by gavage with AFG1 3 microg/kg and AFG1 30 microg/kg respectively, 3 times a week for 24 weeks. The control group was treated with normal saline. All mice were fed with food that was free of AFGs as confirmed by HPLC analysis. The mice were weighed every week throughout the entire experiment, and then sacrificed and examined pathologically at the 58th and 74th weeks respectively.

RESULTSCompared with control mice receiving no AFG1, bronchial epithelial hyperplasia, alveolar hyperplasia and adenocarcinoma of lung were observed in mice receiving AFG1 treatment. The incidences of bronchial epithelial hyperplasia, alveolar hyperplasia and adenocarcinoma of lung were 60.0%, 10.0% and 30.0% for mice receiving 3 microg/kg AFG1 and 28.6%, 35.7%, 42.9% for mice receiving 30 microg/kg of the toxin, respectively.

CONCLUSIONOral administration of AFG1 can induce hyperplastic lesions and adenocarcinoma of lung in NIH mice.

Adenocarcinoma ; chemically induced ; pathology ; Aflatoxins ; toxicity ; Animals ; Aspergillus flavus ; Carcinogens ; toxicity ; Lung Neoplasms ; chemically induced ; pathology ; Mice ; Random Allocation

OBJECTIVETo further explore the carcinogenic activity of Sterigmatocystin (ST) and the possible synergistic carcinogenic effect of deoxynivalenol (DON) in NIH mice.

METHODSNIH mice were randomly divided into 6 groups, 30 in each. Five groups of mice were given by gastric intubation ST 3 microg/kg, ST 30 microg/kg, ST 3 microg/kg + DON 1.5 microg/kg, ST 30 microg/kg + DON 1.5 microg/kg and DON 1.5 microg/kg respectively, 3 times a week for 24 weeks. The remaining group of mice was given normal saline accordingly, serving as control. All mice were fed with HPLC-confirmed mycotoxin-free food, analysis. The mice were killed and pathologically examined at 58th and 74th weeks.

RESULTSNo pathological changes were found in the control group of mice. Adenocarcinoma of lung was observed in 25.0%, 41.7%, 62.5%, 69.2% and 37.5% of mice given ST 3 microg/kg, ST 30 microg/kg, ST 3 microg/kg + DON 1.5 microg/kg, ST 30 microg/kg + DON 1.5 microg/kg and DON 1.5 microg/kg, respectively. In addition, dysplasia of glandular stomach was detected in 50.0%, 58.3%, 37.5%, 53.8% and 25.0% of mice similarly treated.

CONCLUSIONOral administration of ST or DON can induce adenocarcinoma in lung and dysplasia of glandular stomach in NIH mice. There is synergistic carcinogenic effect when both ST and DON are given.

Adenocarcinoma ; chemically induced ; pathology ; Animals ; Female ; Gastric Mucosa ; pathology ; Lung Neoplasms ; chemically induced ; pathology ; Male ; Mice ; Precancerous Conditions ; chemically induced ; pathology ; Sterigmatocystin ; toxicity ; Trichothecenes ; toxicity

Angiogenesis Inhibitors ; adverse effects ; Antibodies, Monoclonal ; adverse effects ; Antibodies, Monoclonal, Humanized ; Bevacizumab ; Carcinoma, Non-Small-Cell Lung ; drug therapy ; Hemorrhage ; chemically induced ; Humans ; Hypertension ; chemically induced ; Lung Neoplasms ; drug therapy ; Proteinuria ; chemically induced ; Thromboembolism ; chemically induced

Humans ; Lung Neoplasms ; chemically induced ; Proportional Hazards Models ; Radon ; adverse effects