Effect of cigarette smoke exposure and mutant Kras overexpression on pancreatic cell proliferation.

Pancreatic cancer is the fourth leading cause of cancer-associated mortality. The major risk factor for pancreatic cancer is cigarette smoking. Kras mutations are commonly observed in human pancreatic cancers.

Inorganic arsenic inhibits the nucleotide excision repair pathway and reduces the expression of XPC.

Chronic exposure to arsenic, most often through contaminated drinking water, has been linked to several types of cancer in humans, including skin and lung cancer. However, the mechanisms underlying its role in causing cancer are not well understood. There is evidence that exposure to arsenic can enhance the carcinogenicity of UV light in inducing skin cancers and may enhance the carcinogenicity of tobacco smoke in inducing lung cancers.

Exposure of Human Lung Cells to Tobacco Smoke Condensate Inhibits the Nucleotide Excision Repair Pathway.

Exposure to tobacco smoke is the number one risk factor for lung cancer. Although the DNA damaging properties of tobacco smoke have been well documented, relatively few studies have examined its effect on DNA repair pathways. This is especially true for the nucleotide excision repair (NER) pathway which recognizes and removes many structurally diverse DNA lesions, including those introduced by chemical carcinogens present in tobacco smoke.

Bhas 42 cell transformation activity of cigarette smoke condensate is modulated by selenium and arsenic.

Cigarette smoking remains a major health risk worldwide. Development of newer tobacco products requires the use of quantitative toxicological assays. Recently, v-Ha-ras transfected BALB/c3T3 (Bhas 42) cell transformation assay was established that simulates the two-stage animal tumorigenesis model and measures tumor initiating and promoting activities of chemicals.

Impact of apigenin and kaempferol on human head and neck squamous cell carcinoma.

Objective: Apigenin and kaempferol are plant flavonoids with reported chemopreventive activities. This study aimed to determine the effect of apigenin and kaempferol on cell viability in cultured cells derived from the pharynx (FaDu cell line), an oral cavity carcinoma (PCI-13 cell line), and a metastatic lymph node (PCI-15B cell line) and in explanted FaDu cells.

Study Design: The in vitro viability of FaDu, PCI-13, and PCI-15B cells treated with apigenin and kaempferol was determined.