RESUMO
Fragile sites are non-staining gaps and breaks on mammalian chromosomes. Several investigators have pointed out that these sites may act as factors that predispose to specific chromosomal rearrangements that are present in some cancer cases. The expression of common fragile sites induced by aphidicolin (Apc) was evaluated on prometaphase chromosomes obtained from the peripheral blood lymphocytes of 15 patients with lung cancer, 20 of their clinically healthy family members, and 20 age-matched normal controls. As a result of cytogenetic evaluation carried out by the High Resolution Banding (HRB) technique, 1q21, 2q33, 3p14, 7q32, 13q13, 16q23, 17q21, and 22q12 are defined as fragile sites in patients and relatives. The rate of total fragile sites and 2q33, 3p14, and 16q23 are statistically significant in both patients and relatives when compared with the control group. Therefore, our results showed that common fragile sites might be unstable factors in the human genome and they can be used as suitable markers for genetic predisposition to lung cancer.
Assuntos
Carcinoma de Células Pequenas/genética , Fragilidade Cromossômica/genética , Cromossomos Humanos/genética , Predisposição Genética para Doença , Neoplasias Pulmonares/genética , Adolescente , Adulto , Idoso , Carcinoma de Células Pequenas/sangue , Aberrações Cromossômicas , Quebra Cromossômica , Sítios Frágeis do Cromossomo , Cromossomos Humanos/ultraestrutura , Citogenética , Feminino , Marcadores Genéticos , Humanos , Neoplasias Pulmonares/sangue , Linfócitos , Masculino , Pessoa de Meia-Idade , LinhagemRESUMO
The chromosomal aberration rates (including gaps and breaks) and expression frequency of fragile sites were determined in peripheral blood lymphocytes cultured with TC 199 medium from 8 patients with squamous cell lung cancer, 10 of their first-degree relatives, and 12 healthy control subjects. As a result of cytogenetic evaluation, both the chromosomal aberration rates and expression frequencies of common fragile sites observed in patients and their relatives were significantly higher than those in healthy control subjects. Our results showed that common fragile sites might be unstable factors in the human genome, and their expression might be affected by some genetic and environmental factors. As a result of this they might play an important role in genetic predisposition to lung cancer. The high expression of fra(3)(p14) in patients and their relatives may be a valid marker for genetic predisposition to lung cancer.
Assuntos
Carcinoma de Células Escamosas/genética , Fragilidade Cromossômica , Neoplasias Pulmonares/genética , Sítios Frágeis do Cromossomo , Feminino , Predisposição Genética para Doença , Humanos , Masculino , Pessoa de Meia-Idade , LinhagemRESUMO
The purpose of our study was to evaluate the effects of cigarette smoking and serum lipids, folate, and vitamin B12 on the development of lung cancer in the Turkish population. The study group consisted of patients with histologically proven lung cancer and the control group comprised healthy smokers being followed in our smoking cessation outpatient department. Smoking history was obtained from all subjects and serum total cholesterol, HDL cholesterol, triglycerides, vitamin B12, and folate levels were measured. Pack/years of cigarettes smoked were significantly higher in the subjects with lung cancer than in the control group (p < 0.01). Serum total cholesterol, HDL cholesterol, triglyceride, serum folate, and vitamin B12 levels were within normal limits in both groups (p < 0.05), but serum vitamin B12 levels were statistically significantly higher (p < 0.01) in the cancer group than in the controls. In our study, we did not observe low levels of serum cholesterol, vitamin B12, or folate in the lung cancer patients.
