{'fraction_non_alphanumeric': 0.029689608636977057, 'fraction_numerical': 0.016194331983805668, 'mean_word_length': 4.979838709677419, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 1, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Oral Tissue Reveals Smoking-Related Risk Nearly One-Third of Adults Get No More Than 6 Hours of Sleep

S A N D I E G O — Smokingrelated cell damage may leave molecular footprints in saliva and oral epithelial cells, offering the potential for noninvasive early diagnosis of lung cancer and of head and neck cancers, researchers reported in separate studies at the annual meeting of the American Association for Cancer Research. “When people smoke cigarettes, the whole field is exposed to carcinogens,” said Dr. Li Mao, professor of thoracic/head and neck medical oncology and systems biology at the University of Texas at Houston. He and his associates theorized that early molecular alterations in oral epithelium might serve as a surrogate for damage in the lungs. To test their idea, they compared cell samples obtained from the lungs to mouth tissue collected with an oral brush in 125 chronic smokers. Using the smokers as their own controls, the investigators found striking similarities in gene expression in lung and oral tissue. For example, they found strong correlations in the inhibition (promoter methylation) of tumor suppressor genes p16 and FHIT (fragile histidine triad) in 1,774 tissue samples. Genetic expression of specific inhibitors (total promoter methylation, inhibition of p16, and inhibition of FHIT, respectively) was found in 23%, 17%, and 35% of bronchial tissues. This also was found, respectively, in 19%, 15%, and 31% of the tissue samples that were