Three simple models for the asbestos-smoking interaction on human lung cancer production are considered. In the first model the excess incidence of lung cancer independently due to asbestos and to smoking adds together when both agents are present (additive model). In the second the addition of each one of the two agents produces an effect (increase in lung cancer incidence) which is proportional to the effect of the other (multiplicative model). In the third, asbestos can only increase lung cancer incidence in the presence of smoking. As previously found by other investigators, the additive model appears the least plausible in the light of the data from two published epidemiological studies. A discrimination between the other two models is attempted through a detailed analysis of the five published epidemiological studies today available which provide information on occupational asbestos exposure, smoking habits and lung cancer risk. Although the data do not allow a definitive discrimination, the multiplicative model appears to be more plausible, being also consistent with a multi-stage carcinogenic mechanism and with evidence from animal (rat) experiments. It is relevant both for biology and for public health that in this model asbestos and smoking are regarded as independently capable of producing lung cancer in humans and that they act synergistically when exposure to both occurs.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1002/ijc.2910200302 | DOI Listing |
Int J Surg
January 2025
Department of Thoracic Surgery, West China hospital, SiChuan University, Chengdu, China.
Background: While recent randomized controlled trials have demonstrated that sublobar resection is non-inferior to lobectomy, the comparative efficacy of these procedures remains uncertain for early-stage non-small cell lung cancer (NSCLC; ≤ 3 cm) exhibiting invasive features postoperatively, such as visceral pleural invasion (VPI) or spread through air spaces (STAS).
Materials And Methods: To identify eligible studies, a comprehensive search of PubMed, Embase, MEDLINE, the Cochrane Library, and Web of Science was conducted through 25 July 2024. Studies were screened according to predefined criteria in accordance with PRISMA guidelines.
J Med Chem
January 2025
College of Chemistry, Zhengzhou University, Zhengzhou 450001, China.
The P2YR is activated by UDP and UDP glucose and is involved in many human inflammatory diseases. Based on the molecular docking analysis of currently reported P2YR antagonists and the crystallographic overlap study between PPTN and compound , a series of 3-substituted 5-amidobenzoate derivatives were designed, synthesized, and identified as promising P2YR antagonists. The optimal compound (methyl 3-(1-benzo[]imidazol-2-yl)-5-(2-(-tolyl) acetamido)benzoate, IC = 0.
View Article and Find Full Text PDFJpn J Clin Oncol
January 2025
Division of International Health Policy Research, Institute for Cancer Control, National Cancer Center, Chuo-ku, Tokyo, Japan.
Cureus
December 2024
Physics and Engineering, London Regional Cancer Program, London, CAN.
Introduction: Radiation may unintentionally injure myocardial tissue, potentially leading to radiation-induced cardiac disease (RICD), with the net benefit of non-small cell lung cancer (NSCLC) radiotherapy (RT) due to the proximity of the lung and heart. RTOG-0617 showed a greater reduction in overall survival (OS) comparing higher doses to standard radiation doses in NSCLC RT. VHeart has been reported as an OS predictor in the first- and fifth-year follow-ups.
View Article and Find Full Text PDFRSC Adv
January 2025
Institute of Chemistry, Vietnam Academy of Science and Technology (VAST) 18 Hoang Quoc Viet, Cau Giay Hanoi Vietnam
Podophyllotoxin, along with its numerous derivatives and related compounds, is well known for its broad-spectrum pharmacological activity, especially for anticancer potential. In this study, several isatin-podophyllotoxin hybrid compounds were successfully synthesized with good yields through microwave-prompted three-component reactions of 2-amino-1,4-naphthoquinone, various substituted isatins, and tetronic acid. Their cytotoxicity was assessed against four types of human cancer cell lines, HepG2 (hepatoma carcinoma), MCF7 (breast cancer), A549 (non-small lung cancer), and KB (epidermoid carcinoma), alongside nontumorigenic HEK-293 human embryonic kidney cells.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!