Although smoking is suggested to be a risk factor for colorectal cancer, the evidence to date is conflicting and may be confounded. Moreover, the effect of tobacco smoke may vary by time since initiation, type of tobacco product, anatomic subsites, and among ethnic groups. Data were derived from two consecutive population-based case-control studies conducted among Caucasians, Japanese, Native Hawaiians, Filipinos, and Chinese in Hawaii, including 1,959 ethnicity-, sex-, and age-matched case-control pairs. A lifetime history of smoking for different tobacco products and information on other risk factors were obtained by in-person interviews. Odds ratios (OR) and corresponding 95% confidence intervals (95% CI) were estimated using conditional logistic regression models with adjustment for potential confounders. Subjects who ever smoked were at an increased risk of colorectal cancer compared with never smokers (OR, 1.23; 95% CI, 0.99-1.52 for men and OR, 1.27; 95% CI, 1.01-1.59 for women). Increasing quartiles of pack-years over all tobacco products showed a clear dose-dependent association in men [for the highest quartile, Q4 (>40 pack-years) versus never smokers: OR, 1.48; 95% CI, 1.12-1.96; P(trend) = 0.002]. The dose-response trend was also present in women [for the highest quartile, Q4 (>30 pack-years) versus never smokers: OR, 1.38; 95% CI, 0.91-1.95; P(trend) = 0.04] and each ethnic group. There was a suggestion of a difference in risk with type of tobacco product. Non-filtered cigarettes increased risk of both colon and rectal cancer [for Q4 versus never smokers: OR, 1.59; 95% CI, 1.15-2.21; P(trend) = 0.001 and OR, 1.84; 95% CI, 1.18-2.86; P(trend) = 0.02, respectively], whereas filtered cigarettes seemed to increase risk of rectal but not colon cancer (OR, 1.37; 95% CI, 0.88-2.13; P(trend) = 0.06 and OR, 1.05; 95% CI, 0.79-1.39; P(trend) = 0.98, respectively). The effect of smoking was not limited to the distant past, and accumulated pack-years of smoking seemed to be more important than the time in which smoking occurred. The data from this large study corroborate previous reports of a positive association between smoking and colorectal cancer and suggest that the association may vary by type of cigarette.
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"The Health Professionals and Nurses' Health study showed an association of at least three to four decades between tobacco exposure and colorectal cancer diagnosis [39, 40]. It is believed that previous research had difficulty identifying this association due to the long latency period and also because of the association due to the extensive time lag between smoking and the occurrence of an adenocarcinoma . The latency estimates provided inTable 2 range from 29.8 years for rectal cancer to 57 years for traverse colon cancer which complement existing research in the field. "
[Show abstract][Hide abstract]ABSTRACT: Mathematical models can be useful tools in exploring population disease trends over time and can be used to gain insight into the fundamental mechanisms of cancer development. In this paper, we provide a systematic comparison between the exact and the approximate solutions for estimating the length of time between the biological initiation of cancer and diagnosis through the development of a Weibull-like survival model. A total of 1,608,484 malignant primary cancers were used in the analysis using cancer incidence data obtained from the National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) program. We find that the approximate solution provides a reliable comparison of the latency periods for different types of cancer and has no significant effect on the estimation accuracy, which differs from the exact solution by 0% to 11.3%. Thirty-five of the 44 cancers in this analysis were found to progress silently for 10 years or longer prior to detection representing 89% of the patients in this analysis. The results of this analysis differentiate cancer types that progress undetected over a period of years to identify new opportunities for early detection which increases the likelihood of successful treatment and alleviates the ever-growing cancer burden.
"Following the increased use of colonoscopy for CRC screening in the 1980s, several studies reported an increase in colorectal adenomas among heavy, long-term cigarette smokers121314151617. After this point, both case–control181920212223 and cohort studies [13, 14,24252627 reported significant increases in colorectal cancer risk for individuals who reported having a smoking history of more than 30 years. The biological mechanism remains unclear but may be due to known colorectal carcinogens (tobaccospecific nitrosamines and heterocyclic amines) that are contained in cigarette smoke [28– 30]. "
[Show abstract][Hide abstract]ABSTRACT: Studies published prior to 1980 failed to find an association between smoking and colorectal cancer, while subsequent studies reported an association after accounting for a three to four decade initiation period. The aims of this study were to determine the effect of accounting for secondhand smoke (SHS) exposure on the association between smoking and colorectal cancer and to determine the association between SHS and colorectal cancer.
Approximately 1,200 colorectal cancer cases treated at Roswell Park Cancer Institute between 1982 and 1998 were matched to 2,400 malignancy-free controls. The effect of accounting for SHS exposure was determined by comparing the odds ratios (OR) for each smoking variable in the overall sample and then for those who reported no current SHS exposure.
A small, significant increase in colorectal cancer odds was noted for heavy, long-term smoking males when not accounting for SHS exposure (>45 PY: OR = 1.34; 95% CI 1.04-1.72). OR increased when the analyses were restricted to individuals reporting no current SHS exposure (>45 PY: OR = 2.40; 95% CI 1.36-4.23).
Accounting for SHS exposure resulted in a substantial increase in the odds of colorectal cancer for all smoking variables in this study. Future studies should account for SHS exposure when examining the association between smoking and colorectal cancer.
Full-text · Article · Apr 2010 · Cancer Causes and Control
"Its real causes are not known. The investigation has shown that people with certain risk factors, like age, diet, smoking or certain genetic alterations, have more probability than others to develop colorectal cancer (Luchtenborg et al., 2007; Schafmayer et al., 2007; Young, 2007). In this sense, the development of tools for search of Colorectal Cancer biomarkers becomes of the major importance (Yasui et al., 2003). "
[Show abstract][Hide abstract]ABSTRACT: The combination of the network theory and the calculation of topological indices (TIs) allow establishing relationships between the molecular structure of large molecules like the genes and proteins and their properties at a biological level. This type of models can be considered quantitative structure-activity relationships (QSAR) for biopolymers. In the present work a QSAR model is reported for proteins, related to human colorectal cancer (HCC) and codified by different genes that have been identified experimentally by Sjöblom et al. [2006. The consensus coding sequences of human breast and colorectal cancers. Science 314, 268-274] among more than 10000 human genes. The 69 proteins related to human colorectal cancer (HCCp) and a control group of 200 proteins not related to HCC (no-HCCp) were represented through an HP Lattice type Network. Starting from the generated graphs we calculate a set of descriptors of electrostatic potential type (xi(k)) that allow to establish, through a linear discriminant analysis (LDA), a QSAR model of relatively high percentage of good classification (higher than 80%) to differentiate between HCCp and no-HCCp proteins. The purpose of this study is helping to predict the possible implication of a certain gene and/or protein (biomarker) in the colorectal cancer. Different procedures of validation of the obtained model have been carried out in order to corroborate its stability, including cross-validation series (CV) and evaluation of an additional series of 200 no-HCCp. This biostatistic methodology could be applied to predict human colorectal cancer biomarkers and to understand much better the biological aspects of this disease.