In the Journals

Cigarette smoking linked to synchronous colorectal cancers

Investigators associated cigarette smoking with an increased risk for synchronous colorectal cancers in a prospective study.

“This association is significantly stronger than that with the risk of solitary CRC,” Andrew T. Chan, MD, MPH, of the division of gastroenterology at Massachusetts General Hospital and Harvard Medical School, and colleagues wrote. “Furthermore, our results suggest that, compared with current smoking, smoking cessation is associated with a reduced risk of synchronous CRCs, implying that the field effect associated with smoking may be paused or reversed in the absence of exposure.”

Andrew T. Chan, MD, MPH

Andrew T. Chan

Chan and colleagues evaluated the link between smoking status and the incidence of solitary and multiple primary CRCs in 134,305 participants within the Health Professionals Follow-up Study and the Nurses’ Health Study. Overall, 1,981 solitary CRCs and 45 synchronous CRCs occurred.

The investigators found that the associations between smoking status and CRC was significantly different depending on tumor synchronicity (P for heterogeneity < .001). Current smokers had a significantly higher risk for synchronous CRC compared with individuals who had never smoked (HR = 5.27; 95% CI, 2.08-13.4) but not for solitary CRC (HR = 0.97; 95% CI, 0.83-1.14).

Further, longer smoking duration measured in cumulative pack years was linked to a higher risk for both synchronous and solitary CRCs, but the association was stronger for synchronous CRCs (P for heterogeneity = .006).

Similarly, longer duration of smoking cessation appeared to be associated with a reduced risk for synchronous CRCs compared with that of individuals who had never smoked (P for heterogeneity = .001). Multivariable analysis showed that having quit smoking for at least 10 years was associated with a significantly lower risk for synchronous CRC compared with that of current smokers (HR = 0.42; 95% CI, 0.19-0.95), but this effect was no observed for solitary CRC.

Finally, the link between smoking and synchronous CRC appeared more significant than the link between smoking and solitary CRCs that were positive for CpG island methylator phenotype-high, microsatellite instability-high or BRAF mutation subtypes (P for heterogeneity = .002).

“Our results provide insight into the mechanisms of colorectal carcinogenesis and add further scientific support for the field effect theory of carcinogenesis,” the investigators concluded. “Moreover, these findings also highlight the importance of smoking cessation and abstinence as a component of CRC prevention strategies.” – by Adam Leitenberger

Disclosures: Chan reports he previously served as a consultant for Bayer Healthcare, Millennium Pharmaceuticals, Aralaz Pharmaceuticals and Pfizer. Please see the full study for a list of all other researchers’ relevant financial disclosures.

Investigators associated cigarette smoking with an increased risk for synchronous colorectal cancers in a prospective study.

“This association is significantly stronger than that with the risk of solitary CRC,” Andrew T. Chan, MD, MPH, of the division of gastroenterology at Massachusetts General Hospital and Harvard Medical School, and colleagues wrote. “Furthermore, our results suggest that, compared with current smoking, smoking cessation is associated with a reduced risk of synchronous CRCs, implying that the field effect associated with smoking may be paused or reversed in the absence of exposure.”

Andrew T. Chan, MD, MPH

Andrew T. Chan

Chan and colleagues evaluated the link between smoking status and the incidence of solitary and multiple primary CRCs in 134,305 participants within the Health Professionals Follow-up Study and the Nurses’ Health Study. Overall, 1,981 solitary CRCs and 45 synchronous CRCs occurred.

The investigators found that the associations between smoking status and CRC was significantly different depending on tumor synchronicity (P for heterogeneity < .001). Current smokers had a significantly higher risk for synchronous CRC compared with individuals who had never smoked (HR = 5.27; 95% CI, 2.08-13.4) but not for solitary CRC (HR = 0.97; 95% CI, 0.83-1.14).

Further, longer smoking duration measured in cumulative pack years was linked to a higher risk for both synchronous and solitary CRCs, but the association was stronger for synchronous CRCs (P for heterogeneity = .006).

Similarly, longer duration of smoking cessation appeared to be associated with a reduced risk for synchronous CRCs compared with that of individuals who had never smoked (P for heterogeneity = .001). Multivariable analysis showed that having quit smoking for at least 10 years was associated with a significantly lower risk for synchronous CRC compared with that of current smokers (HR = 0.42; 95% CI, 0.19-0.95), but this effect was no observed for solitary CRC.

Finally, the link between smoking and synchronous CRC appeared more significant than the link between smoking and solitary CRCs that were positive for CpG island methylator phenotype-high, microsatellite instability-high or BRAF mutation subtypes (P for heterogeneity = .002).

“Our results provide insight into the mechanisms of colorectal carcinogenesis and add further scientific support for the field effect theory of carcinogenesis,” the investigators concluded. “Moreover, these findings also highlight the importance of smoking cessation and abstinence as a component of CRC prevention strategies.” – by Adam Leitenberger

Disclosures: Chan reports he previously served as a consultant for Bayer Healthcare, Millennium Pharmaceuticals, Aralaz Pharmaceuticals and Pfizer. Please see the full study for a list of all other researchers’ relevant financial disclosures.