scholarly journals Second cancer risk in adults receiving autologous haematopoietic SCT for cancer: a population-based cohort study

2014 ◽  
Vol 49 (5) ◽  
pp. 691-698 ◽  
Author(s):  
I A Bilmon ◽  
◽  
L J Ashton ◽  
R E Le Marsney ◽  
A J Dodds ◽  
...  
2021 ◽  
Vol 11 ◽  
Author(s):  
Yin-Che Lu ◽  
Pin-Tzu Chen ◽  
Mei-Chen Lin ◽  
Che-Chen Lin ◽  
Shi-Heng Wang ◽  
...  

Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce mortality in patients with cancer, especially breast cancer, but their influence on second cancer risk is uncertain. This study aimed to examine whether NSAID use is associated with second cancer risk in patients with breast cancer. This population-based propensity score-matched cohort study using Taiwan’s National Health Insurance Research Database enrolled patients with newly diagnosed breast cancer (n = 7356) with and without (n = 1839) NSAID therapy from 2000 to 2009. They were followed up until the diagnosis of second cancer, death, or end of 2011. Cox proportional hazard models were used to estimate adjusted hazard ratios (aHR). The NSAID cohort had a lower incidence rate of second cancer than the non-NSAID cohort (5.57 vs. 9.19 per 1,000 person-years), with an aHR of 0.63 (95% confidence interval (CI) 0.46–0.87). When compared with the non-NSAID cohort, the second cancer incidence was lower in patients taking non-cyclooxygenase 2 inhibitors (aHR 0.67, 95% CI 0.47–0.94) and in those receiving multiple NSAIDs during follow-up (aHR 0.55, 95% CI 0.37–0.84). A dose–response relationship existed in NSAID cumulative days. The findings demonstrate that NSAID use reduces second cancer risk in a dose-dependent manner in patients with primary breast cancer.


Author(s):  
Sonia Guleria ◽  
Allan Jensen ◽  
Vanna Albieri ◽  
Bugge Nøhr ◽  
Kirsten Frederiksen ◽  
...  

2014 ◽  
Vol 62 (2) ◽  
pp. 311-316 ◽  
Author(s):  
Dana L. Casey ◽  
Danielle N. Friedman ◽  
Chaya S. Moskowitz ◽  
Patrick D. Hilden ◽  
Charles A. Sklar ◽  
...  

1992 ◽  
Vol 3 (5) ◽  
pp. 419-425 ◽  
Author(s):  
Hans-Olov Adami ◽  
Joseph K. McLaughlin ◽  
Ann W. Hsing ◽  
Alicja Wolk ◽  
Anders Ekbom ◽  
...  

2014 ◽  
Vol 110 (3) ◽  
pp. 471-476 ◽  
Author(s):  
Yasser Abo-Madyan ◽  
Muhammad Hammad Aziz ◽  
Moamen M.O.M. Aly ◽  
Frank Schneider ◽  
Elena Sperk ◽  
...  

2009 ◽  
Vol 27 (6) ◽  
pp. 967-973 ◽  
Author(s):  
Anil K. Chaturvedi ◽  
Ruth A. Kleinerman ◽  
Allan Hildesheim ◽  
Ethel S. Gilbert ◽  
Hans Storm ◽  
...  

Purpose Although cervical squamous cell carcinoma (SCC) and adenocarcinoma (AC) are both caused by human papillomavirus (HPV) infection, they differ in cofactors such as cigarette smoking. We assessed whether these cofactor differences translate into differences in second cancer risk. Patients and Methods We assessed second cancer risk among 85,109 cervical SCC and 10,280 AC survivors reported to population-based cancer registries in Denmark, Finland, Norway, Sweden, and the United States. Risks compared to the general population were assessed using standardized incidence ratios (SIR). Results Overall cancer risk was significantly increased among both cervical SCC survivors (n = 10,559 second cancers; SIR, 1.31; 95% CI, 1.29 to 1.34) and AC survivors (n = 920 second cancers; SIR, 1.29; 95% CI, 1.22 to 1.38). Risks of HPV-related and radiation-related cancers were increased to a similar extent among cervical SCC and AC survivors. Although significantly increased in both groups when compared with the general population, risk of smoking-related cancers was significantly higher among cervical SCC than AC survivors (P = .015; SIR for cervical SCC = 2.07 v AC = 1.78). This difference was limited to lung cancer (SIR for cervical SCC = 2.69 v AC = 2.18; P = .026). The increased lung cancer risk among cervical AC survivors was observed for both lung SCC and lung AC. SIRs for second cancers of the colon, soft tissue, melanoma, and non-Hodgkin's lymphoma were significantly higher among cervical AC than SCC survivors. Conclusion The second cancer profiles among cervical SCC and AC survivors mirror the similarities and differences in cofactors for these two histologies. Because smoking is not a cofactor for cervical AC, the increased lung cancer risk suggests a role for additional factors.


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