Fertility drugs increase cancer risk

2008 ◽  
Vol 200 (2686) ◽  
pp. 14
Author(s):  
Alison Motluk ◽  
Celeste Biever
Author(s):  
Patrick J. Sheehan ◽  
Ryan C. Lewis ◽  
Christopher R. Kirman ◽  
Heather N. Watson ◽  
Eric D. Winegar ◽  
...  

Given ubiquitous human exposure to ethylene oxide (EO), regardless of occupation or geography, the current risk-specific concentrations (RSCs: 0.0001–0.01 ppb) from the U.S. Environmental Protection Agency (EPA) cancer risk assessment for EO are not useful metrics for managing EO exposures to the general U.S. population. The magnitude of the RSCs for EO are so low, relative to typical endogenous equivalent metabolic concentrations (1.1–5.5 ppb) that contribute ~93% of total exposure, that the RSCs provide little utility in identifying excess environmental exposures that might increase cancer risk. EO monitoring data collected in the vicinity of eight EO-emitting facilities and corresponding background locations were used to characterize potential excess exogenous concentrations. Both 50th and 90th percentile exogenous exposure concentrations were combined with the 50th percentile endogenous exposure concentration for the nonsmoking population, and then compared to percentiles of total equivalent concentration for this population. No potential total exposure concentration for these local populations exceeded the normal total equivalent concentration 95th percentile, indicating that excess facility-related exposures are unlikely to require additional management to protect public health.


2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
QingAn Yu ◽  
XiaoYing Lv ◽  
KunPeng Liu ◽  
DaKun Ma ◽  
YaoHua Wu ◽  
...  

Associations have been demonstrated between fertility drugs and a variety of hormone-sensitive carcinomas. The purpose of this study was to determine the relationship between fertility drugs used in the treatment of female infertility and the risk of thyroid cancer. To investigate the clinical significance of fertility drugs used for the treatment of female infertility and the risk associated with thyroid cancer, we performed a literature search using PubMed, MEDLINE, the Cochrane Library, the Web of Science, and EBSCOHOST for comparative studies published any time prior to July 21, 2017. The studies included women who were treated for infertility with fertility drugs, such as clomiphene citrate, gonadotropins, or other unspecified fertility agents, which reported the incidence of thyroid cancer as the main outcome. Eight studies were included in the meta-analyses. Among women with infertility, there was a significant positive association between thyroid cancer risk and the use of fertility drugs (relative risk [RR] = 1.35; 95% confidence interval [CI] 1.12–1.64; P=0.002). Additionally, among women with infertility, the use of clomiphene citrate was associated with an increased risk of thyroid cancer compared to women who did not use fertility drugs (RR = 1.45; 95% CI 1.12–1.88; P=0.005). After pooling results, we found that the parity status of infertile women using fertility drugs was not associated with thyroid cancer risk (RR = 0.99; 95% CI 0.61–1.58, P=0.95). In summary, clomiphene citrate (the most commonly used fertility drug) and other fertility drugs are associated with an increased risk of thyroid cancer.


2017 ◽  
Vol 45 (9) ◽  
pp. 1213-1224 ◽  
Author(s):  
G. L.-H. Wong ◽  
Y.-K. Tse ◽  
T. C.-F. Yip ◽  
H. L.-Y. Chan ◽  
K. K.-F. Tsoi ◽  
...  

Blood ◽  
2012 ◽  
Vol 120 (18) ◽  
pp. 3764-3773 ◽  
Author(s):  
Shuyun Rao ◽  
Sang-Yun Lee ◽  
Alejandro Gutierrez ◽  
Jacqueline Perrigoue ◽  
Roshan J. Thapa ◽  
...  

Abstract Ribosomal protein (RP) mutations in diseases such as 5q− syndrome both disrupt hematopoiesis and increase the risk of developing hematologic malignancy. However, the mechanism by which RP mutations increase cancer risk has remained an important unanswered question. We show here that monoallelic, germline inactivation of the ribosomal protein L22 (Rpl22) predisposes T-lineage progenitors to transformation. Indeed, RPL22 was found to be inactivated in ∼ 10% of human T-acute lymphoblastic leukemias. Moreover, monoallelic loss of Rpl22 accelerates development of thymic lymphoma in both a mouse model of T-cell malignancy and in acute transformation assays in vitro. We show that Rpl22 inactivation enhances transformation potential through induction of the stemness factor, Lin28B. Our finding that Rpl22 inactivation promotes transformation by inducing expression of Lin28B provides the first insight into the mechanistic basis by which mutations in Rpl22, and perhaps some other RP genes, increases cancer risk.


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