Lung Cancer and Environmental Chemical Exposure: A Review of Our Current State of Knowledge With Reference to the Role of Hormones and Hormone Receptors as an Increased Risk Factor for Developing Lung Cancer in Man

Fucic, Alexandra; Gamulin, Marija; Ferenčić, Željko; Rokotov, Dinko Stancic; Katic, Jelena; Bartoňová, Alena; Lovasić, Ingrid Belac; Merlo, Domenico Franco

doi:10.1177/0192623310378136

Cited by 37 publications

(23 citation statements)

References 90 publications

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“…In fact, regulations on pollutants should take into account new scientific evidences on age and gender differential susceptibilities [105,106].…”

Section: Resultsmentioning

confidence: 99%

“…Substances with estrogenic actiivity may promote neoplastic changes in specific tissues, as in case of breast and lung cancer [18][19][20][21]; the case of another major cancer, colorectal cancer, is more difficult. Colon epithelium is rich of ERbeta receptors and an estrogenic action may significantly increase the cancer metastic potency [22]; however, the impacts, whether protective or adverse, of estrogen and estrogen-acrtive substances on cancer promotion are still matter of discussion [23,24].…”

Section: Introductionmentioning

confidence: 99%

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Gender and Age Related Modulation of Xenoestrogen-Induced Tumorigenesis

Fučić¹,

Mantovani²

2015

TOBIOTJ

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Susceptibility to environmental stressors, same as cancer incidence is both age and gender related. Understanding the complexity of responses to living environment has been impaireddue to research based on reductionisms and lack of methods, models and sophisticated softwares which enable analysis of complex pathways which may be disturbed by xenobotics. Impact of estrogen on development, maturation and homeostasis of organism in both genders is now well recognised and environmental investigations are currently making major efforts to understand how xenoestrogens affect organisms at very low doses.Additionally, it is of great interest to learn possible synergistic or antagonistic effects of xenoestrogen mixtures on adult organism and during development. The aim of this paper is to review the findings on the association between cancer risk and the endocrine disrupters which directly or indirectly mimic estrogen action.

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“…In fact, regulations on pollutants should take into account new scientific evidences on age and gender differential susceptibilities [105,106].…”

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Gender and Age Related Modulation of Xenoestrogen-Induced Tumorigenesis

Fučić¹,

Mantovani²

2015

TOBIOTJ

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“…Additionally, exposure to environmental-chemical carcinogens are other associated risk factors (3). The mechanism of lung tumorigenesis is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Single-nucleotide polymorphism (c.309T>G) in the MDM2 gene and lung cancer risk

et al. 2014

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Abstract. Murine double minute 2 (MDM2) is a negative regulator of p53. A single-nucleotide polymorphism (SNP) (rs2279744: c.309T>G) in the promoter region of the MDM2 gene has been shown to result in higher levels of MDM2 RNA and protein. Regarding the contribution of c.309T>G in the MDM2 gene to the lung cancer risk, previous studies are conflicting. In order to evaluate the association between c.309T>G and the lung cancer risk, a case-control study was performed. The MDM2 genotypes were determined in 762 lung cancer patients and in 700 cancer-free control subjects using the Smart Amplification Process. Statistical adjustment was performed for gender, age and pack-years of smoking. The distributions of c.309T>G (T/T, T/G, G/G) were 20.1, 49.7, 30.2% in the case group and 21.7, 47.9, 30.4% in the healthy-control group. There were no overall associations between the MDM2 genotypes and the risk of lung cancer [T/G genotype: Adjusted odds ratio (AOR), 1.30; 95% confidence interval (CI), 0.88-1.93; and G/G genotype: AOR, 1.18; 95% CI, 0.78-1.80]. The subgroup analysis of gender, histology, smoking status and epidermal growth factor receptor mutation status also indicated that there was no association with lung cancer. Additionally, the genotypes did not have an effect on the age at the time of diagnosis of lung cancer (P=0.25). In conclusion, the G allele frequency in the lung cancer cases was 0.551, which was similar to other studies. The results of the present study suggest that the c.309T>G is not significantly associated with lung cancer.

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“…These inflammatory mediators may further promote neoplasia by inducing preneoplastic mutation, proliferation, resistance to apoptosis, invasiveness, angiogenesis, and secretion of immune suppressive factors [3]. Aside from the tumorigenic effects of NNK alone, emerging data suggested that other environmental toxicants are also considered to play significant roles in the development of lung cancer [4]. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a member of the polyhalogenated aromatic hydrocarbon family and is one of the most toxic environmental compounds produced by industrial combustion and chemical manufacturing processes [5].…”

Section: Introductionmentioning

confidence: 99%

The regulation of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumor promotion by estradiol in female A/J mice

et al. 2013

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Epidemiological studies indicate that women are at a higher risk developing lung cancer than men are. It is suggested that estrogen is one of the most important factors in lung cancer development in females. Additionally, cigarette smoke, and environmental pollutants, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), may play salient roles in female lung carcinogenesis. However, the mechanisms responsible for the interaction of these factors in the promotion of lung cancer are still poorly understood. The present study was designed to explore two ideas: first, the synergistic lung tumorigenic effects of 4-(methylnitrosamino)-1-(3-pyridyl)-butanol (NNK) combined with TCDD, 17b-estradiol (E2) or both through a long-term treatment experiment, and second, to identify early changes in the inflammatory and signaling pathways through short-term treatment experiments. The results indicate that A/J mice given E2 had strong effects in potentiating NNK-induced activation of MAPK signaling, NFkB, and COX-2 expression. In the long-term exposure model, E2 had a strong tumor promoting effect, whereas TCDD antagonized this effect in A/J mice. We conclude that treatment with NNK combined with either E2 or TCDD induces lung carcinogenesis and the promotion effects could be correlated with lung inflammation. E2 was shown to potentiate NNK-induced inflammation, cell proliferation, thereby leading to lung tumorigenesis.

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Lung Cancer and Environmental Chemical Exposure: A Review of Our Current State of Knowledge With Reference to the Role of Hormones and Hormone Receptors as an Increased Risk Factor for Developing Lung Cancer in Man

Cited by 37 publications

References 90 publications

Gender and Age Related Modulation of Xenoestrogen-Induced Tumorigenesis

Gender and Age Related Modulation of Xenoestrogen-Induced Tumorigenesis

Single-nucleotide polymorphism (c.309T>G) in the MDM2 gene and lung cancer risk

The regulation of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumor promotion by estradiol in female A/J mice

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