Gene Polymorphisms in Detoxification Enzymes as Susceptibility Factor for Head and Neck Cancer?

Gronau, Silke; Koenig-Greger, D.; Jerg, M; Riechelmann, Herbert

doi:10.1016/s0194-59980300176-1

Cited by 9 publications

(2 citation statements)

References 15 publications

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“…GST activities toward CDNB did not differ between the cisplatin‐treated Gstm1 / Gstt1 ‐DKO and WT mice, suggesting that other GST family members or other enzymes involved in cisplatin metabolism may have a compensating mechanism. This result is consistent with those of previous studies, which found that those with GSTM1 null mutation had equivalent GST enzyme activity to individuals who had a functional GSTM1 enzyme 67,68 …”

Section: Discussionsupporting

confidence: 93%

“…This result is consistent with those of previous studies, which found that those with GSTM1 null mutation had equivalent GST enzyme activity to individuals who a functional GSTM1 enzyme. 67,68 NRF2 regulates the expression of numerous antioxidant genes that are vital for the cellular defense system, particularly in the management of oxidative stress. 69 GSTM1 is a direct target of NRF2.…”

Section: Discussionmentioning

confidence: 99%

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Gstm1/Gstt1 is essential for reducing cisplatin ototoxicity in CBA/CaJ mice

Liu

Wang

et al. 2022

The FASEB Journal

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Cisplatin is a widely used chemotherapeutic agent. However, its clinical utility is limited because of cisplatin‐induced ototoxicity. Glutathione S‐transferase (GST) was found to play a vital role in reducing cisplatin ototoxicity in mice. Deletion polymorphisms of GSTM1 and GSTT1, members of the GST family, are common in humans and are presumed to be associated with cisplatin‐induced hearing impairment. However, the specific roles of GSTM1 and GSTT1 in cisplatin ototoxicity are not completely clear. Here, under cisplatin treatment, simultaneous deletion of Gstm1 and Gstt1 lead to a more profound hearing loss in CBA/CaJ mice (Gstm1/Gstt1‐DKO) than in wild‐type mice. The Gstm1/Gstt1‐DKO mice, in which phase II detoxification genes were upregulated, exhibited more severe oxidative stress and higher outer hair cell apoptosis in the cochleae than the control mice. Thus, our study revealed that Gstm1 and Gstt1 protect auditory hair cells from cisplatin‐induced ototoxicity in the CBA/CaJ mice, and genetic screening for GSTM1 and GSTT1 polymorphisms could help determine a standard cisplatin dose for cancer patients undergoing chemotherapy.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Gstm1/Gstt1 is essential for reducing cisplatin ototoxicity in CBA/CaJ mice

Liu

Wang

et al. 2022

The FASEB Journal

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Smoking and drinking can induce p15 methylation in the upper aerodigestive tract of healthy individuals and patients with head and neck squamous cell carcinoma

Chang

Ling

Wei

et al. 2004

Cancer

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BACKGROUND The consumption of tobacco and alcohol has been implicated in the development of head and neck squamous cell carcinoma (HNSCC). Promoter methylation of tumor suppressor genes is common in HNSCC. In this study, the authors evaluated the effects of tobacco and alcohol on p15 gene methylation of cells in cells from the mouth and throat of physically healthy individuals and patients with HNSCC. METHODS The study participants were divided into 3 groups, including a group of 37 healthy nonsmokers and nondrinkers, a group of 22 healthy smokers and/or drinkers and a group of 31 patients with HNSCC. RESULTS Methylation of p15 was detected in cells obtained from mouth and throat (M&T) rinsing fluid samples from 3 of 37 healthy individuals (8%) who did not drink or smoke, from 15 of 22 healthy smokers and/or drinkers (68%), and from 15 of 31 patients (48%) with HNSCC. Among 31 patients with HNSCC, 20 patients (65%) had methylated p15 gene in their tumor biopsies. With the use of β‐actin as a reference, the ratio of methylated p15 to β‐actin was calculated as an index of the percentage of cells with p15 methylation. The percentage of exfoliated cells from M&T rinsing fluid samples that had p15 methylation ranged from 0% to 11% for patients with HNSCC and from 0% to 21% for healthy smokers/drinkers, respectively. The methylation index of tumor cells with p15 methylation ranged from 0% to 65%. CONCLUSIONS The results suggest that p15 gene methylation can be induced by chronic smoking and drinking and may play a role in the very early stages of carcinogenesis in HNSCC. Cancer 2004. © 2004 American Cancer Society.

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