erbB expression changes in ethanol and 7,12- dimethylbenz (a)anthracene-induced oral carcinogenesis

Jacinto-Alemán, Luís Fernando; García‐Carrancá, Alejandro; Leyba-Huerta, Elba Rosa; Zenteno, Edgar; Jiménez-Farfán, María Dolores; Hernández‐Guerrero, Juan Carlos

doi:10.4317/medoral.18068

Cited by 4 publications

(2 citation statements)

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“…Among the HPV-negative patients, ERBB2 gene amplification occurred only in moderate and heavy alcohol drinkers. In a murine model, ERBB2 expression was increased in alcohol-exposed mucosa, dysplasia, and invasive oral carcinomas [ 17 ], which may support our results. Concerning esophageal [ 18 ] and breast cancer [ 19 ], in both of which alcohol consumption is a risk factor [ 7 ] and ERBB2 gene amplification was reported.…”

Section: Discussionsupporting

confidence: 87%

Distinct Effects of Alcohol Consumption and Smoking on Genetic Alterations in Head and Neck Carcinoma

et al. 2013

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BackgroundTobacco and alcohol consumption are risk factors for head and neck squamous cell carcinoma (HNSCC). Recently, whole-exome sequencing clarified that smoking increased TP53 and other mutations in HNSCC; however, the effects of alcohol consumption on these genetic alterations remain unknown. We explored the association between alcohol consumption and somatic copy-number alterations (SCNAs) across the whole genome in human papillomavirus (HPV)-negative HNSCCs, and compared with the effects of smoking on genetic alterations.MethodsSCNA and TP53 mutations in tumor samples were examined by high-resolution comparative genomic hybridization microarray 180K and by direct sequencing, respectively, and statistically analyzed for associations with alcohol consumption and smoking during the 20 years preceding diagnosis of HNSCC. Probes with a corrected p-value (=q-value) less than 0.05 and fold change greater than 1.2 or less than -1.2 were considered statistically significant.ResultsA total of 248 patients with HNSCC were enrolled. In the HPV-negative patients (n=221), heavy alcohol consumption was significantly associated with SCNAs of oncogenes/oncosuppressors that were previously reported to occur frequently in HNSCCs: CDKN2A (q=0.005), FHIT (q=0.005), 11q13 region including CCND1, FADD and CTTN (q=0.005), ERBB2 (HER2) (q=0.009), 3q25-qter including CCNL1, TP63, DCUN1D1 and PIK3CA (q=0.014), and CSMD1 (q=0.019). But, TP53 mutations were not affected. In contrast, smoking was associated with increased risk of TP53 mutations, but did not induce any significant SCNAs of oncogenes/oncosuppressors. ConclusionThese results suggest that both alcohol consumption and smoking had distinct effects on genetic alterations in HNSCCs. Heavy alcohol consumption may trigger previously known and unknown SCNAs, but may not induce TP53 mutation. In contrast, smoking may induce TP53 mutation, but may not trigger any SCNAs.

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Section: Discussionsupporting

confidence: 87%

Distinct Effects of Alcohol Consumption and Smoking on Genetic Alterations in Head and Neck Carcinoma

et al. 2013

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“…Some research groups implemented our hamster model of sequential carcinogenesis in order to evaluate the expression of biomarkers such as P53, BCL2, RB1 and ERBB2 (24). An Indian group used the hamster model of sequential carcinogenesis in order to study the role of Wnt/β-catenin signaling pathway during progression of oral squamous cell carcinoma.…”

Section: Articles Citing the Foundation Report On The Hamster Model Omentioning

confidence: 99%

The Hamster Model of Sequential Oral Carcinogenesis: An Update

Yapijakis

Kalogera²,

Papakosta

et al. 2019

In Vivo

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Characterization of Chemically Induced Ovarian Carcinomas in an Ethanol-Preferring Rat Model: Influence of Long-Term Melatonin Treatment

et al. 2013

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Ovarian cancer is the fourth most common cause of cancer deaths among women, and chronic alcoholism may exert co-carcinogenic effects. Because melatonin (mel) has oncostatic properties, we aimed to investigate and characterize the chemical induction of ovarian tumors in a model of ethanol-preferring rats and to verify the influence of mel treatment on the overall features of these tumors. After rats were selected to receive ethanol (EtOH), they were surgically injected with 100 µg of 7,12-dimethyl-benz[a]anthracene (DMBA) plus sesame oil directly under the left ovarian bursa. At 260 days old, half of the animals received i.p. injections of 200 µg mel/100 g b.w. for 60 days. Four experimental groups were established: Group C, rats bearing ovarian carcinomas (OC); Group C+EtOH, rats voluntarily consuming 10% (v/v) EtOH and bearing OC; Group C+M, rats bearing OC and receiving mel; and Group C+EtOH+M, rats with OC consuming EtOH and receiving mel. Estrous cycle and nutritional parameters were evaluated, and anatomopathological analyses of the ovarian tumors were conducted. The incidence of ovarian tumors was higher in EtOH drinking animals 120 days post-DMBA administration, and mel efficiently reduced the prevalence of some aggressive tumors. Although mel promoted high EtOH consumption, it was effective in synchronizing the estrous cycle and reducing ovarian tumor mass by 20%. While rats in the C group displayed cysts containing serous fluid, C+EtOH rats showed solid tumor masses. After mel treatment, the ovaries of these rats presented as soft and mobile tissues. EtOH consumption increased the incidence of serous papillary carcinomas and sarcomas but not clear cell carcinomas. In contrast, mel reduced the incidence of sarcomas, endometrioid carcinomas and cystic teratomas. Combination of DMBA with EtOH intake potentiated the incidence of OC with malignant histologic subtypes. We concluded that mel reduces ovarian masses and the incidence of adenocarcinomas in ethanol-deprived rats.

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erbB expression changes in ethanol and 7,12- dimethylbenz (a)anthracene-induced oral carcinogenesis

Cited by 4 publications

References 28 publications

Distinct Effects of Alcohol Consumption and Smoking on Genetic Alterations in Head and Neck Carcinoma

Distinct Effects of Alcohol Consumption and Smoking on Genetic Alterations in Head and Neck Carcinoma

The Hamster Model of Sequential Oral Carcinogenesis: An Update

Characterization of Chemically Induced Ovarian Carcinomas in an Ethanol-Preferring Rat Model: Influence of Long-Term Melatonin Treatment

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